Agents and endogenous substances that antagonize or inhibit the development of new blood vessels.
Six-carbon alicyclic hydrocarbons.
A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.
Angiostatic proteins that are formed from proteolytic cleavage of COLLAGEN TYPE XVIII.
The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.
Circulating 38-kDa proteins that are internal peptide fragments of PLASMINOGEN. The name derives from the fact that they are potent ANGIOGENESIS INHIBITORS. Angiostatins contain four KRINGLE DOMAINS which are associated with their potent angiostatic activity.
An extracellular matrix glycoprotein from platelets and a variety of normal and transformed cells of both mesenchymal and epithelial origin. Thrombospondin-1 is believed to play a role in cell migration and proliferation, during embryogenesis and wound repair. Also, it has been studied for its use as a potential regulator of tumor growth and metastasis.
The original member of the family of endothelial cell growth factors referred to as VASCULAR ENDOTHELIAL GROWTH FACTORS. Vascular endothelial growth factor-A was originally isolated from tumor cells and referred to as "tumor angiogenesis factor" and "vascular permeability factor". Although expressed at high levels in certain tumor-derived cells it is produced by a wide variety of cell types. In addition to stimulating vascular growth and vascular permeability it may play a role in stimulating VASODILATION via NITRIC OXIDE-dependent pathways. Alternative splicing of the mRNA for vascular endothelial growth factor A results in several isoforms of the protein being produced.
Agents that induce or stimulate PHYSIOLOGIC ANGIOGENESIS or PATHOLOGIC ANGIOGENESIS.
A non-fibrillar collagen found in BASEMENT MEMBRANE. The C-terminal end of the alpha1 chain of collagen type XVIII contains the ENDOSTATIN peptide, which can be released by proteolytic cleavage.
Intercellular signaling peptides and proteins that regulate the proliferation of new blood vessels under normal physiological conditions (ANGIOGENESIS, PHYSIOLOGICAL). Aberrant expression of angiogenic proteins during disease states such as tumorigenesis can also result in PATHOLOGICAL ANGIOGENESIS.
Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
An extra-embryonic membranous sac derived from the YOLK SAC of REPTILES; BIRDS; and MAMMALS. It lies between two other extra-embryonic membranes, the AMNION and the CHORION. The allantois serves to store urinary wastes and mediate exchange of gas and nutrients for the developing embryo.
A 200-230-kDa tyrosine kinase receptor for vascular endothelial growth factors found primarily in endothelial and hematopoietic cells and their precursors. VEGFR-2 is important for vascular and hematopoietic development, and mediates almost all endothelial cell responses to VEGF.
A family of angiogenic proteins that are closely-related to VASCULAR ENDOTHELIAL GROWTH FACTOR A. They play an important role in the growth and differentiation of vascular as well as lymphatic endothelial cells.
These growth factors are soluble mitogens secreted by a variety of organs. The factors are a mixture of two single chain polypeptides which have affinity to heparin. Their molecular weight are organ and species dependent. They have mitogenic and chemotactic effects and can stimulate endothelial cells to grow and synthesize DNA. The factors are related to both the basic and acidic FIBROBLAST GROWTH FACTORS but have different amino acid sequences.
Mutant mice homozygous for the recessive gene "nude" which fail to develop a thymus. They are useful in tumor studies and studies on immune responses.
A family of closely related RECEPTOR PROTEIN-TYROSINE KINASES that bind vascular endothelial growth factors. They share a cluster of seven extracellular Ig-like domains which are important for ligand binding. They are highly expressed in vascular endothelial cells and are critical for the physiological and pathological growth, development and maintenance of blood and lymphatic vessels.
Soluble protein factors generated by activated lymphocytes that affect other cells, primarily those involved in cellular immunity.
The outermost extra-embryonic membrane surrounding the developing embryo. In REPTILES and BIRDS, it adheres to the shell and allows exchange of gases between the egg and its environment. In MAMMALS, the chorion evolves into the fetal contribution of the PLACENTA.
Endothelial cells that line venous vessels of the UMBILICAL CORD.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.
Precursor of plasmin (FIBRINOLYSIN). It is a single-chain beta-globulin of molecular weight 80-90,000 found mostly in association with fibrinogen in plasma; plasminogen activators change it to fibrinolysin. It is used in wound debriding and has been investigated as a thrombolytic agent.
Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.
A single-chain polypeptide growth factor that plays a significant role in the process of WOUND HEALING and is a potent inducer of PHYSIOLOGIC ANGIOGENESIS. Several different forms of the human protein exist ranging from 18-24 kDa in size due to the use of alternative start sites within the fgf-2 gene. It has a 55 percent amino acid residue identity to FIBROBLAST GROWTH FACTOR 1 and has potent heparin-binding activity. The growth factor is an extremely potent inducer of DNA synthesis in a variety of cell types from mesoderm and neuroectoderm lineages. It was originally named basic fibroblast growth factor based upon its chemical properties and to distinguish it from acidic fibroblast growth factor (FIBROBLAST GROWTH FACTOR 1).
The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.
A carcinoma discovered by Dr. Margaret R. Lewis of the Wistar Institute in 1951. This tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse. The tumor does not appear to be grossly hemorrhagic and the majority of the tumor tissue is a semifirm homogeneous mass. (From Cancer Chemother Rep 2 1972 Nov;(3)1:325) It is also called 3LL and LLC and is used as a transplantable malignancy.
New blood vessels originating from the corneal veins and extending from the limbus into the adjacent CORNEAL STROMA. Neovascularization in the superficial and/or deep corneal stroma is a sequel to numerous inflammatory diseases of the ocular anterior segment, such as TRACHOMA, viral interstitial KERATITIS, microbial KERATOCONJUNCTIVITIS, and the immune response elicited by CORNEAL TRANSPLANTATION.
Experimental transplantation of neoplasms in laboratory animals for research purposes.
Compounds that differ from COUMARINS in having the positions of the ring and ketone oxygens reversed so the keto oxygen is at the 1-position of the molecule.
A highly vascularized extra-embryonic membrane, formed by the fusion of the CHORION and the ALLANTOIS. It is mostly found in BIRDS and REPTILES. It serves as a model for studying tumor or cell biology, such as angiogenesis and TISSUE TRANSPLANTATION.
Proteins that specifically inhibit the growth of new blood vessels (ANGIOGENESIS, PHYSIOLOGIC).
In vivo methods of screening investigative anticancer drugs, biologic response modifiers or radiotherapies. Human tumor tissue or cells are transplanted into mice or rats followed by tumor treatment regimens. A variety of outcomes are monitored to assess antitumor effectiveness.
The minute vessels that connect the arterioles and venules.
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
Triple-looped protein domains linked by disulfide bonds. These common structural domains, so-named for their resemblance to Danish pastries known as kringlers, play a role in binding membranes, proteins, and phospholipids as well as in regulating proteolysis. Kringles are also present in coagulation-related and fibrinolytic proteins and other plasma proteinases.
Cell adhesion molecules present on virtually all monocytes, platelets, and granulocytes. CD31 is highly expressed on endothelial cells and concentrated at the junctions between them.
A cell line derived from cultured tumor cells.
Benzopyrroles with the nitrogen at the number one carbon adjacent to the benzyl portion, in contrast to ISOINDOLES which have the nitrogen away from the six-membered ring.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
A family of related, adhesive glycoproteins which are synthesized, secreted, and incorporated into the extracellular matrix of a variety of cells, including alpha granules of platelets following thrombin activation and endothelial cells. They interact with a number of BLOOD COAGULATION FACTORS and anticoagulant factors. Five distinct forms have been identified, thrombospondin 1, -2, -3, -4, and cartilage oligomeric matrix protein (COMP). They are involved in cell adhesion, platelet aggregation, cell proliferation, angiogenesis, tumor metastasis, VASCULAR SMOOTH MUSCLE growth, and tissue repair.
A polypeptide substance comprising about one third of the total protein in mammalian organisms. It is the main constituent of SKIN; CONNECTIVE TISSUE; and the organic substance of bones (BONE AND BONES) and teeth (TOOTH).
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).
Venous vessels in the umbilical cord. They carry oxygenated, nutrient-rich blood from the mother to the FETUS via the PLACENTA. In humans, there is normally one umbilical vein.
A multifunctional protein that is found primarily within membrane-bound organelles. In the ENDOPLASMIC RETICULUM it binds to specific N-linked oligosaccharides found on newly-synthesized proteins and functions as a MOLECULAR CHAPERONE that may play a role in PROTEIN FOLDING or retention and degradation of misfolded proteins. In addition calreticulin is a major storage form for CALCIUM and functions as a calcium-signaling molecule that can regulate intracellular calcium HOMEOSTASIS.
Transplantation between animals of different species.
A 180-kDa VEGF receptor found primarily in endothelial cells that is essential for vasculogenesis and vascular maintenance. It is also known as Flt-1 (fms-like tyrosine kinase receptor-1). A soluble, alternatively spliced isoform of the receptor may serve as a binding protein that regulates the availability of various ligands for VEGF receptor binding and signal transduction.
Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.
Cells grown in vitro from neoplastic tissue. If they can be established as a TUMOR CELL LINE, they can be propagated in cell culture indefinitely.
The finer blood vessels of the vasculature that are generally less than 100 microns in internal diameter.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
The developmental entity of a fertilized chicken egg (ZYGOTE). The developmental process begins about 24 h before the egg is laid at the BLASTODISC, a small whitish spot on the surface of the EGG YOLK. After 21 days of incubation, the embryo is fully developed before hatching.
A non-fibrillar collagen found in the structure of BASEMENT MEMBRANE. Collagen type IV molecules assemble to form a sheet-like network which is involved in maintaining the structural integrity of basement membranes. The predominant form of the protein is comprised of two alpha1(IV) subunits and one alpha2(IV) subunit, however, at least six different alpha subunits can be incorporated into the heterotrimer.
Mice homozygous for the mutant autosomal recessive gene "scid" which is located on the centromeric end of chromosome 16. These mice lack mature, functional lymphocytes and are thus highly susceptible to lethal opportunistic infections if not chronically treated with antibiotics. The lack of B- and T-cell immunity resembles severe combined immunodeficiency (SCID) syndrome in human infants. SCID mice are useful as animal models since they are receptive to implantation of a human immune system producing SCID-human (SCID-hu) hematochimeric mice.
Regulatory proteins and peptides that are signaling molecules involved in the process of PARACRINE COMMUNICATION. They are generally considered factors that are expressed by one cell and are responded to by receptors on another nearby cell. They are distinguished from HORMONES in that their actions are local rather than distal.
Cell surface receptors that bind growth or trophic factors with high affinity, triggering intracellular responses which influence the growth, differentiation, or survival of cells.
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A variation of the PCR technique in which cDNA is made from RNA via reverse transcription. The resultant cDNA is then amplified using standard PCR protocols.
Agents that modulate the PHYSIOLOGIC ANGIOGENESIS process. This is accomplished by endogenous ANGIOGENIC PROTEINS and a variety of other chemicals and pharmaceutical agents.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Tumors or cancer of the LUNG.
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
A mutant strain of Rattus norvegicus without a thymus and with depressed or absent T-cell function. This strain of rats may have a small amount of hair at times, but then lose it.
Compounds that include the amino-N-phenylamide structure.
Techniques and strategies which include the use of coding sequences and other conventional or radical means to transform or modify cells for the purpose of treating or reversing disease conditions.
A family of serine proteinase inhibitors which are similar in amino acid sequence and mechanism of inhibition, but differ in their specificity toward proteolytic enzymes. This family includes alpha 1-antitrypsin, angiotensinogen, ovalbumin, antiplasmin, alpha 1-antichymotrypsin, thyroxine-binding protein, complement 1 inactivators, antithrombin III, heparin cofactor II, plasminogen inactivators, gene Y protein, placental plasminogen activator inhibitor, and barley Z protein. Some members of the serpin family may be substrates rather than inhibitors of SERINE ENDOPEPTIDASES, and some serpins occur in plants where their function is not known.
Large, noncollagenous glycoprotein with antigenic properties. It is localized in the basement membrane lamina lucida and functions to bind epithelial cells to the basement membrane. Evidence suggests that the protein plays a role in tumor invasion.
A class of cellular receptors that have an intrinsic PROTEIN-TYROSINE KINASE activity.
Organic compounds that include a cyclic ether with three ring atoms in their structure. They are commonly used as precursors for POLYMERS such as EPOXY RESINS.
An important compound functioning as a component of the coenzyme NAD. Its primary significance is in the prevention and/or cure of blacktongue and PELLAGRA. Most animals cannot manufacture this compound in amounts sufficient to prevent nutritional deficiency and it therefore must be supplemented through dietary intake.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Single preparations containing two or more active agents, for the purpose of their concurrent administration as a fixed dose mixture.
The transparent anterior portion of the fibrous coat of the eye consisting of five layers: stratified squamous CORNEAL EPITHELIUM; BOWMAN MEMBRANE; CORNEAL STROMA; DESCEMET MEMBRANE; and mesenchymal CORNEAL ENDOTHELIUM. It serves as the first refracting medium of the eye. It is structurally continuous with the SCLERA, avascular, receiving its nourishment by permeation through spaces between the lamellae, and is innervated by the ophthalmic division of the TRIGEMINAL NERVE via the ciliary nerves and those of the surrounding conjunctiva which together form plexuses. (Cline et al., Dictionary of Visual Science, 4th ed)
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Drugs which have received FDA approval for human testing but have yet to be approved for commercial marketing. This includes drugs used for treatment while they still are undergoing clinical trials (Treatment IND). The main heading includes drugs under investigation in foreign countries.
Organic salts and esters of benzenesulfonic acid.
The uptake of naked or purified DNA by CELLS, usually meaning the process as it occurs in eukaryotic cells. It is analogous to bacterial transformation (TRANSFORMATION, BACTERIAL) and both are routinely employed in GENE TRANSFER TECHNIQUES.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Proteins prepared by recombinant DNA technology.
Culture media containing biologically active components obtained from previously cultured cells or tissues that have released into the media substances affecting certain cell functions (e.g., growth, lysis).
Domesticated bovine animals of the genus Bos, usually kept on a farm or ranch and used for the production of meat or dairy products or for heavy labor.
Glycoproteins which have a very high polysaccharide content.
An angiopoietin that is closely related to ANGIOPOIETIN-1. It binds to the TIE-2 RECEPTOR without receptor stimulation and antagonizes the effect of ANGIOPOIETIN-1. However its antagonistic effect may be limited to cell receptors that occur within the vasculature. Angiopoietin-2 may therefore play a role in down-regulation of BLOOD VESSEL branching and sprouting.
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)
The first to be discovered member of the angiopoietin family. It may play a role in increasing the sprouting and branching of BLOOD VESSELS. Angiopoietin-1 specifically binds to and stimulates the TIE-2 RECEPTOR. Several isoforms of angiopoietin-1 occur due to ALTERNATIVE SPLICING of its mRNA.
Antibodies from non-human species whose protein sequences have been modified to make them nearly identical with human antibodies. If the constant region and part of the variable region are replaced, they are called humanized. If only the constant region is modified they are called chimeric. INN names for humanized antibodies end in -zumab.
Tumors or cancers of the KIDNEY.
A group of compounds consisting in part of two rings sharing one atom (usually a carbon) in common.
The outer covering of the body that protects it from the environment. It is composed of the DERMIS and the EPIDERMIS.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.
A subclass of EXOPEPTIDASES that act on the free N terminus end of a polypeptide liberating a single amino acid residue. EC 3.4.11.
A group of compounds that contain the structure SO2NH2.
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
A TIE receptor tyrosine kinase that is found almost exclusively on ENDOTHELIAL CELLS. It is required for both normal embryonic vascular development (NEOVASCULARIZATION, PHYSIOLOGIC) and tumor angiogenesis (NEOVASCULARIZATION, PATHOLOGIC).
A heterogeneous group of sporadic or hereditary carcinoma derived from cells of the KIDNEYS. There are several subtypes including the clear cells, the papillary, the chromophobe, the collecting duct, the spindle cells (sarcomatoid), or mixed cell-type carcinoma.
The main trunk of the systemic arteries.
A sarcoma derived from deep fibrous tissue, characterized by bundles of immature proliferating fibroblasts with variable collagen formation, which tends to invade locally and metastasize by the bloodstream. (Stedman, 25th ed)
Compounds with a six membered aromatic ring containing NITROGEN. The saturated version is PIPERIDINES.
Works about pre-planned studies of the safety, efficacy, or optimum dosage schedule (if appropriate) of one or more diagnostic, therapeutic, or prophylactic drugs, devices, or techniques selected according to predetermined criteria of eligibility and observed for predefined evidence of favorable and unfavorable effects. This concept includes clinical trials conducted both in the U.S. and in other countries.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)
Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).
A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.
Established cell cultures that have the potential to propagate indefinitely.
Hypoxia-inducible factor 1, alpha subunit is a basic helix-loop-helix transcription factor that is regulated by OXYGEN availability and is targeted for degradation by VHL TUMOR SUPPRESSOR PROTEIN.
A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.
Tumors or cancer of the PROSTATE.
Elements of limited time intervals, contributing to particular results or situations.
Tumors or cancer of the COLON.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
Adherence of cells to surfaces or to other cells.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
A malignant epithelial tumor with a glandular organization.
An integrin that binds to a variety of plasma and extracellular matrix proteins containing the conserved RGD amino acid sequence and modulates cell adhesion. Integrin alphavbeta3 is highly expressed in OSTEOCLASTS where it may play role in BONE RESORPTION. It is also abundant in vascular smooth muscle and endothelial cells, and in some tumor cells, where it is involved in angiogenesis and cell migration. Although often referred to as the vitronectin receptor there is more than one receptor for vitronectin (RECEPTORS, VITRONECTIN).
An antineoplastic agent. It has significant activity against melanomas. (from Martindale, The Extra Pharmacopoeia, 31st ed, p564)
The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.
Immunologic techniques based on the use of: (1) enzyme-antibody conjugates; (2) enzyme-antigen conjugates; (3) antienzyme antibody followed by its homologous enzyme; or (4) enzyme-antienzyme complexes. These are used histologically for visualizing or labeling tissue specimens.
Antibodies produced by a single clone of cells.
Formation of new blood vessels originating from the retinal veins and extending along the inner (vitreal) surface of the retina.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
Linear POLYPEPTIDES that are synthesized on RIBOSOMES and may be further modified, crosslinked, cleaved, or assembled into complex proteins with several subunits. The specific sequence of AMINO ACIDS determines the shape the polypeptide will take, during PROTEIN FOLDING, and the function of the protein.
The action of a drug in promoting or enhancing the effectiveness of another drug.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
Restoration of integrity to traumatized tissue.
A class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. Among their common properties are a requirement for metabolic activation to intermediates with antitumor efficacy and the presence in their chemical structures of N-methyl groups, that after metabolism, can covalently modify cellular DNA. The precise mechanisms by which each of these drugs acts to kill tumor cells are not completely understood. (From AMA, Drug Evaluations Annual, 1994, p2026)
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Agents that inhibit PROTEIN KINASES.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
A common neoplasm of early childhood arising from neural crest cells in the sympathetic nervous system, and characterized by diverse clinical behavior, ranging from spontaneous remission to rapid metastatic progression and death. This tumor is the most common intraabdominal malignancy of childhood, but it may also arise from thorax, neck, or rarely occur in the central nervous system. Histologic features include uniform round cells with hyperchromatic nuclei arranged in nests and separated by fibrovascular septa. Neuroblastomas may be associated with the opsoclonus-myoclonus syndrome. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2099-2101; Curr Opin Oncol 1998 Jan;10(1):43-51)
Unique slender cells with multiple processes extending along the capillary vessel axis and encircling the vascular wall, also called mural cells. Pericytes are imbedded in the BASEMENT MEMBRANE shared with the ENDOTHELIAL CELLS of the vessel. Pericytes are important in maintaining vessel integrity, angiogenesis, and vascular remodeling.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
A condition of decreased oxygen content at the cellular level.
The giving of drugs, chemicals, or other substances by mouth.
A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.
The blood vessels which supply and drain the RETINA.
The formation of LYMPHATIC VESSELS.
A family of structurally-related angiogenic proteins of approximately 70 kDa in size. They have high specificity for members of the TIE RECEPTOR FAMILY.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
A secreted endopeptidase homologous with INTERSTITIAL COLLAGENASE, but which possesses an additional fibronectin-like domain.
Ability of neoplasms to infiltrate and actively destroy surrounding tissue.
An endopeptidase that is structurally similar to MATRIX METALLOPROTEINASE 2. It degrades GELATIN types I and V; COLLAGEN TYPE IV; and COLLAGEN TYPE V.
The treatment of a disease or condition by several different means simultaneously or sequentially. Chemoimmunotherapy, RADIOIMMUNOTHERAPY, chemoradiotherapy, cryochemotherapy, and SALVAGE THERAPY are seen most frequently, but their combinations with each other and surgery are also used.
A protein-serine-threonine kinase that is activated by PHOSPHORYLATION in response to GROWTH FACTORS or INSULIN. It plays a major role in cell metabolism, growth, and survival as a core component of SIGNAL TRANSDUCTION. Three isoforms have been described in mammalian cells.
Small double-stranded, non-protein coding RNAs (21-31 nucleotides) involved in GENE SILENCING functions, especially RNA INTERFERENCE (RNAi). Endogenously, siRNAs are generated from dsRNAs (RNA, DOUBLE-STRANDED) by the same ribonuclease, Dicer, that generates miRNAs (MICRORNAS). The perfect match of the siRNAs' antisense strand to their target RNAs mediates RNAi by siRNA-guided RNA cleavage. siRNAs fall into different classes including trans-acting siRNA (tasiRNA), repeat-associated RNA (rasiRNA), small-scan RNA (scnRNA), and Piwi protein-interacting RNA (piRNA) and have different specific gene silencing functions.
Relatively complete absence of oxygen in one or more tissues.
A basic helix-loop-helix transcription factor that plays a role in APOPTOSIS. It is composed of two subunits: ARYL HYDROCARBON RECEPTOR NUCLEAR TRANSLOCATOR and HYPOXIA-INDUCIBLE FACTOR 1, ALPHA SUBUNIT.
The property of blood capillary ENDOTHELIUM that allows for the selective exchange of substances between the blood and surrounding tissues and through membranous barriers such as the BLOOD-AIR BARRIER; BLOOD-AQUEOUS BARRIER; BLOOD-BRAIN BARRIER; BLOOD-NERVE BARRIER; BLOOD-RETINAL BARRIER; and BLOOD-TESTIS BARRIER. Small lipid-soluble molecules such as carbon dioxide and oxygen move freely by diffusion. Water and water-soluble molecules cannot pass through the endothelial walls and are dependent on microscopic pores. These pores show narrow areas (TIGHT JUNCTIONS) which may limit large molecule movement.
Time schedule for administration of a drug in order to achieve optimum effectiveness and convenience.
Experimentally induced tumor that produces MELANIN in animals to provide a model for studying human MELANOMA.
Period after successful treatment in which there is no appearance of the symptoms or effects of the disease.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
An enzyme that catalyzes the transfer of 2-deoxy-D-ribose from THYMIDINE to orthophosphate, thereby liberating thymidine.
Compounds that inhibit the enzyme activity or activation of MATRIX METALLOPROTEINASES.
Dimeric cell surface receptor involved in angiogenesis (NEOVASCULARIZATION, PHYSIOLOGICAL) and axonal guidance. Neuropilin-1 is a 140-kDa transmembrane protein that binds CLASS 3 SEMAPHORINS, and several other growth factors. Neuropilin-1 forms complexes with plexins or VEGF RECEPTORS, and binding affinity and specificity are determined by the composition of the neuropilin dimer and the identity of other receptors complexed with it. Neuropilin-1 is expressed in distinct patterns during neural development, complementary to those described for NEUROPILIN-2.
Processes required for CELL ENLARGEMENT and CELL PROLIFERATION.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
A vascular connective tissue formed on the surface of a healing wound, ulcer, or inflamed tissue. It consists of new capillaries and an infiltrate containing lymphoid cells, macrophages, and plasma cells.
A negative regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Cellular signaling in which a factor secreted by a cell affects other cells in the local environment. This term is often used to denote the action of INTERCELLULAR SIGNALING PEPTIDES AND PROTEINS on surrounding cells.

Recombinant adenovirus expressing wild-type p53 is antiangiogenic: a proposed mechanism for bystander effect. (1/4006)

Angiogenesis is required for the growth and progression of malignancies. Recent studies have demonstrated that genetic alterations may accompany acquisition of the angiogenic phenotype. The tumor suppressor gene p53 is most frequently mutated in human cancers and is also known to be a transcriptional regulator of a variety of genes. Here, we investigated the antiangiogenic effect of the wild-type p53 (wt-p53) gene transfer on a human non-small cell lung cancer cell line. Mutant p53-expressing H226Br non-small cell lung cancer cells were transduced with the wt-p53 gene using a recombinant adenoviral vector (Ad5CMVp53) and applied to semiquantitative reverse transcription-PCRs for the detection of altered mRNA expression of angiogenic and/or antiangiogenic factors. In vivo neovascularization assay of Ad5CMVp53-infected cells was then performed using a membrane-diffusion chamber system s.c. transplanted in nu/nu mice. We also evaluated the effect of Ad5CMVp53-infected H226Br cells on nontransduced tumor cells in vivo by s.c. inoculating mixture of cells into nu/nu mice. Ad5CMVp53 infection markedly inhibited the expression of an angiogenic factor, vascular endothelial growth factor, and increased the expression of a novel antiangiogenic factor, brain-specific angiogenesis inhibitor 1, resulting in reduced neovascularization in vivo. Mixing experiments showed that tumor cells transduced with the wt-p53 gene inhibited the in vivo tumor growth of adjacent nontransduced cells. Our data suggest that a recombinant adenovirus expressing the wt-p53 gene is antiangiogenic, which may explain, in part, the mechanism of the bystander effect induced by the wt-p53 gene transfer on adjacent tumor cells.  (+info)

Calreticulin and calreticulin fragments are endothelial cell inhibitors that suppress tumor growth. (2/4006)

Several angiogenesis inhibitors are fragments of larger proteins that are themselves not active as angiogenesis inhibitors. Vasostatin, the N-terminal domain of calreticulin inclusive of amino acids 1-180, is an angiogenesis inhibitor that exerts antitumor effects in vivo. In the present study, we examined whether the full-length calreticulin molecule shares the antiangiogenic and antitumor activities of vasostatin. Similar to vasostatin, calreticulin selectively inhibited endothelial cell proliferation in vitro, but not cells of other lineages, and suppressed angiogenesis in vivo. When inoculated into athymic mice, calreticulin inhibited Burkitt tumor growth comparably with vasostatin. Calreticulin lacking the N-terminal 1-120 amino acids inhibited endothelial cell proliferation in vitro and Burkitt tumor growth in vivo comparably with vasostatin. An internal calreticulin fragment encompassing amino acids 120-180 also inhibited endothelial cell proliferation in vitro and angiogenesis in vivo comparably with calreticulin and vasostatin. These results suggest that the antiangiogenic activities of vasostatin reside in a domain that is accessible from the full-length calreticulin molecule and localize to calreticulin N-terminal amino acids 120-180. Thus, calreticulin and calreticulin fragments are inhibitors of angiogenesis that directly target endothelial cells, inhibit angiogenesis, and suppress tumor growth. This information may be critical in designing targeted inhibitors of pathological angiogenesis that underlies cancer and other diseases.  (+info)

Inhibition of angiogenesis and intrahepatic growth of colon cancer by TAC-101. (3/4006)

We demonstrated in this study that inhibition of intra-hepatic growth of colon cancer by TAC-101 is mediated by inhibition of angiogenesis. In vitro experiments showed that TAC-101 inhibited the proliferation of murine hepatic sinusoidal endothelial (HSE) cells induced by coculture with murine colon 26-L5 (L5) cells. HSE cell proliferation was also enhanced by conditioned medium of L5 cells (CM-L5), and this enhancement of proliferation was abrogated by anti-vascular endothelial growth factor antibody. CM-L5 also induced in vitro tube formation of HSE cells on Matri-gel, and this activity of CM-L5 was abrogated by TAC-101 in a concentration-dependent manner. On the other hand, p.o. administration of TAC-101 inhibited tumor-induced angiogenesis in vivo and decreased the weights of L5 tumors in the mouse liver. Reverse transcriptase-PCR analysis using in vivo tumor tissue suggested that repression of vascular endothelial growth factor expression by TAC-101 was associated with the antiangiogenic activity. TAC-101 alone and 5-fluorouracil (5-FU)/D,L-leucovorin (LV) significantly inhibited the intrahepatic growth of L5 tumors (P = 0.002 and 0.001, respectively), whereas 5-FU alone did not (P = 0.088). When TAC-101 was administered with 5-FU/LV, marked enhancement of antitumor activity was observed (95% inhibition; P<0.001). This enhanced antitumor effect was also observed in experiments using Co-3 human colon adenocarcinoma. Concurrent treatment with TAC-101 and 5-FU/LV and sequential treatment with 5-FU/LV followed by TAC-101 resulted in significant augmentation of antitumor activity against Co-3 (overall P = 0.007 and 0.015, respectively). These findings indicate that TAC-101 inhibits tumor angiogenesis and suggest that it may be effective against hepatic metastasis of colon cancer.  (+info)

A pharmacokinetically guided Phase II study of carboxyamido-triazole in androgen-independent prostate cancer. (4/4006)

We conducted a Phase II clinical trial of the antiproliferative, antimetastatic, and antiangiogenic agent carboxyamido-triazole (CAI), using pharmacokinetic assessment to guide drug dosing. Fifteen patients who had stage D2 androgen-independent prostate cancer with soft tissue metastases were enrolled. Because CAI previously had been shown to decrease prostate-specific antigen secretion in vitro, this marker was not used to assess disease status. The dose of CAI used in this study was calculated so that plasma steady-state maximum concentrations between 2.0 and 5.0 microg/ml would be maintained. Following the initial dosage adjustment, 93% (14 of 15) of patients were within the predicted range. Fourteen of 15 patients were evaluable for response. All of the 14 evaluable patients demonstrated progressive disease at approximately 2 months. Twelve patients progressed by computed tomography and or bone scan at 2 months, whereas two patients demonstrated clinical progression at 1.5 and 2 months. One patient was removed from study at 6 weeks due to grade II peripheral neuropathy lasting >1 month. Although no clinical responses were noted, a 27.7% decrease in serum vascular endothelial growth factor concentration was observed. CAI does not possess clinical activity in patients with androgen-independent prostate cancer and soft tissue metastases. Pharmacokinetically guided dosing, although found to be feasible using a Bayesian approach, was not found to be of practical benefit. Although plasma CAI concentrations were maintained within the designated range, grade III toxicity requiring drug discontinuation was still observed.  (+info)

Angiogenesis inhibitor endostatin is a distinct component of elastic fibers in vessel walls. (5/4006)

Theendothelial cell inhibitor endostatin (22 kDa) is part of the carboxyl-terminal globular domain of collagen XVIII and shows a widespread tissue distribution. Immunohistology of adult mouse tissues demonstrated a preferred localization in many vessel walls and some other basement membrane zones. A strong immunogold staining was observed across elastic fibers in the multiple elastic membranes of aorta and other large arteries. Staining was less strong along sparse elastic fibers of veins and almost none was observed in the walls of arterioles and capillaries. Strong evidence was also obtained for some intracellular and basement membrane associations. Immunogold double staining of elastic fibers showed a close colocalization of endostatin with fibulin-2, fibulin-1, and nidogen-2, but not with perlecan. Reasonable amounts of endostatin could be extracted from aorta and skin by EDTA, followed by detergents, with aorta being the richest source of the inhibitor identified so far. Solubilizations with collagenase and elastase were approximately fivefold less efficient. Immunoblots of aortic extracts detected major endostatin components of 22-25 kDa whereas skin extracts also contained some larger components. Solid-phase assays demonstrated distinct binding of recombinant mouse endostatin to the fibulins and nidogen-2, consistent with their tissue colocalization. Together, the data indicate several different ways for endostatin to be associated with the extracellular matrix, and its release may determine biological activation. This also defines a novel function for some elastic tissues.  (+info)

Antiangiogenic activity of prostate-specific antigen. (6/4006)

BACKGROUND: Measurement of serum levels of prostate-specific antigen (PSA) is widely used as a screening tool for prostate cancer. However, PSA is not prostate specific, having been detected in breast, lung, and uterine cancers. In one study, patients whose breast tumors had higher levels of PSA had a better prognosis than patients whose tumors had lower PSA levels. To test the hypothesis that PSA may have antiangiogenic properties, we evaluated the effects of PSA on endothelial cell proliferation, migration, and invasion, which are key steps in angiogenesis, the process by which tumors develop a blood supply. METHODS: To assess the antiproliferative effects of PSA, we treated bovine endothelial cells and human endothelial cell lines (HUVEC and HMVEC-d) with purified human PSA (0.1-10 microM) and then stimulated them with 10 ng/mL fibroblast growth factor-2 (FGF-2). Effects on FGF-2- or vascular endothelial growth factor (VEGF)-stimulated endothelial cell migration, invasion, and tube formation were measured by use of one cell line only (HUVEC). PSA was administered to mice at 9 microM for 11 consecutive days after intravenous inoculation of B16BL6 melanoma cells to assess its ability to inhibit the formation of lung colonies (i.e., metastatic tumors). RESULTS: PSA inhibited endothelial cell proliferation, migration, and invasion at IC(50) (i. e., the concentration at which inhibition was 50%) values ranging from 0.3-5 microM. In addition, PSA inhibited endothelial cell responses to both angiogenic stimulators tested, FGF-2 and VEGF. In a mouse model of metastatic disease, daily PSA treatment resulted in a 40% reduction in the mean number of lung tumor nodules compared with phosphate-buffered saline treatment (two-sided P =.003). CONCLUSION: To our knowledge, this is the first report that PSA may function in tumors as an endogenous antiangiogenic protein. This function may explain, in part, the naturally slow progression of prostate cancer. Our findings call into question various strategies to inhibit the expression of PSA in the treatment of prostate cancer.  (+info)

Antifungal activities of antineoplastic agents: Saccharomyces cerevisiae as a model system to study drug action. (7/4006)

Recent evolutionary studies reveal that microorganisms including yeasts and fungi are more closely related to mammals than was previously appreciated. Possibly as a consequence, many natural-product toxins that have antimicrobial activity are also toxic to mammalian cells. While this makes it difficult to discover antifungal agents without toxic side effects, it also has enabled detailed studies of drug action in simple genetic model systems. We review here studies on the antifungal actions of antineoplasmic agents. Topics covered include the mechanisms of action of inhibitors of topoisomerases I and II; the immunosuppressants rapamycin, cyclosporin A, and FK506; the phosphatidylinositol 3-kinase inhibitor wortmannin; the angiogenesis inhibitors fumagillin and ovalicin; the HSP90 inhibitor geldanamycin; and agents that inhibit sphingolipid metabolism. In general, these natural products inhibit target proteins conserved from microorganisms to humans. These studies highlight the potential of microorganisms as screening tools to elucidate the mechanisms of action of novel pharmacological agents with unique effects against specific mammalian cell types, including neoplastic cells. In addition, this analysis suggests that antineoplastic agents and derivatives might find novel indications in the treatment of fungal infections, for which few agents are presently available, toxicity remains a serious concern, and drug resistance is emerging.  (+info)

Tumor development under angiogenic signaling: a dynamical theory of tumor growth, treatment response, and postvascular dormancy. (8/4006)

The effects of the angiogenic inhibitors endostatin, angiostatin, and TNP-470 on tumor growth dynamics are experimentally and theoretically investigated. On the basis of the data, we pose a quantitative theory for tumor growth under angiogenic stimulator/inhibitor control that is both explanatory and clinically implementable. Our analysis offers a ranking of the relative effectiveness of these inhibitors. Additionally, it reveals the existence of an ultimate limitation to tumor size under angiogenic control, where opposing angiogenic stimuli come into dynamic balance, which can be modulated by antiangiogenic therapy. The competitive influences of angiogenically driven growth and inhibition underlying this framework may have ramifications for tissue size regulation in general.  (+info)

Angiogenesis is defined as the formation of new blood vessels from pre-existing vasculature. Angiogenesis is relevant not just to disease tumors and to non-neoplastic diseases most notably macular degeneration, psoriasis, endometriosis, {and,as well as arthritis. The development {and,because well as metastasis of tumors tend to be really critically dependent upon angiogenesis. Therefore, the inhibition of angiogenesis grew to become {an,a particular,a few sort of,some of important therapeutic approach for cancer. Although the existing anti-angiogenesis options have been stated to have less toxicity than conventional chemo {or, alternatively perhaps radiotherapy, they are frequently connected with clinical side impacts, {and,since well also limited tumor regression. Therefore, there has become {an,a particular,a bunch of type of,a few of increased focus towards development of novel angiogenesis inhibitors {and,also as book approaches to improve the anti-angiogenic options .. Human apolipoprotein ...
Sigma-Aldrich offers abstracts and full-text articles by [Jae Hyeon Kim, Jin-Kyu Kim, Eun-Kyung Ahn, Hye-Jin Ko, Young-Rak Cho, Choong Hyun Lee, Yong Kee Kim, Gyu-Un Bae, Joa Sub Oh, Dong-Wan Seo].
The Antiangiogenic Compound Aeroplysinin-1 Induces Apoptosis in Endothelial Cells by Activating the Mitochondrial Pathway. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
To further investigate the role of CD11b+Gr1+ cells in refractoriness to anti-VEGF, we also treated the same tumors with mFlt(1-3)-IgG, a high affinity chimeric-soluble VEGFR-1 variant that not only neutralizes VEGF-A but also PlGF and VEGF-B ( 23). We saw no difference between anti-VEGF or mFlt(1-3)-IgG-treated groups in the efficiency of tumor formation or in the accumulation of CD11b+Gr1+ cells, suggesting that VEGFR-1 selective ligands do not compensate for the lack of VEGF-A, at least under these experimental circumstances. In apparent conflict with these conclusions, Fisher and colleagues ( 24) recently reported that targeting PlGF alone with neutralizing antibodies elicits significant antitumor effects in some anti-VEGF refractory models. Elucidating the reasons for such discrepancy will require further investigation. In addition, to address whether a lack of response to anti-VEGF might reflect a general refractoriness to other antitumor agents, we treated tumor-bearing mice with several ...
TL-118 is an anti-angiogenic drug combination designed for the treatment of cancer. The investigational product Tl-118 comprises of four well-known active components. The therapy is administrated at a unique dosing regimen that was found to be effective and advantageous in terms of safety. The product is formulated as an oral suspension, conveniently administrated by the patients at home and not requiring medical staff assistance. This Phase II clinical trial aims to evaluate the efficacy, safety and tolerability of TL-118 in Gemcitabine treated Pancreatic Cancer ...
University of Pittsburgh scientists have shown that triggering an anti-tumor immune response significantly potentiates the effects of the anti-angiogenic drug endostatin in animal models, leading to permanent and complete regression...
The treatment of the most common cancers (colon, breast, lung, liver and kidney) has recently added a new therapeutic class known as the anti-angiogenic. It was born from a better understanding of tumor growth requires the development of neo-vessels. These new vessels are of major importance for the viability of the tumor but also the birth of metastases. This neo-angiogenesis is complex and results from an imbalance between pro-angiogenic factors and anti-angiogenic factors. Growth factor VEGF and its receptors (VEGFR-1, VEGFR-2 and VEGFR-3) are a way of survival of endothelial cells required for tumor neoangiogenesis. The anti-angiogenic drugs currently available on the market are bevacizumab (Avastin ®), sunitinib (Sutent ®) and sorafenib (Nexavar ®). The mechanism of anti-angiogenic action of these three main drugs are pharmacological inhibition of the VEGF pathway.. These new anti-angiogenic therapies, however, have significant adverse effects are common and some other more serious but ...
TY - JOUR. T1 - Vascular Mimicry. T2 - A Novel Neovascularization Mechanism Driving Anti-Angiogenic Therapy (AAT) Resistance in Glioblastoma. AU - Angara, Kartik. AU - Borin, Thaiz Ferraz. AU - Arbab, Ali Syed. PY - 2017/8/1. Y1 - 2017/8/1. N2 - Glioblastoma (GBM) is a hypervascular neoplasia of the central nervous system with an extremely high rate of mortality. Owing to its hypervascularity, anti-angiogenic therapies (AAT) have been used as an adjuvant to the traditional surgical resection, chemotherapy, and radiation. The benefits of AAT have been transient and the tumors were shown to relapse faster and demonstrated particularly high rates of AAT therapy resistance. Alternative neovascularization mechanisms were shown to be at work in these resilient tumors to counter the AAT therapy insult. Vascular Mimicry (VM) is the uncanny ability of tumor cells to acquire endothelial-like properties and lay down vascular patterned networks reminiscent of host endothelial blood vessels. The VM channels ...
The central importance of angiogenesis and our understanding of how new blood vessels are formed have led to the development of novel antiangiogenic therapies. Although the number of agents in development has grown exponentially, only one phase III trial in breast cancer has been completed. In that study the addition of bevacizumab to capecitabine did not extend the progression-free survival of patients with refractory disease as compared with capecitabine monotherapy. Early enthusiasm for antiangiogenic therapy must give way to clinical reality. Our challenge now is to exploit better the activity of antiangiogenic agents seen in the early clinical studies.
The approval of the first antiangiogenic agent for clinical use in patients with colorectal carcinoma has taught us many lessons, the most important of which is that these agents must be used in combination with agents that target cancer cells to have an appreciable impact on patient survival. Increasing the dose of antiangiogenic agent may harm normal tissues and destroy too much of the tumor vasculature, leading to hypoxia and poor drug delivery in the tumor and to toxicity in normal tissues. However, optimal doses and schedules of these reagents tailored to the angiogenic profile of tumors can normalize tumor vasculature and microenvironment without harming normal tissue.. At least three major challenges must be met before therapies based on this vascular normalization model can be successfully translated to the clinic. The first challenge is to determine which other direct or indirect antiangiogenic therapies lead to vascular normalization. In principle, any therapy that restores the balance ...
The antiangiogenic effects need to be fine-tuned and adapted over time to obtain the best antitumor response possible because suboptimal antiangiogenic therapy might, in some cases, lead to potentially more aggressive tumor progression (23). Combined with conventional cytotoxic drugs, the extent of the antiangiogenic activity might determine whether the combination is synergistic, for instance, by transient normalization of the tumor vasculature resulting in temporarily better oxygenation and drug deposition (24), otherwise, the combination could be antagonistic. A further layer of complexity derives from the finding that most conventional, and many targeted antitumor agents, exert accidental antiangiogenic effects (25). Indeed, if given in a metronomic fashion (i.e., administered frequently in comparatively low doses over prolonged periods with no prolonged breaks), traditional cytotoxic drugs might act primarily via antiangiogenic mechanisms that are accompanied by only low-grade toxicity ...
Beverly Teicher and a panel of distinguished investigators survey the state-of-the-art of antiangiogenesis research from the lab bench to clinical trials. Timely and authoritative, the contributors summarize our current understanding of tumor growth and its dependence on vascular development, as well as the present status of antiangiogenic agents in preclinical and clinical development. In addition, the book also examines what is known about the mechanisms by which these therapeutic agents interfere with tumor vasculature and grapples with the problem of establishing criteria by which to assess their clinical efficacy. Antiangiogenic Agents in Cancer Therapy offers a unique cutting-edge compendium of antiangiogenic research, taking stock of what has been accomplished , where the experimental therapeutics of antiangiogenic agents is going, and the continuing evolution of their role in cancer treatment and novel drug development ...
Poster (2011, January 31). DNA methylation and histone deacetylation are two key epigenetic modifications that play central role in regulation of gene expression. Several studies have shown that histone deacetylases (HDAC) and DNA ... [more ▼]. DNA methylation and histone deacetylation are two key epigenetic modifications that play central role in regulation of gene expression. Several studies have shown that histone deacetylases (HDAC) and DNA methyltransferases (DNMT) inhibitors are potent anti-angiogenic compounds. Though combination of HDAC and DNMT inhibitors are now being examined in clinical trials of hematological malignancies, little work has been done to understand the effect of this combination on physiological and tumoral angiogenesis. We have designed and tested a family of twin drugs with intrinsic HDAC and DNMT inhibitory activities in relevant models of angiogenesis in vitro (Human Umbilical Vein Endothelial Cells - HUVEC and aortic ring) and in vivo (chick chorioallantoic ...
In chapter 1, we sought a proof of principle to confirm that the blocking of angiogenesis does indeed improve cartilage formation when using genetically-modified nasal chondrocytes (NCs) or antiangiogenic peptides associated with NCs. For this purpose, NCs were genetically-modified to express mouse soluble VEGF receptor-2 (sFlk-1) or were associated with an antiangiogenic peptide in order to have their chondrogenic capacity assessed in vitro and in vivo. Improved cartilage regeneration could be observed after in vivo implantation of NCs in an ectopic nude mouse model. Whereas the anti-angiogenic approaches did not improve chondrogenesis in vitro, frank chondrogenesis occured in vivo only in the constructs generated by NCs expressing sFlk-1 or treated with the peptide. Blood vessel ingrowth was significantly hampered in the anti-angiogenic experimental groups when compared with naïve NCs, which correlated with chondrogenis improvement. Strikingly, the anti-angiogenic effect was even more evident ...
View more ,Cancer is one of the leading causes of death worldwide. Despite extensive research cancer is predicated to be the leading cause of death by 2020. One element of cancer development, which has been successfully targeted clinically resulting in impaired tumour growth and spread (metastases), is the process by which tumours enroll vasculature. This is referred to as tumour angiogenesis. However, the problems currently associated with current anti-angiogenic therapies (eg. Avastin) is that they are prone to adaptive resistance (the process of initial response, followed by hypoxia and rapid relapse). Furthermore, such therapies target normal aspects of human biology, including the immune system, wound healing and vascular homeostasis. This leads to unintended and adverse side-affects. Bone marrow (BM) derived Endothelial Progenitor Cells (EPCs) play a critical role in tumour angiogenesis and adaptive resistance. Therefore, targeting these cells offers a novel anti-angiogenic therapy, which ...
Health, ...The beneficial effects of anti-angiogenesis drugs in the treatment of ... Our findings suggest that antiangiogenesis therapy can increase patie...Cediranib inhibits the potent angiogenesis factor VEGF which is known... We frequently see beneficial effects from drugs in patients without f...,Angiogenesis,inhibitor,improves,brain,tumor,survival,by,reducing,edema,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
New blood vessel formation, or angiogenesis, is a critical hallmark of solid tumor growth and anti-angiogenic agents have become a vital component of current cancer treatment regimens. The appeal of anti-angiogenic therapy can be attributed to several advantages of targeting the endothelial cells that line blood vessels, rather than the tumor cells themselves. First, endothelial cells are directly exposed to circulating blood, facilitating drug delivery and enabling the use of high molecular weight therapeutics. Second, each vessel capillary supports hundreds of tumor cells. Third, endothelial cells are genetically stable and their ability to develop resistance may be limited. Finally, this type of therapy should be applicable to a wide variety of tumor types. Several anti-angiogenic agents that target the vascular endothelial growth factor (VEGF) pathway have been approved for the treatment of cancer. However, tumors can exploit alternative angiogenesis mechanisms when the VEGF pathway is ...
Anti-angiogenic compounds, like sunitinib, targeting the VEGF receptor have shown activity in various tumor types. Currently no biomarkers are available to select patients or may function as early response predictor. Previously, we showed that radiolabeled ranibizumab, an anti-VEGF Fab tracer with high affinity for all VEGF-A isoforms, allows non-invasive, frequent, quantitative and rapid insight in VEGF levels in the tumor and its microenvironment. Therefore, radiolabeled ranibizumab was used to monitor sunitinib treatment to obtain insight in locoregional changes in tracer uptake during therapy. Method: Direct cytotoxicity of sunitinib was evaluated in vitro in a high VEGF producing human A2780 ovarian tumor cell line. Nude mice were inoculated with A2780 cells. When the tumor was established, mice were treated 1) once daily with sunitinib (60 mg/kg ip) or vehicle (ip) for 7 days followed by a stop week, thus reflecting the patient regimen, or 2) sunitinib/vehicle was continued for 7 days. ...
Negative feedback is a crucial physiological regulatory mechanism, but no such regulator of angiogenesis has been established. Here we report a novel angiogenesis inhibitor that is induced in endothelial cells (ECs) by angiogenic factors and inhibits angiogenesis in an autocrine manner. We have performed cDNA microarray analysis to survey VEGF-inducible genes in human ECs. We characterized one such gene, KIAA1036, whose function had been uncharacterized. The recombinant protein inhibited migration, proliferation, and network formation by ECs as well as angiogenesis in vivo. This inhibitory effect was selective to ECs, as the protein did not affect the migration of smooth muscle cells or fibroblasts. Specific elimination of the expression of KIAA1036 in ECs restored their responsiveness to a higher concentration of VEGF. The expression of KIAA1036 was selective to ECs, and hypoxia or TNF-α abrogated its inducible expression. As this molecule is preferentially expressed in ECs, we designated it ...
A team of CNIO researchers, in collaboration with the Spanish Oncology Genitourinary Group (SOGUG) and the University Hospitals Leuven (Belgium), has discovered various potential biomarkers predictive of tyrosine kinase inhibitors (TKIs) response in metastatic renal cancer. In their study, published in JCI Insight, the researchers identify various miRNAs that define a group of patients refractory to TKI treatment -a type of anti-angiogenic agent widely used to treat renal cell carcinoma- and with poor prognosis. The study, conducted on 139 patient samples, is the most robust to date in this tumour type.
Negative feedback is a crucial physiological regulatory mechanism, but no such regulator of angiogenesis has been established. Here we report a novel angiogenesis inhibitor that is induced in endothelial cells (ECs) by angiogenic factors and inhibits angiogenesis in an autocrine manner. We have performed cDNA microarray analysis to survey VEGF-inducible genes in human ECs. We characterized one such gene, KIAA1036, whose function had been uncharacterized. The recombinant protein inhibited migration, proliferation, and network formation by ECs as well as angiogenesis in vivo. This inhibitory effect was selective to ECs, as the protein did not affect the migration of smooth muscle cells or fibroblasts. Specific elimination of the expression of KIAA1036 in ECs restored their responsiveness to a higher concentration of VEGF. The expression of KIAA1036 was selective to ECs, and hypoxia or TNF-α abrogated its inducible expression. As this molecule is preferentially expressed in ECs, we designated it ...
Phase I Study of Gemcitabine With Antiangiogenic Vaccine [angiogenesis inhibitor vaccine] Therapy Using Epitope Peptide Restricted to HLA [human leukocyte antigen]-A-2402 Derived From VEGFR2 [vascular endothelial grwoth factor receptor 2] in Patients With Unresectable, Locally Advanced, Recurrent or Metastatic Pancreatic Cancer ...
Figure 1a-d: Imaging results of a patient with glioblastoma undergoing bevacizumab therapy. First column: MRI (MP-RAGE with contrast enhancement); second column: 18F-FET-PET (parametric images scaled to mean uptake in a right temporal reference region); third column: image fusion. (A) scan prior to therapy 07/2010; (B) scan after 8 weeks of bevacizumab 09/2010; (C) scan after 16 weeks of bevacizumab 11/2010; (D) scan after re-irradiation with 20 Gy, 01/2011. Bevacizumab therapy was continued. For details, see ...
The use of antivascular endothelial growth factors such as bevacizumab and ranibizumab has brought about a revolution in management protocols of various ophthalmic disorders. A lot has been written about these agents, still lacunae exist in our understanding due to paucity of randomized control trials with large number of patients. This brief review attempts to throw light on the clinical applications of these molecules for glaucoma.. ...
The evolving landscape of treatment for advanced gastric cancer and the role of anti-angiogenic therapy: implications from results of the INTEGRATE study
We are proud to announce a group of new titles from Bentham Science are now available through Elsevier and ScienceDirect. Please enjoy a free sample chapter on Anti-Angiogenic Therapy and Cardiovascular Diseases: Current Strategies and Future Perspectives.
Principal Investigator:HOSOI Yutaka,小見山 高士, Project Period (FY):1998 - 1999, Research Category:Grant-in-Aid for Scientific Research (C), Section:一般, Research Field:General surgery
Historically, VEGFR-1 was assigned a role as a nonsignaling decoy receptor because of the low activity and embryonic dispensability of its tyrosine kinase function. More recently, its role has become more interesting because VEGFR-1 signaling has been reported both to promote (6, 7) and suppress (8) VEGF-A-driven angiogenesis. We report not only that PlGF-1 inhibits inflammatory CNV, extending the scope of VEGFR-1 function, but also what we believe is the unprecedented observation that VEGF-A itself can suppress angiogenesis. Multiple lines of evidence emerging from genetic ablation, antibody neutralization, and receptor-selective ligand activation all strongly support the thesis that the antiangiogenic action of VEGF-A is mediated by VEGFR-1. Previously, VEGF-A has been reported to reduce VEGF-E-induced VEGFR-2 tyrosine kinase phosphorylation in capillary endothelial cells in vitro, raising the provocative hypothesis that VEGF-A could limit its own angiogenic activity through VEGFR-1 (29). We ...
Purpose: Vascular endothelial growth factor (VEGF) is an angiogenic cytokine which is important in developmental blood vessel formation. In kidneys of embryonic to adult humans and mice, VEGF is detected in epithelial cells of the glomeruli and endothelial cells of glomeruli, tubules and peritubular capillaries. Some low birth weight (LBW) infants are known to have a decrease in nephron number and kidney size even after catch up growth. In order to find the potential therapy of infants with impaired renal development, we first generated the murine model, and investigated the effect of retinoic acid (RA). Materials and Methods: An angiogenesis inhibitor (SU1498) was injected subcutaneously to day 3 C57BL/6 newborn mice to create a model of arrested renal development. RA (2g/kg) was injected intraperitoneally for 10 consecutive days for the duration of renal development. Morphometric analysis of the renal cortex and glomerulus using light microscopic findings and electron microscopic examination ...
We investigated the anti-vascular activity of local hyperthermia (44 degrees C, 60 min) in s.c. BT4An rat gliomas, and the influence on tumour growth of hyperthermia and the anti-angiogenic compound batimastat (30 mg/kg i.p.). Heat-induced vascular damage was assessed in small (82 mm3) and large (171 mm3) tumours using confocal ...
Health,...Anti-angiogenesis drug prolonged progression-free survival study find...SATURDAY May 31 (HealthDay News) -- Adding the drug Avastin to chemot...Previous studies have found that adding Avastin (bevacizumab) to the c...Avastin is already approved for use in metastatic colon cancer non-sm...,Avastin,Added,to,Chemo,Helps,Women,With,Advanced,Breast,Cancer,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
We used semiautomated segmentation software to quantify total as well as the focal and diffuse components of leakage before and after anti-VEGF therapy. Anti-VEGF therapy effectively reduced total leakage as well as diffuse and focal leakage. However, the absolute and percent reduction in diffuse leakage was significantly greater than the reduction in focal leakage. These findings suggested that diffuse leakage is significantly more responsive to a moderate course of anti-VEGF therapy (approximately 5 injections on average). Numerous investigators have subtyped DME as diffuse or focal according to various criteria and using variable tools, which include biomicroscopy,21-29 fundus photography.23,24,27,28,30,31 FA,31-40 and OCT.41-44 To date, the utility of classifying DME based on FA has been limited by inherent subjectivity, multiple definitions and challenges in reproducibility.15,19 Fluorescein angiography has been used to distinguish diffuse and focal DME in numerous studies31,34,36,38,40 and ...
2-methoxyoestradiol (2-MeOE2) is a potent anti-angiogenic agent. Its 3- and 17-sulphamoylated derivatives have been demonstrated to induce G2-M cell cycle arrest and apoptosis in breast cancer cells in vitro as well as tumour regression in rats in vivo with greater potency than the parent oestrogen. To determine whether the anti-cancer properties of these derivatives can be synergistically enhanced with low-dose TNF-alpha co-treatment, we investigated the effects of these treatments in adult human fibroblasts and human umbilical vein endothelial cells (HUVECs). Treatment of fibroblasts with 0.1 microM 2-methoxyoestradiol-3,17-bis sulphamate (2-MeOE2bisMATE) but not 2-MeOE2 caused a reversible morphology change and induced G2-M arrest (from 12 to 33%) but not subsequent apoptosis. In contrast, treatment of HUVECs did not induce morphology change or G2-M arrest. Using a nucleosomal ELISA assay, we showed that TNF-alpha (20 ng/ml) combination treatment synergistically increases 0.1 microM 2-MeOE2bisMATE
Advanced imaging techniques may be able to distinguish which patients tumors will respond to treatment with antiangiogenic drugs and which will not.
TY - JOUR. T1 - A vascular targeted pan phosphoinositide 3-kinase inhibitor prodrug, SF1126, with antitumor and antiangiogenic activity. AU - Garlich, Joseph R.. AU - De, Pradip. AU - Dey, Nandini. AU - Jing, Dong Su. AU - Peng, Xiaodong. AU - Miller, Antoinette. AU - Murali, Ravoori. AU - Lu, Yiling. AU - Mills, Gordon B.. AU - Kundra, Vikas. AU - Shu, H. K.. AU - Peng, Qiong. AU - Durden, Donald L.. PY - 2008/1/1. Y1 - 2008/1/1. N2 - PTEN and the pan phosphoinositide 3-kinase (PI3K) inhibitor 2-(4-morpholinyl)-8-phenyl-4H-1benzopyran-4-one (LY294002) exert significant control over tumor-induced angiogenesis and tumor growth in vivo. The LY294002 compound is not a viable drug candidate due to poor pharmacologic variables of insolubility and short half-life. Herein, we describe the development and antitumor activity of a novel RGDS-conjugated LY294002 prodrug, termed SF1126, which is designed to exhibit increased solubility and bind to specific integrins within the tumor compartment, resulting ...
Usha Chakravarthy, MD, FRCS, FRCOphth, PhD, shares thoughts on recent research of systemic effects of anti-VEGF agents. She discusses clinical trials that monitor adverse events associated with anti-VEGF therapy and gives insight into the potential o…
Diffuse optical spectroscopic imaging (DOSI) has been described as a method to assess tumor vascularity and oxygenation by measuring tissue hemoglobin
2. Failure of one prior antiangiogenic therapy (patients must have received at least 4 weeks of prior therapy). Antiangiogenic agents include sorafenib, bevacizumab and brivanib. Failure is defined as either a) documented progressive disease (per RECIST version 1.1) while receiving prior therapy or after the last dose of prior therapy; or b) intolerance to the prior antiangiogenic therapy. Intolerance to prior antiangiogenic therapy (at any dose and/or duration) is defined as documented treatment-related grade 3 or 4 adverse events that led to treatment discontinuation ...
Fingerprint Dive into the research topics of WMJ-S-001, a novel aliphatic hydroxamate derivative, exhibits anti-angiogenic activities via Src-homology-2-domaincontaining protein tyrosine phosphatase 1. Together they form a unique fingerprint. ...
In order for tumor cells to multiple and spread, they must develop their own blood supply through a process called angiogenesis. Angiogenesis inhibitor chemotherapy drugs work to stop or slow down this process, thereby controlling tumor growth. Metronomic chemotherapy is one example of angiogenesis inhibition treatment, which is becoming a popular treatment option for pets…
While it is true that the limitations of anti-VEGF therapy are becoming more evident as our experience with these agents increases, it is also undeniable that a subset of cancer patients treated with bevacizumab do show objective clinical responses and improved survival. However, we have yet to identify predictive biomarkers that have been validated in multiple, independent studies and can reliably distinguish patients who are likely to respond from those who will not. The identification of such biomarkers will be critical in harnessing the full potential of anti-VEGF therapy and in minimizing the rates of adverse side effects. The design and implementation of clinical trials based on proven, predictive biomarkers should allow for the enrichment of proper patient cohorts and facilitate the understanding of therapeutic mechanisms behind anti-VEGF therapy.. Several cytokines have been proposed in the literature as a possible predictive biomarker for anti-VEGF therapy. However, VEGF-A, the target ...
Results: 71 patients were treated, and the MTD was identified at the highest dose level (bevacizumab 15 mg/kg, bortezomib 1.3 mg/m2 ...
Interference with the activity of TSP-1 and its antiangiogenic peptides by soluble GST-CD36 fusion proteins. Increasing concentrations of CD36 fusion proteins
Angiogenesis is a very important step in the development of cancer. Several antiangiogenic biological agents have been studied during the past two …
The identification of patients likely to respond to antiangiogenic treatment has high priority. In this translational study, we analyzed the predictive value of the angiogenic couple, EGFL7 and miR126, in primary tumors from patients with mCRC treated with first-line chemotherapy and bevacizumab. The results indicated that the EGFL7 VA has a predictive value in this setting.. We analyzed two cohorts of patients with mCRC. The only difference between the two investigated cohorts was a higher fraction of patients with resected tumors compared with endoscopic biopsies in cohort 2. This difference, however, did not influence any of the clinical endpoints and, thus, allowed us to consider the two patient cohorts as one when analyzing the investigated parameters.. The present results demonstrate a significant difference in median EGFL7 VA in the tumor resections according to RR. Patients with low EGFL7 VA were more likely to respond to chemotherapy combined with anti-VEGF-A. With these findings, we ...
BioVision develops and offers a wide variety of products including assay kits, antibodies, recombinant proteins & enzymes, and other innovative research tools for studying Apoptosis, Metabolism, Cell Proliferation, Cellular Stress, Cell Damage and Repair, Diabetes, Obesity and Metabolic Syndrome, Stem Cell Biology, Gene Regulation, Signal Transduction, etc. BioVisions products are currently being sold in more than 60 countries worldwide.
TY - JOUR. T1 - Anti-vascular endothelial growth factor therapy for neovascular ocular diseases other than age-related macular degeneration. AU - Ciulla, Thomas A.. AU - Rosenfeld, Philip J.. PY - 2009/5/1. Y1 - 2009/5/1. N2 - The discovery of VEGF-As role in the pathogenesis of neovascular ocular disease provided a strong rationale for the development of anti-VEGF-based therapies. There is now ample evidence that anti-VEGF therapies are viable treatment options for these diseases. Nevertheless, large, randomized controlled trials are still awaited to confirm early safety and efficacy findings from small, open-label prospective studies.. AB - The discovery of VEGF-As role in the pathogenesis of neovascular ocular disease provided a strong rationale for the development of anti-VEGF-based therapies. There is now ample evidence that anti-VEGF therapies are viable treatment options for these diseases. Nevertheless, large, randomized controlled trials are still awaited to confirm early safety and ...
Title: Imaging in the Age of Molecular Medicine: Monitoring of Anti-Angiogenic Treatments. VOLUME: 13 ISSUE: 4. Author(s):W. Lederle, M. Palmowski and F. Kiessling. Affiliation:Department of Experimental Molecular Imaging, University of Aachen (RWTH), Pauwelsstrasse 20, 52074 Aachen, Germany.. Keywords:Angiogenesis, imaging, CT, MRI, nuclear imaging, optical imaging, ultrasound, characterization of different angiogenic steps, numerous angiogenesis inhibitors, anti-angiogenic treatment, longitudinal treatment monitoring, molecular imaging, tumor vessels. Abstract: Angiogenesis is a complex multistep process and a crucial pre-requisite for tumor growth, invasion and metastasis. A profound knowledge of the mechanisms including the elucidation of markers for angiogenic vessels is essential for the generation of new anti-angiogenic chemotherapeutic agents and the improvement of specific imaging techniques. During the last decades, numerous angiogenesis inhibitors have been developed and some of them ...
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A translational research project aiming to identify predictive markers for response to bevacizumab treatment in HER2-negative breast cancer from GeparQuinto study has been published in Clinical Cancer Research.
Studies comparing the effect of antiangiogenic agents targeting different angiogenic pathways are sparse. The purpose of this study was to compare the effect of properdistatin and sunitinib treatment in a preclinical model of malignant melanoma. Properdistatin is a small peptide derived from the thrombospondin-1 domain of the plasma protein properdin, and sunitinib is a tyrosine kinase inhibitor targeting several receptors including the vascular endothelial growth factor receptors. R-18 human melanoma xenografts growing in dorsal window chambers were treated with properdistatin, sunitinib, or vehicle. Parameters describing the morphology of tumor vasculature were assessed from high-resolution transillumination images, and BST (blood supply time; the time needed for arterial blood to flow from the main supplying artery to downstream microvessels) was assessed from first-pass imaging movies recorded after a bolus of fluorescence-labeled dextran had been administered intravenously. Tumor hypoxia was
Studies comparing the effect of antiangiogenic agents targeting different angiogenic pathways are sparse. The purpose of this study was to compare the effect of properdistatin and sunitinib treatment in a preclinical model of malignant melanoma. Properdistatin is a small peptide derived from the thrombospondin-1 domain of the plasma protein properdin, and sunitinib is a tyrosine kinase inhibitor targeting several receptors including the vascular endothelial growth factor receptors. R-18 human melanoma xenografts growing in dorsal window chambers were treated with properdistatin, sunitinib, or vehicle. Parameters describing the morphology of tumor vasculature were assessed from high-resolution transillumination images, and BST (blood supply time; the time needed for arterial blood to flow from the main supplying artery to downstream microvessels) was assessed from first-pass imaging movies recorded after a bolus of fluorescence-labeled dextran had been administered intravenously. Tumor hypoxia was
Corneal expression levels of the proinflammatory and pro(lymph)angiogenic cytokines IL-1β, TNFα, VEGF-A, VEGF-C, and VEGF-D were analyzed by real-time PCR after suture placement and treatment with serum eyedrops, bevacizumab eyedrops, or a combination of both. After 2 days of treatment, only bevacizumab affected IL-1β expression (serum mean of 95.6%, n.s.; bevacizumab mean of 74.3%, P , 0.01; and serum and bevacizumab mean of 96.4%, n.s.), whereas after 7 days of treatment, all treatment groups had significantly reduced IL-1β expression (serum mean of 48.4%, P , 0.001; bevacizumab mean of 58.9%, P , 0.001; and serum and bevacizumab mean of 53.2%, P , 0.001) (Fig. 5, top left). After 2 days of treatment, TNFα expression was significantly impaired only by bevacizumab (serum mean of 106.1%, n.s.; bevacizumab mean of 68.4%, P , 0.05; and serum and bevacizumab mean of 93.0%, n.s.), while after 7 days of treatment, the combination of serum and bevacizumab also showed considerable inhibition of ...
In this issue of the BJO, Boyd et al (pp 440 and 448) present data that confirm an important role for vascular endothelial growth factor-A (VEGF-A) and, to a lesser extent, basic fibroblast growth factor (bFGF) in angiogenic growth in and around uveal melanomas. Using a range of approaches, they assayed these factors in ocular fluids and postmortem specimens from patients, grew co-cultures of tumour cells and endothelium in vitro, and concluded that anti-angiogenic therapy may be a worthwhile approach for treatment of eyes harbouring uveal melanomas. In many of these tumours VEGF-A was expressed at high levels, and this was especially true in patients who developed secondary retinal and iris neovascularisation following ionising radiation treatment of their tumours. VEGF-A expression was shown to be particularly high in the ocular fluids of this subset of patients and Boyd et al conclude that this phenomenon makes the case for anti-VEGF-A treatment as an adjunctive therapy in the treatment of ...
The dependence of tumor growth and metastasis on blood vessels makes tumor angiogenesis a rational target for therapy. Strategies have been pursued to inhibit neovascularization and to destroy existing tumor vessels, or both. These include direct targeting of endothelial cells, and indirect targeting by inhibiting the release of proangiogenic growth factors by cancer or stromal cells. Many patients benefit from antiangiogenic therapies; thus, development of noninvasive biomarkers of disease response and relapse is a crucial objective to aid in their management. A number of non-invasive tools are described with their potential benefits and limitations. We review currently available candidate biomarkers of anti-angiogenic agent effect. Including these markers into clinical trials may provide insight into appropriate dosing for desired biological effects, appropriate timing of additional therapy, and prediction of individual response. This has important consequences for the clinical use of angiogenesis
To investigate the effect of intravitreal bevacizumab and ranibizumab on wound tension and by histopathology during cutaneous wound healing in a rabbit model and to compare this effect to placebo intravitreal saline controls 1 and 2 weeks following i
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Colorectal cancer is one of the leading causes of cancer-related mortality in the United States (14). Given its biologic complexity and poor prognosis, it is important to evaluate novel treatment strategies that might potentially improve treatment outcome in patients. The essential dietary trace element, selenium, has been shown to act as an effective chemopreventive agent reducing the risk and mortality associated with cancer (15, 16). MSC is an organoselenium compound that has been shown to exert potent antiangiogenic activity in vivo (8, 9, 17, 18). The antiangiogenic effects of selenium have previously been demonstrated in ectopic subcutaneous models of human head and neck, colorectal and lung cancer (8, 9).. Monitoring of subcutaneous (ectopic) tumors in small animals can be performed easily through the combination of visual inspection and simple caliper-based measurements of tumor dimension. In contrast, tumors established in orthotopic tumor sites cannot be assessed by visual examination ...
Previs, Rebecca A. et al Dual Metronomic Chemotherapy with Nab-Paclitaxel and Topotecan Has Potent Antiangiogenic Activity in Ovarian Cancer. Molecular Cancer Therapeutics 14.12 (2015): 2677-2686. Web. 09 Aug. 2020. ...
Data Availability StatementThe datasets used and analyzed during the current research are available in the corresponding writer on reasonable demand. week in we.p. dosages of 10?mg/kg before mice became moribund. Healing effects were examined by identifying tumor web host survival time, evaluating tumor development and angiogenic activity Carbidopa by quantitative analyses of histological arrangements, and calculating the appearance of angiogenesis-related genes by quantitative PCR. Outcomes Meningeal A-07 melanomas demonstrated higher appearance of VEGF-A than meningeal D-12 melanomas, whereas the appearance of IL8 and ANGPT2, two essential angiogenesis motorists in melanoma, was higher in D-12 than in A-07 tumors. Bevacizumab treatment inhibited tumor angiogenesis and extended host success in mice with A-07 tumors however, not in mice with D-12 tumors. Meningeal A-07 tumors in bevacizumab-treated mice paid out for the decreased VEGF-A activity by up-regulating a lot of angiogenesis-related ...
There is a very strong link between the vascularization of a tumour and the spread of the disease, both locally and to distant sites (Gimbrone et al., 1974, J. Natl. Cancer Inst. 52, 413-27; Muthukkaruppan et al, 1982, J. Natl. Cancer Inst. 69, 699-704; Ellis & Fiddler, 1995, Lancet 346, 388-9). A tumour becomes vascularized by a process known as angiogenesis. Tumour angiogenesis is initiated by the release of diffusible substances by the tumour, whereby neighbouring capillary vessels are stimulated to grow and eventually penetrate the tumour. Anti-angiogenesis has been proposed as a potential strategy for the treatment of cancer (Folkman, 1995, Nature Med. 1, 21-31; Harris et al, 1996, Breast Cancer Res. Treat. 38, 97-108). In this paper, a mathematical model of the development of the tumour vasculature is presented. By suitable manipulation of the model parameters, we simulate various anti-angiogenesis strategies and we examine the roles that haptotaxis and chemotaxis may play during the ...
Sulfamoylation of 2-methoxyestrone (2-MeOE1) was shown previously to enhance its potency as an anti-proliferative agent against breast cancer cells. We have examined the ability of a series of 2-methoxyestradiol (2-MeOE2) and 2-ethylestradiol (2-EtE2) sulfamates to inhibit angiogenesis in vitro. 2-MeOE2 bis-sulfamate and 2-EtE2 sulfamate were potent inhibitors of human umbilical vein endothelial cell (HUVEC) proliferation with IC(50) values of 0.05 microM and 0.01 microM, respectively. A novel co-culture system, in which endothelial cells were cultured in a matrix of human dermal fibroblasts, was also used to assess the anti-angiogenic potential of these drugs. In this system endothelial cells proliferate and migrate through the culture matrix to form tubule structures. Whereas 2-MeOE2 (1.0 microM) caused a small reduction in tubule formation, both 2-MeOE2 bis-sulfamate (0.1 microM) and 2-EtE2 sulfamate (0.1 microM) almost completely abolished tubule formation. 2-MeOE2 bis-sulfamate and 2-EtE2 sulfamate
FDA has given Genentechs antiangiogenesis agent Avastin (bevacizumab) accelerated approval for use in combination with paclitaxel for the first-line treatment of metastatic HER2-negative breast cancer.
Preoperative bevacizumab may predominantly benefit breast cancer patients with a high baseline microvessel density, according to a new study.
Poster (2006, May). Tumour development is often accompanied by the formation of new blood vessels from existing vasculature. This new intratumoral blood network is driven by the process of angiogenesis, providing the ... [more ▼]. Tumour development is often accompanied by the formation of new blood vessels from existing vasculature. This new intratumoral blood network is driven by the process of angiogenesis, providing the essential nutrients for growth, invasion and metastasis. At the present time, it is well established that inhibitors of angiogenesis prevent the growth and progression of tumours, offering a new therapeutic approach for treatment of cancer. Several studies have already showed that the N-terminal fragment of the human prolactin, 16k-Da PRL, has a potent anti-angiogenic activity. Recently, research groups have demonstrated that the 16k-Da PRL inhibits tumour development in animal models. Despite the fact that several studies leading to improve our knowledge of 16k-Da PRL ...
SOUTH SAN FRANCISCO -- Genentech has given compounding pharmacies a months reprieve from its plan to stop selling them bevacizumab (Avastin), which they repackage as a low-cost alternative to ranibiz
Ethanol, RA and thalidomide treatments lead to major global gene expression changes in human EBs. (A) Histogram of the total number of up-regulated (blue) and d
Understanding of structural and functional characteristics of the vascular microenvironment in gliomas and the impact of antiangiogenic treatments is essential for developing better therapeutic strategies. Although a number of methods exist in which this process can be studied experimentally, no single noninvasive test has the capacity to provide information concerning both microvascular function and morphology. The purpose of present study is to demonstrate the feasibility of using a novel three-dimensional ?R2-based microscopic magnetic resonance angiography (3D ?R2-µMRA) technique for longitudinal imaging of tumor angiogenesis and monitoring the effects of antiangiogenic treatment in rodent brain tumor models. Using 3D ?R2-µMRA, a generally consistent early pattern of vascular development in gliomas was revealed, in which a single feeding vessel was visualized first (arteriogenesis), followed by sprouting angiogenesis. Considerable variability of the tumor-associated vasculature was then ...
Kaempferol offers been reported to reduce the risk of ovarian malignancy, but the mechanism is not completely understood. cells, and better characterized kaempferol toward chemoprevention. angiogenesis caused by ovarian malignancy cells, and the pathways involve regulation on HIF1- and ERR- gene expressions (Luo et al., 2009). Anti-angiogenesis is probably the most feasible strategy for current chemoprevention of ovarian cancers, given the fact that these early-stage tiny tumors cannot be successfully diagnosed but their continued development desperately depends on the establishment of a new blood vessel network (Bertl et al., 2006; Carmeliet et al., 2000). Tumor-free adults, on the other hand, have virtually zero need for angiogenesis in normal situations (Fotsis et al., 1993; Glade-Bender et al., 2003). Thus our findings about kaempferols anti-angiogenesis effects (Luo et al., 2009) become more relevant in this context. Nevertheless, the previously investigated pathways for kaempferol are not ...
Avastin (bevacizumab) is an effective, first-line option when used together with other medicines for certain types of cancers, but it has to be given in a clinic or hospital and it has many severe side effects. If you have heart or kidney problems, Avastin (bevacizumab) may increase your risk of side effects.
Almac Discovery today announced the licensing of its novel anti-angiogenic peptide ALM201 to Shin Poong Pharmaceutical Company Ltd for clinical development and marketing in South Korea. Shin Poong will make an undisclosed upfront payment and pay milestones and royalties as part of the deal. The Shin Poong programme in South Korea will run in parallel with Almac Discoverys own development programme in Europe.
Since VEGF is known to activate FAK - which plays a role in cellular signaling - in the endothelial cells that line pulmonary blood vessels, the researchers analyzed levels of the enzyme at the sites of induced vascular leakiness and found them to be elevated. Blocking the activity of FAK in lung endothelial cells reduced both vascular permeability and the adhesion of metastatic cells to those tissues. Additional genetic experiments revealed that FAK produces these effects through increased local expression of the cellular adhesion molecule E-selectin, says Dai Fukumura, MD, PhD, of the Steele Lab, a co-senior author of the report.. Co-senior author Dan G. Duda, DMD, PhD, also of the Steele Lab, adds, Anti-metastatic therapy is the ultimate frontier for cancer therapy, but existing treatments - both traditional chemotherapy and newer antiangiogenesis agents - have limited effectiveness in preventing the development of metastases. Our findings provide proof of principle that FAK inhibition is ...
Anti-angiogenesis occurs when new blood formation (angiogenesis) is stopped. Drugs that are used to stop angiogenesis are called anti-angiogenesis drugs.. Tags: A, Cancer Dictionary, Uncategorized. ...
Pazopanib is a novel antiangiogenic inhibitor of tyrosine kinases (TKIs) with high activity against vascular endothelial growth factor receptor (VEGFR1-3), platelet-derived growth factor receptor (PDGFRα+β), and c-Kit. Here we report on a patient with prostate cancer and type 2 diabetes whose glycemic control has been significantly improved with pazopanib during anticancer therapy and describe a potential mechanism of action.. The 73-year-old patient was diagnosed with prostate cancer in 1999 and underwent prostatectomy and radiotherapy, sequential hormonal therapies, and, in 2008, first line chemotherapy. Due to disease progression he was enrolled in a phase I trial with pazopanib (400 mg p.o. daily, day 1 to 21 every 3 weeks) in combination with epirubicine (75 mg/m2 i.v. q3w every 3 weeks). Type 2 diabetes was diagnosed when the patient was 69 years and weighed 103 kg (BMI 33.6 kg/m2). He was treated with glibenclamide resulting in moderate to poor glycemic control (A1C 7.5-10.9%).. In ...
One of the most recent methods that is being developed for the delivery of anti-angiogenesis factors to tumour regions in cancer sufferers is using genetically modified bacteria that are able to colonize solid tumors in vivo. This method involves genetically engineering bacterial species such as Clostridium, Bifidobacteria and Salmonella by adding the genes for anti-angiogenic factors such as endostatin or IP10 chemokine and removing any harmful virulence genes. A target can also be added to the outside of the bacteria so that they are sent to the correct organ in the body. The bacteria can then be injected into the patient and they will locate themselves to the tumor site, where they release a continual supply of the desired drugs in the vicinity of a growing cancer mass, preventing it from being able to gain access to oxygen and ultimately starving the cancer cells.[11] This method has been shown to work both in vitro and in vivo in mice models, with very promising results.[12] It is expected ...
Disclosed is a method for monitoring early treatment response of a cancer treatment comprising measuring by magnetic resonance spectroscopy (MRS), for example, proton MRS, the amount of Choline present in the tissue adjoining or surrounding the cancerous tissue before and after treatment; the treatment comprises administration of an angiogenesis inhibitor, for example, a VEGF inhibitor, whereby a decrease in the amount of Choline after treatment is indicative of a positive response. The decrease in the amount of Choline represents the decrease in the internal cell membrane as a result of down regulation of the organelles and their secretory granules and their transport vesicles. Disclosed also is a method for determining effectiveness of an angiogenesis inhibitor in the treatment of cancer. Also disclosed are methods of monitoring early treatment response in diseases where an angiogenesis effector, i.e., an inhibitor or promoter of angiogenesis, is employed. Also disclosed is a method for monitoring
Sometimes called antiangiogenic therapy, this treatment may prevent the growth of cancer by blocking the formation of new blood vessels.
Our mission is to build healthier lives, free of cardiovascular diseases and stroke. That single purpose drives all we do. The need for our work is beyond question. Find Out More about the American Heart Association. ...
Since anti-VEGF therapies have shown good potential for slowing vascular leakage and preventing vision loss associated with wet AMD, ophthalmologists...
Angiogenesis inhibitors interfere with blood vessel formation by interfering with the angiogenesis signalling cascade. They are ... "Angiogenesis Inhibitors". National Cancer Institute. May 2018. Retrieved 2018-02-19. Rosella D, Papi P, Giardino R, Cicalini E ... Another suggested factor is inhibition of angiogenesis due to bisphosphonates; this effect remains uncertain. Several studies ... March 2005). "Zoledronic acid-related angiogenesis modifications and survival in advanced breast cancer patients". Journal of ...
Prolactin modulators: Prolactin inhibitors: D2 receptor agonists (e.g., bromocriptine, cabergoline); Prolactin releasers: D2 ...
Angiogenesis inhibitor ("-anibi-"). Humanized ("-anibizu-"). *Ranibizumab. Growth factor ("-gr(o)-"). Human ("-gru-"). * ...
"Borrelidin is an angiogenesis inhibitor; disruption of angiogenic capillary vessels in a rat aorta matrix culture model". The ... "Biosynthesis of the angiogenesis inhibitor borrelidin by Streptomyces parvulus Tü4055: cluster analysis and assignment of ... "Biosynthesis of the angiogenesis inhibitor borrelidin by Streptomyces parvulus Tü4055: insights into nitrile formation". ... First discovered in 1949 from Streptomyces rochei, Borrelidin shows antibacterial activity by acting as an inhibitor of ...
This research has been used in anti-tumor therapeutic research, including an observation that angiogenesis inhibitors enhanced ... "Clinical translation of angiogenesis inhibitors". Nature Reviews Cancer. 2 (10): 727-739. doi:10.1038/nrc905. PMID 12360276. ... characterizing the effects of angiogenesis inhibitors on the effectiveness of anti-tumor therapies, has been cited over 900 ... Chen, Yun; Gorski, David H. (1 February 2008). "Regulation of angiogenesis through a microRNA (miR-130a) that down-regulates ...
Sorbera LA, Bayes M (2005). "ABT-510: oncolytic angiogenesis inhibitor". Drugs of the Future. Prous Science. 30 (11): 1081-6. ... April 2005). "Thrombospondin-1 mimetic peptide inhibitors of angiogenesis and tumor growth: design, synthesis, and optimization ... Since tumors overexpressing TSP-1 typically grow slower, exhibit less angiogenesis, and have fewer metastases, TSP1 is an ... functions for TSP-1 have been found in multiple biological processes including angiogenesis, apoptosis, activation of TGF-beta ...
Inhibition of TNF-α is not the mechanism of thalidomide's inhibition of angiogenesis since numerous other TNF-α inhibitors do ... D'Amato RJ, Loughnan MS, Flynn E, Folkman J (April 1994). "Thalidomide is an inhibitor of angiogenesis". Proc. Natl. Acad. Sci ... Additionally, these analogs are more potent inhibitors of angiogenesis than thalidomide. As well, the amino-thalidomide and ... "Angiogenesis inhibitors derived from thalidomide". Bioorganic & Medicinal Chemistry Letters. 15 (24): 5509-5513. doi:10.1016/j. ...
... who was looking for angiogenesis inhibitors, discovered in 1994 that thalidomide inhibited angiogenesis and was effective in ... D'Amato RJ, Loughnan MS, Flynn E, Folkman J (April 1994). "Thalidomide is an inhibitor of angiogenesis". Proceedings of the ... Ribatti D (2008). "Judah Folkman, a pioneer in the study of angiogenesis". Angiogenesis. 11 (1): 3-10. doi:10.1007/s10456-008- ... As of 2015, the main theories were inhibition of the process of angiogenesis, its inhibition of cereblon, a ubiquitin ligase, ...
... was looking for angiogenesis inhibitors, and discovered that thalidomide inhibited angiogenesis in 1994. Around that time, the ... In 2004, the first angiogenesis inhibitor, bevacizumab (Avastin), was approved by the FDA, as a treatment for colon cancer. It ... D'Amato RJ, Loughnan MS, Flynn E, Folkman J (1994). "Thalidomide is an inhibitor of angiogenesis". Proceedings of the National ... Ribatti D (2008). "Judah Folkman, a pioneer in the study of angiogenesis". Angiogenesis. 11 (1): 3-10. doi:10.1007/s10456-008- ...
D'Amato RJ, Loughnan MS, Flynn E, Folkman J (April 1994). "Thalidomide is an inhibitor of angiogenesis". Proceedings of the ... since potent TNF inhibitors including rolipram and pentoxifylline do not inhibit myeloma cell growth or angiogenesis. ... Pomalidomide directly inhibits angiogenesis and myeloma cell growth. This dual effect is central to its activity in myeloma, ... April 2002). "S-3-Amino-phthalimido-glutarimide inhibits angiogenesis and growth of B-cell neoplasias in mice". Cancer Research ...
Withaferin A potent inhibitor of angiogenesis. References[edit]. *^ Hannink M, Donoghue DJ (1989). "Structure and function of ... PDGF plays a role in embryonic development, cell proliferation, cell migration, and angiogenesis.[19] Over-expression of PDGF ... Wortmannin is a PI3K-specific inhibitor, and treatment of cells with Wortmannin in combination with PDGF resulted in enhanced ... which are active in angiogenesis and endothelial cell growth, and placenta growth factor (PlGF) which is also active in ...
Among anti-angiogenesis inhibitors, endostatin has a wide range of anti-cancer spectrum targets, increasing its significance ... Endogenous inhibitors of angiogenesis are present in both normal tissue and cancerous tissue. Overall, endostatin down ... Endostatin is a broad-spectrum angiogenesis inhibitor and may interfere with the pro-angiogenic action of growth factors such ... Hohenester, E.; Sasaki, T.; Olsen, B.R.; Timpl, R. (1998). "Crystal structure of the angiogenesis inhibitor endostatin at 1.5 A ...
Stetler-Stevenson WG, Seo DW (2005). "TIMP-2: an endogenous inhibitor of angiogenesis". Trends in Molecular Medicine. 11 (3): ... Tissue inhibitor of metalloproteinases 2 (TIMP2) is a gene and a corresponding protein. The gene is a member of the TIMP gene ... Zucker S, Drews M, Conner C, Foda HD, DeClerck YA, Langley KE, Bahou WF, Docherty AJ, Cao J (January 1998). "Tissue inhibitor ... Bigg HF, Shi YE, Liu YE, Steffensen B, Overall CM (June 1997). "Specific, high affinity binding of tissue inhibitor of ...
Brain-specific angiogenesis inhibitor InterPro: IPR008077 BAI1; BAI2; BAI3 CD97 antigen InterPro: IPR003056 CD97 EMR hormone ... calcium-independent receptors for latrotoxin and brain-specific angiogenesis inhibitor receptors amongst others. They are ...
Lee, A; Langer, R (16 September 1983). "Shark cartilage contains inhibitors of tumor angiogenesis". Science. 221 (4616): 1185-7 ...
Various angiogenesis inhibitors have been developed to interfere with different steps in the process. Bevacizumab (Avastin) is ... Sorafenib and sutinib are additional angiogenesis inhibitors that bind and block receptors on endothelial cells that have ... Cook, Kristina M.; Figg, William D. (2010-07-01). "Angiogenesis inhibitors: current strategies and future prospects". CA: A ... Shih, Ted; Lindley, Celeste (2006-11-01). "Bevacizumab: an angiogenesis inhibitor for the treatment of solid malignancies". ...
Ryeom S, Folkman J (March 2009). "Role of endogenous angiogenesis inhibitors in Down syndrome". The Journal of Craniofacial ... Since 2008 there have been other therapies (e.g. kinase inhibitors and anti-VEGF) drugs available. Laser photocoagulation can ...
... is a relatively specific phosphodiesterase 5 inhibitor. Vatalanib - a structurally related angiogenesis inhibitor ... a Specific Inhibitor of Cyclic GMP Phosphodiesterase, on Human Platelet Aggregation". The Journal of Pharmacology and ...
... an angiogenesis inhibitor". Biochemistry. United States. 42 (2): 450-7. doi:10.1021/bi0267792. ISSN 0006-2960. PMID 12525172. ...
Li Q, Shen PY, Wu G, Chen XZ (Jan 2003). "Polycystin-2 interacts with troponin I, an angiogenesis inhibitor". Biochemistry. 42 ... Perry SV (Jan 1999). "Troponin I: inhibitor or facilitator". Molecular and Cellular Biochemistry. 190 (1-2): 9-32. doi:10.1023/ ... "Troponin I is present in human cartilage and inhibits angiogenesis". Proceedings of the National Academy of Sciences of the ... "Troponin I is present in human cartilage and inhibits angiogenesis". Proceedings of the National Academy of Sciences of the ...
... a potent inhibitor of angiogenesis". Science. 285 (5425): 245-8. doi:10.1126/science.285.5425.245. PMID 10398599. Mori K, Duh E ... They found that PEDF was a previously uncharacterized protein and a member of the serpin (serine protease inhibitor) family. ... This action interferes with VEGF signaling thereby inhibiting angiogenesis. Laminin receptor is also a target for PEDF, and the ... Tong JP, Yao YF (Mar 2006). "Contribution of VEGF and PEDF to choroidal angiogenesis: a need for balanced expressions". ...
... angiogenesis inhibitors like bevacizumab, known to sometimes cause bone pain; and surgery, which may produce post-operative ... Aromatase inhibitors can cause diffuse muscle and joint pain and stiffness, and may increase the likelihood of osteoporosis and ... the proteasome inhibitors such as bortezomib, and the platinum-based drugs cisplatin, oxaliplatin and carboplatin. Whether CIPN ...
... is a monoclonal antibody that functions as an angiogenesis inhibitor. It works by slowing the growth of new blood ... Bevacizumab was the first available angiogenesis inhibitor in the United States. Bevacizumab was originally derived from a ... Shih T, Lindley C (November 2006). "Bevacizumab: an angiogenesis inhibitor for the treatment of solid malignancies". Clinical ... it became the first clinically used angiogenesis inhibitor. Its development was based on the discovery of human vascular ...
... endogenous angiogenesis inhibitors, fumagillin analogues, statins, cyclo-oxygenase-2 inhibitors, phytochemical compounds, ... Angiogenesis inhibitors lack clinical evidence of efficacy in endometriosis therapy. Under experimental in vitro and in vivo ... Examples of aromatase inhibitors include anastrozole and letrozole. Evidence for aromatase inhibitors is limited due to the ... Aromatase inhibitors are medications that block the formation of estrogen and have become of interest for researchers who are ...
Poster[permanent dead link] Matsumoto K, Nakamura T (April 2003). "NK4 (HGF-antagonist/angiogenesis inhibitor) in cancer ... Moreover, MET inhibitors, such as Crizotinib or PF-04254644, have been tested by short-term treatments in cellular and ... MP470 (SuperGen) is a novel inhibitor of c-KIT, MET, PDGFR, Flt3, and AXL. Phase I clinical trial of MP470 had been announced ... The major limitation of HGF inhibitors is that they block only HGF-dependent MET activation. NK4 competes with HGF as it binds ...
Miao RQ, Agata J, Chao L, Chao J (2002). "Kallistatin is a new inhibitor of angiogenesis and tumor growth". Blood. 100 (9): ... Chai KX, Chen LM, Chao J, Chao L (Dec 1993). "Kallistatin: a novel human serine proteinase inhibitor. Molecular cloning, tissue ... Miao RQ, Chen V, Chao L, Chao J (2003). "Structural elements of kallistatin required for inhibition of angiogenesis" (PDF). Am ... The MEROPS online database for peptidases and their inhibitors: I04.003 SERPINA4+protein,+human at the US National Library of ...
It is an endogenous angiogenesis inhibitor (i.e., it blocks the growth of new blood vessels). Clinical trials have been ... October 1994). "Angiostatin: a novel angiogenesis inhibitor that mediates the suppression of metastases by a Lewis lung ... "The X-ray Crystallographic Structure of the Angiogenesis Inhibitor Angiostatin". Journal of Molecular Biology. 318 (4): 1009- ... However studies have shown that avB3-integrins are not critically essential for angiogenesis, so more investigation is require ...
Miao RQ, Agata J, Chao L, Chao J (November 2002). "Kallistatin is a new inhibitor of angiogenesis and tumor growth". Blood. 100 ... Serpins are therefore the largest and most diverse superfamily of protease inhibitors. Most serpins are protease inhibitors, ... Some serpins are both protease inhibitors and perform additional roles. For example, the nuclear cysteine protease inhibitor ... Serpins are classed as irreversible inhibitors and as suicide inhibitors since each serpin protein permanently inactivates a ...
... angiogenesis inhibitors like bevacizumab, known to sometimes cause bone pain; surgery, which may produce post-operative pain, ... non-steroidal anti-inflammatory drugs or COX-2 inhibitors. Then, if complete pain relief is not achieved or disease progression ...
It is described as an angiogenesis inhibitor and a phytoestrogen. It was first isolated in 1899 from the dyer's broom, Genista ... Genistein and other isoflavones have been identified as angiogenesis inhibitors, and found to inhibit the uncontrolled cell ... Genistein's chief method of activity is as a tyrosine kinase inhibitor. Tyrosine kinases are less widespread than their ser/thr ... The main known activity of genistein is tyrosine kinase inhibitor, mostly of epidermal growth factor receptor (EGFR). Tyrosine ...
Angiolillo (1995). „Human interferon-inducible protein 10 is a potent inhibitor of angiogenesis in vivo". J. Exp. Med. 182: 155 ...
Cell growth, proliferation, angiogenesis, and migrationEdit. The above processes are part and parcel to tissue integrity and ... Seckl MJ, Higgins T, Widmer F, Rozengurt E (Jan 1997). "[D-Arg1,D-Trp5,7,9,Leu11]substance P: a novel potent inhibitor of ... "Inhibitor of apoptosis proteins (IAPs) and their antagonists regulate spontaneous and tumor necrosis factor (TNF)-induced ...
angiogenesis. • neuron differentiation. • Wnt signaling pathway involved in dorsal/ventral axis specification. • canonical Wnt ...
... entry inhibitors - Env - envelope - enzyme - enzyme-linked immunosorbent assay (ELISA) - eosinophil - eosinophilic folliculitis ... angiogenesis - angiomatosis - anorexia - antenatal - antibiotic - antibodies - antibody-dependent cell-mediated cytotoxicity ( ... integrase inhibitors - interaction - interferon - interleukin-1 (IL-1) - interleukin-2 (IL-2) - interleukin-4 (IL-4) - ... protease inhibitors - protease-sparing regimen - proteins - protocol - protozoa - provirus - pruritus - pseudo-Cushing's ...
HER2 kinase inhibitors, such as lapatinib, have also demonstrated clinical efficacy in HER2 overexpressing breast cancers by ... Evidence from cell lines and primary breast cancer cultures in vitro". Angiogenesis. 8 (3): 197-204. doi:10.1007/s10456-005- ... challenging the belief that VEGF's role in cancer is limited to angiogenesis. Instead, this research suggests that VEGF ... EGFR-specific tyrosine kinase inhibitors such as gefitinib have shown limited therapeutic success. This resistance is proposed ...
Brain-specific angiogenesis inhibitor 1. *Bromazepam. *Bulu tangkis Denmark. *Bus. C. *Cannone da 90/53 ...
... specifically binds to the 165 isoform of VEGF, a protein that plays a critical role in angiogenesis (the formation ... Kinase inhibitors: Altiratinib. *CE-245677. *Rebastinib. *Antibodies: Evinacumab (against angiopoietin 3). *Nesvacumab (against ...
Non-specific inhibitors (apigenin, sulfated glycosaminoglycans) or crude enzyme extracts have been used to test most hypotheses ... Hyaluronidases are also thought to play a role in the process of angiogenesis, although most hyaluronidase preparations are ... "Differential selectivity of hyaluronidase inhibitors toward acidic and basic hyaluronidases". Glycobiology. 16 (1): 11-21. doi: ...
Brain-specific angiogenesis inhibitor (1. *2. *3). *Cadherin (1. *2. *3). *Calcitonin ...
Inhibition of TNF-α is not the mechanism of thalidomide's inhibition of angiogenesis since numerous other TNF-α inhibitors do ... D'Amato RJ, Loughnan MS, Flynn E, Folkman J (April 1994). "Thalidomide is an inhibitor of angiogenesis". Proc. Natl. Acad. Sci ... Additionally, these analogs are more potent inhibitors of angiogenesis than thalidomide. As well, the amino-thalidomide and ... "Angiogenesis inhibitors derived from thalidomide". Bioorganic & Medicinal Chemistry Letters. 15 (24): 5509-5513. doi:10.1016/j. ...
Adapting AR inhibitors could as well prevent sepsis complications, prevent angiogenesis, ameliorate mild or asymptomatic ... Fatmawati S, Ersam T, Yu H, Zhang C, Jin F, Shimizu K (September 2014). "20(S)-Ginsenoside Rh2 as aldose reductase inhibitor ... Grewal AS, Bhardwaj S, Pandita D, Lather V, Sekhon BS (2016-01-01). "Updates on Aldose Reductase Inhibitors for Management of ... Gupta S, Singh N, Jaggi AS (March 2014). "Alkaloids as aldose reductase inhibitors, with special reference to berberine". ...
"Matrix metalloproteinase inhibitors". Georgetown University Hospital, Vincent T. Lombardi Cancer Center, Division of Medical ... Neurogenesis saling terkait dengan angiogenesis juga terjadi bergelombang yang diawali dengan migrasi neuroblas dengan ekspresi ... "Reducing bleeding complications after thrombolytic therapy for stroke: clinical potential of metalloproteinase inhibitors and ... faktor jaringan dan tissue factor pathway inhibitor.[22] Disfungsi endotelial yang menyebabkan defisiensi sawar darah otak, ...
... including pathways associated with angiogenesis, inflammation, the immune response, the mechanistic target of rapamycin (mTOR) ... "A human aminoacyl-tRNA synthetase as a regulator of angiogenesis". Proceedings of the National Academy of Sciences of the ...
These compounds also act as phosphodiesterase inhibitors, which produces additional anti-inflammatory effects, and makes them ...
... serves to block angiogenesis in both frog embryos and human cells. It has also been shown to serve as a vascular ... inhibitors. Azoles (lanosterol 14α-. demethylase inhibitors). Imidazoles. *Topical: bifonazole‡. *butoconazole. *chlormidazole‡ ... Genes responsible for the maintenance of cell walls in yeast have been shown to be responsible for angiogenesis in vertebrates ...
... they promote angiogenesis (the growth of new blood vessels), or guide cells to tissues that provide specific signals critical ... and that sustained delivery of such inhibitors have the capacity of long-term infection control.[13] The association of ... "Peptide and protein-based inhibitors of HIV-1 co-receptors". Experimental Biology and Medicine. 238 (5): 442-9. doi:10.1177/ ...
... and inhibitors of angiogenesis, such as pigment epithelium-derived factor (PEDF), rAAV-mediated expression of PEDF, angiostatin ...
It is thought to have a role in the cell growth and angiogenesis required for tumour survival. In this way it has been ... a new inhibitor of the chemokine receptors CXCR1 and CXCR2". Biochem. Pharmacol. 69 (3): 385-94. doi:10.1016/j.bcp.2004.10.007 ...
Other ineffective treatments include leukocyte elastase protease inhibitors, the EIPH Patch, hyperbaric oxygen therapy, ... and bronchial angiogenesis. ... phosphodiesterase inhibitors (e.g., sildenafil), and endothelin ...
Brain-specific angiogenesis inhibitor (1. *2. *3). *Cadherin (1. *2. *3). *Calcitonin ...
Prolactin modulators: Prolactin inhibitors: D2 receptor agonists (e.g., bromocriptine, cabergoline); Prolactin releasers: D2 ...
Angiogenesis Inhibitors for Cancer - from The Angiogenesis Foundation, 23 June 2009. *Angiogenesis Inhibitors for Eye Disease ... An angiogenesis inhibitor is a substance that inhibits the growth of new blood vessels (angiogenesis). Some angiogenesis ... and are thus destroyed by angiogenesis inhibitors.[28] Angiogenesis inhibitors are also used as treatment for the wet form of ... downregulate angiogenesis stimulators and inhibit cell migration of endothelial cells. IL-12. stimulate angiogenesis inhibitor ...
angiogenesis. • insulin receptor signaling pathway via phosphatidylinositol 3-kinase. • glucose metabolic process. • ... Pharmaceutical companies are designing and characterizing potential p110α isoform specific inhibitors.[14][15] ...
Moždano specifični angiogenezni inhibitor (1, 2, 3) • Cadherin (1, 2, 3) • Kalcitonin • CALCRL • CD97 • Kortikotropin- ... Feoktistov I, Ryzhov S, Goldstein AE, Biaggioni I (2003). "Mast cell-mediated stimulation of angiogenesis: cooperative ...
Angiogenesis inhibitors and other cancer therapeutics are used in combination to reduce cancer morbidity and mortality.[210] ... Angiogenesis inhibitors were once incorrectly thought to have potential as a "silver bullet" treatment applicable to many types ... "Five-alpha-reductase Inhibitors for prostate cancer prevention". The Cochrane Database of Systematic Reviews (2): CD007091. doi ... Another common example is the class of Bcr-Abl inhibitors, which are used to treat chronic myelogenous leukemia (CML).[4] ...
CysLTR2 inhibitors[edit]. There are as yet no selective inhibitors of CysLTR2 that are in clinical use (see Clinical ... positive regulation of angiogenesis. • G-protein coupled receptor signaling pathway. Sources:Amigo / QuickGO. ... of CysLTR2 in the allergic and hypersensitivity diseases of humans must await the development of selective CysLTR2 inhibitors. ...
As a clinical application, a bNOS inhibitor could be produced to decrease the load of Gram positive bacteria. Nitric oxide ... It helps modulate vascular tone, insulin secretion, airway tone, and peristalsis, and is involved in angiogenesis and neural ... is an NOS inhibitor that is under development as a neuroprotective agent for the treatment of traumatic brain injury.[1] Other ... is involved in regulation of cardiac function and angiogenesis (growth of new blood vessels). NO produced by eNOS has been ...
Brain-specific angiogenesis inhibitor (1. *2. *3). *Cadherin (1. *2. *3). *Calcitonin ...
Angiogenesis Inhibitors for Cancer - from The Angiogenesis Foundation, 23 June 2009. *Angiogenesis Inhibitors for Eye Disease ... An angiogenesis inhibitor is a substance that inhibits the growth of new blood vessels (angiogenesis). Some angiogenesis ... and are thus destroyed by angiogenesis inhibitors.[28] Angiogenesis inhibitors are also used as treatment for the wet form of ... downregulate angiogenesis stimulators and inhibit cell migration of endothelial cells. IL-12. stimulate angiogenesis inhibitor ...
Many other angiogenesis inhibitors are now being studied as well.. Angiogenesis inhibitors have different side effects from ... But angiogenesis inhibitors only prevent new blood vessels from forming. The side effects from angiogenesis inhibitors are ... Angiogenesis Inhibitors. Facebook Twitter Linkedin Pinterest Print. Cancer Breast Cancer Biopsies What is angiogenesis?. ... Scientists have studied the effect of angiogenesis inhibitors on certain kinds of tumors and cells. Several of the angiogenesis ...
Many other angiogenesis inhibitors are now being studied as well.. Angiogenesis inhibitors have different side effects from ... But angiogenesis inhibitors only prevent new blood vessels from forming. The side effects from angiogenesis inhibitors are ... Scientists have studied the effect of angiogenesis inhibitors on certain kinds of tumors and cells. Several of the angiogenesis ... What are angiogenesis inhibitors and how do they work?. A chemical that interferes with the signals to form new blood vessels ...
Potent inhibitor of angiogenesis and tumor growth in vitro and in vivo; specifically inhibits endothelial cell proliferation.. ... Endostatin is a potent inhibitor of angiogenesis and tumor growth in vitro and in vivo; specifcally inhibits endothelial cell ... However, it does not have an overall impact on wound healing. As it is a potent inhibitor of angiogenesis, it also strongly ... A specific inhibitor of endothelial cell growth and angiogenesis. More active relative to kringles 1-4. Studies with ...
Home > Treatments > Biological Therapies > Angiogenesis Inhibitors Angiogenesis Inhibitors. Angiogenesis is the process which ... PubMed Central search for free-access publications about Angiogenesis Inhibitors. MeSH term: Angiogenesis Inhibitors. US ... Inhibitors work in different ways: * by blocking angiogenesis growth factors (substances, such as VEGF, which promote the ... Many synthetic inhibitors of angiogenesis have not only come into force but also resulted in some severe adverse effects. ...
Patients with macular edema related to retinal vein occlusion had significant improvement in vision when treated with ranibizumab (Lucentis) in each of two dosages, randomized clinical trials showed.
... αPIGF inhibited tumor angiogenesis and lymphangiogenesis, as well as tumor recruitment of proangiogenic macrophages. αPIGF ... inhibitor-resistant tumors without affecting healthy vessels. Cell 131, 463-475 (2007). [PubMed] ... is not required for normal development and maintenance of the vasculature but has been implicated in pathological angiogenesis ...
Pharmacological Actions : Angiogenesis Inhibitors, Anti-Inflammatory Agents. Additional Keywords : Angiogenesis Inhibitors, ... Pharmacological Actions : Angiogenesis Inhibitors, Hypoxia-inducible factor-1 (HIF-1) inhibitor, NF-kappaB Inhibitor, Vascular ... Pharmacological Actions : Angiogenesis Inhibitors, Antiproliferative , Apoptotic. Additional Keywords : Angiogenesis Inhibitors ... Angiogenesis Inhibitors, Vascular Endothelial Growth Factor A Inhibitor, Vascular Endothelial Growth Factor C Inhibitor, ...
Taylor, S., and Folkman, J., 1982, Protamine is an inhibitor of angiogenesis. Nature 297: 307.PubMedCrossRefGoogle Scholar ... Moses, M.A., and Langer, R., 1991a, Inhibitors of angiogenesis. Biotechnology 9: 630.PubMedCrossRefGoogle Scholar ... Lee, A., and Langer, R., 1983, Shark cartilage contains inhibitors of tumor angiogenesis. Science 221: 1185.PubMedCrossRef ... Rastinejad, F., Polverini, P. J. and Bouck N. P., 1989, Regulation of the activity of a new inhibitor of angiogenesis by a ...
Brain-specific angiogenesis inhibitor 2 is a protein that in humans is encoded by the BAI2 gene. It is a member of the adhesion ... BAI1, a p53-target gene, encodes brain-specific angiogenesis inhibitor, a seven-span transmembrane protein and is thought to be ... 2002). "Expression of brain-specific angiogenesis inhibitor 2 (BAI2) in normal and ischemic brain: involvement of BAI2 in the ... "Entrez Gene: BAI2 brain-specific angiogenesis inhibitor 2". Stacey, edited by Simon Yona, Martin (2010). Adhesion-GPCRs : ...
... concerned with the bifurcation phenomenon of a free-boundary problem modeling the tumor growth under the action of angiogenesis ... and inhibitor. Taking the surface tension coefficient γ... ... stemming from angiogenesis. The appearance of inhibitor and the ... In this paper, we study a mathematical model of tumor growth under the action of angiogenesis and inhibitor. Angiogenesis is an ... As a result of angiogenesis, the tumor possesses its own vasculature. Then the nutrient and the inhibitor may be supplied to ...
Angiogenesis-inhibitors for metastatic thyroid cancer. There is currently no reliable evidence from randomized controlled ... To evaluate the benefits and risks of angiogenesis-inhibitors for metastatic thyroid cancer when given alone, or in combination ... Tan A, Xia N, Gao F, Mo Z, Cao Y. Angiogenesis-inhibitors for metastatic thyroid cancer. Cochrane Database of Systematic ... We planned to include randomized controlled trials that compared angiogenesis-inhibitors with other treatments, no treatment, ...
... Int J Cancer. 2002 Jan 20;97(3):290-6. doi: 10.1002/ijc.1602. ... suggesting that a gene-transcription effect was involved in the inhibition of angiogenesis by FK228. These results indicate ...
HUMAN METHIONINE AMINOPEPTIDASE 2 COMPLEXED WITH ANGIOGENESIS INHIBITOR FUMAGILLIN. *DOI: 10.2210/pdb1BOA/pdb ...
OSCC is a highly vascularized tumor but despite the crucial role of angiogenesis in OSCC, there is no antiangiogenic agent in ... Several pathways are involved in mediating angiogenesis, and vascular endothelial growth factor (VEGF) pathway is the most ... Angiogenesis is a hallmark of cancer and it is crucial for tumor growth, invasion, and metastasis formation. ... antibody-based agents and VEGF receptor tyrosine kinase inhibitors (TKIs). Antiangiogenic agents have been approved by the US ...
Therapeutic potential of selective cyclooxygenase-2 inhibitors in the management of tumor angiogenesis.. Gately S1, Kerbel R. ... The reported success of selective COX-2 inhibitors in cancer prevention could be related to angiogenesis inhibition [109]. As ... Intervention with angiogenesis inhibitors at this early stage of carcinogenesis has been shown to attenuate tumor growth in ... The effects of selective COX-2 inhibitors on angiogenesis may also be due, in part, to COX-independent mechanisms [123-125]. ...
Angiogenesis Inhibitors. What is angiogenesis?. Angiogenesis is the formation of new blood vessels. The process is controlled ... Many other angiogenesis inhibitors are now being studied as well.. Angiogenesis inhibitors have different side effects from ... But angiogenesis inhibitors only prevent new blood vessels from forming. The side effects from angiogenesis inhibitors are ... Scientists have studied the effect of angiogenesis inhibitors on certain kinds of tumors and cells. Several of the angiogenesis ...
Inhibitors of endothelial cell proliferation can usually function as inhibitors of angiogenesis. To find out if s3f inhibits ... Semaphorin-3F Is an Inhibitor of Tumor Angiogenesis. Ofra Kessler, Niva Shraga-Heled, Tali Lange, Noga Gutmann-Raviv, Edmond ... Semaphorin-3F Is an Inhibitor of Tumor Angiogenesis. Ofra Kessler, Niva Shraga-Heled, Tali Lange, Noga Gutmann-Raviv, Edmond ... Semaphorin-3F Is an Inhibitor of Tumor Angiogenesis. Ofra Kessler, Niva Shraga-Heled, Tali Lange, Noga Gutmann-Raviv, Edmond ...
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C11 is a novel selective FGFR1 inhibitor that exhibits potent activity against breast cancer metastasis and angiogenesis. ... C11 was a selective FGFR1 inhibitor with an IC50 of 19 nM among a panel of 20 tyrosine kinases. C11 inhibited cell ... Furthermore, the anti-angiogenesis activity of C11 was verified in endothelial cells and chicken chorioallantoic membranes ( ... Here, we identified a new selective FGFR inhibitor, C11, and assessed its antitumor activities. ...
6. Classification of Angiogenesis Inhibitors. 6.1 Direct Endogenous Inhibitors of Angiogenesis. 6.2 Indirect Inhibitors of ... Global Cancer Angiogenesis Inhibitors Clinical Pipeline: 146 Drugs. - Marketed Cancer Angiogenesis Inhibitors Drugs: 11 Drugs ... 9. Global Angiogenesis Inhibitors Market overview. 9.1 Current Market Scenario. 9.2 Global Cancer Angiogenesis Inhibitors ... One of the major segments of cancer therapy is occupied by the angiogenesis inhibitors. The market for angiogenesis inhibitors ...
... an endogenous angiogenesis inhibitor known to down-regulate a variety of growth- and angiogenesis-related genes in a wide range ... and angiogenesis-associated genes in the endothelium because this phenomenon is induced by a potent angiogenesis inhibitor, ... Rifampicin as an Oral Angiogenesis Inhibitor Targeting Hepatic Cancers. Masayoshi Shichiri, Nozomi Fukai, Yutaka Kono and ... Rifampicin as an Oral Angiogenesis Inhibitor Targeting Hepatic Cancers. Masayoshi Shichiri, Nozomi Fukai, Yutaka Kono and ...
View and select products within our Angiogenesis Inhibitors category available for immediate purchase. ... Angiogenesis Inhibitors. Santa Cruz Biotechnology now offers a broad range of Angiogenesis Inhibitors. Angiogenesis Inhibitors ... A potent inhibitor of angiogenesis, a vimentin and proteasome inhibitor. 5119-48-2. sc-200381. sc-200381A. 1 mg. 10 mg. $115.00 ... An inhibitor of PDGFR-β, Flk-1, and angiogenesis. 168836-03-1. sc-205984. sc-205984A. 1 mg. 5 mg. $48.00. $200.00. 0. ...
The membrane-anchored MMP inhibitor RECK is a key regulator of extracellular matrix integrity and angiogenesis.. Oh J1, ... results support a role for RECK in the regulation of MMP-2 in vivo and implicate RECK downregulation in tumor angiogenesis. ...
Drug: usage oral angiogenesis inhibitor Drug: stop oral angiogenesis inhibitor Phase 4 ... Angiogenesis Inhibitors. Angiogenesis Modulating Agents. Growth Substances. Physiological Effects of Drugs. Growth Inhibitors. ... Study to the Optimal Duration of Therapy With Oral Angiogenesis Inhibitors. The safety and scientific validity of this study is ... However, angiogenesis inhibitors have a rather cytostatic than cytotoxic effect compared to chemotherapeutics, as a result of ...
Angiogenesis,inhibitor,improves,brain,tumor,survival,by,reducing,edema,medicine,medical news today,latest medical news,medical ... Cediranib inhibits the potent angiogenesis factor VEGF which is known... We frequently see beneficial effects from drugs in ... The beneficial effects of anti-angiogenesis drugs in the treatment of ... Our findings suggest that antiangiogenesis therapy ... Angiogenesis inhibitor improves brain tumor survival by reducing edema. ...The beneficial effects of anti-angiogenesis drugs in ...
... an angiogenesis inhibitor developed by AEterna Laboratories Inc., a Canadian biotechnology corporation, in the treatment of ... In our work to date with patients, AEterna s AE-941/Neovastat has demonstrated to be an interesting angiogenesis inhibitor for ... NCI to Sponsor Phase III Trials of Liquid Shark Cartilage Angiogenesis Inhibitor. January 1, 1999 ... an angiogenesis inhibitor developed by AEterna Laboratories Inc., a Canadian biotechnology corporation, in the treatment of ...
... Cancer Biother Radiopharm. ... Extent of intratumoral angiogenesis, as indicated by microvessel tortuosity and microvessel density, was significantly reduced ...
BAI1 (brain-specific angiogenesis inhibitor 1) is a member of the so-called adhesion-type family of 7-transmembrane receptors ( ... Brain angiogenesis inhibitor 1 (BAI1) is a pattern recognition receptor that mediates macrophage binding and engulfment of Gram ... Brain angiogenesis inhibitor 1 (BAI1) is a receptor that recognizes apoptotic cells through its conserved type I thrombospondin ... Brain angiogenesis inhibitor 1 (BAI1) is a pattern recognition receptor that mediates macrophage binding and engulfment of Gram ...
  • Inhibition of the VEGF pathway has become the focus of angiogenesis research as approximately 60% of malignant tumors express high concentrations of VEGF. (wikipedia.org)
  • Strategies to inhibit the VEGF pathway include antibodies directed against VEGF or VEGFR, soluble VEGFR/VEGFR hybrids, and tyrosine kinase inhibitors. (wikipedia.org)
  • [4] [5] The most widely used VEGF pathway inhibitor on the market today is Bevacizumab . (wikipedia.org)
  • It inhibits angiogenesis by blocking the pro-angiogenic activities of VEGF and FGF-basic. (sigmaaldrich.com)
  • SU 5416 is a vascular endothelial growth factor (VEGF) receptor protein tyrosine kinase 1/2 inhibitor. (sigmaaldrich.com)
  • by blocking angiogenesis growth factors (substances, such as VEGF, which promote the process of developing new blood vessels). (cancerindex.org)
  • VEGF inhibitors in renal cell carcinoma. (cancerindex.org)
  • The arrival of targeted therapies-vascular endothelial growth factor (VEGF) pathway inhibitors and mammalian target of rapamycin (mTOR) inhibitors-and programmed death 1 (PD-1) inhibitors has transformed the management of renal cell carcinoma (RCC). (cancerindex.org)
  • It then discusses the pivotal trials that have investigated VEGF inhibitors in metastatic RCC, as well as in adjuvant and neoadjuvant settings. (cancerindex.org)
  • Finally, it addresses some practical considerations and future directions in the use of VEGF inhibitors in RCC. (cancerindex.org)
  • Noting that placental growth factor [PIGF, a member of the VEGF family that binds VEGF receptor 1 (VEGFR-1)] is not required for normal development and maintenance of the vasculature but has been implicated in pathological angiogenesis, Fischer et al . (sciencemag.org)
  • VEGF is a key molecular target for specific polyphenols found in tea, apples and cocoa which potently inhibit VEGF signalling and angiogenesis at physiological concentrations. (greenmedinfo.com)
  • Several pathways are involved in mediating angiogenesis, and vascular endothelial growth factor (VEGF) pathway is the most important one. (frontiersin.org)
  • Two major categories of agents have been developed to target VEGF pathway: antibody-based agents and VEGF receptor tyrosine kinase inhibitors (TKIs). (frontiersin.org)
  • In a mouse corneal neovascularization assay, this compound inhibited VEGF-induced angiogenesis. (nih.gov)
  • s3f also inhibited VEGF 165 , as well as bFGF-induced in vivo angiogenesis as determined by the alginate micro-encapsulation and Matrigel plug assays. (aacrjournals.org)
  • Indeed, s3a was found to inhibit capillary sprouting in an in vitro assay of angiogenesis and VEGF 165 -induced migration of endothelial cells. (aacrjournals.org)
  • Cediranib inhibits the potent angiogenesis factor VEGF which is known. (bio-medicine.org)
  • Cediranib inhibits the potent angiogenesis factor VEGF, which is known to be abundantly present in glioblastomas and play a critical role in tumor blood vessel formation. (bio-medicine.org)
  • Jain also notes that it will be important to identify biomarkers that may indicate which patients are most likely to benefit from treatment with angiogenesis inhibitors and to identify the mechanisms by which glioblastomas and other tumors resist anti-VEGF therapies. (bio-medicine.org)
  • Although VEGF has growth factor activity for some cancers, its bigger role in cancer spread is to promote angiogenesis by aiding multiplication and survival of the endothelial cells that form the new blood vessels. (oasisofhope.com)
  • PD-1/PD-L1 checkpoint inhibitors have been associated with promising activity as monotherapy in patients with HCC, and VEGF inhibition with bevacizumab has shown "modest activity" in this population. (onclive.com)
  • The benzoquinone ansamycin Hsp90 inhibitors geldanamycin and/or its derivatives 17-allylamino-17-demethoxygeldanamycin (17-AAG) and 17-(dimethylaminoethylamino)-17-demethoxygeldanamycin inhibited production of vascular endothelial growth factor (VEGF)-A by tumor cells and blocked proliferative responses of human endothelial cells at nanomolar concentrations. (aacrjournals.org)
  • Vascular endothelial growth factor (VEGF) is one of the most important proangiogenic factors that can drive tumor angiogenesis ( 6 , 7 ), although platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF) also play an important role. (aacrjournals.org)
  • In contrast, to inhibit lymph angiogenesis, so far there are only a few experimental approaches (e.g., the use of a VEGF R1R2 -Trap 5 or of a blocking anti-VEGFR3-antibody 9 ) but there is no U.S. Food and Drug Administration (FDA)-approved substance available yet. (arvojournals.org)
  • Introduction of non-platinum based PARP inhibitors and VEGF inhibitors in second and third-line settings has changed the treatment regime for ovarian cancer dramatically. (marketresearch.com)
  • Keywords: CCR7, esophageal squamous carcinoma, angiogenesis, VEGF Introduction Esophageal squamous cell carcinoma (ESCC) is usually one of the most aggressive tumors and is usually also the most common cause of esophagus malignancy deaths WZ8040 worldwide [1]. (acancerjourney.info)
  • Tumor angiogenesis WZ8040 is usually a result of an imbalance between pro-angiogenic factors, such as the vascular endothelial growth factor (VEGF) family and inhibitors of angiogenesis, including endostatin, angiostatin and other related molecules [6]. (acancerjourney.info)
  • VEGF-A regulates the sprouting and proliferation of endothelial cells and can stimulate tumor angiogenesis. (acancerjourney.info)
  • A number of currently-used anti-angiogenesis drugs function by inhibiting pro-angiogenic factors, for example the monoclonal antibody bevacizumab binds to VEGF-A and prevents it from binding to the VEGF receptors, and sunitinib and sorafenib are small molecules that attach to VEGF-R and prevent the binding of VEGF-A [8]. (acancerjourney.info)
  • VEGF promotes angiogenesis by aiding multiplication and survival of the endothelial cells needed to form new blood vessels. (oasisofhopecancercenter.com)
  • We also utilize NF-kappaB inhibitors and EGFR inhibitors because they both boost tumor production of VEGF and other angiogenic growth factors. (oasisofhopecancercenter.com)
  • VEGF or other angiogenesis factors produced by tumor cells or nearby cells can cause the development of blood vessels that feed the growing tumor. (cancerquest.org)
  • Disappointing results were reported with oral VEGF inhibitors plus erlotinib in pretreated patients with EGFR wild type NSCLC. (explorationpub.com)
  • citation needed] Some common components of human diets also act as mild angiogenesis inhibitors and have therefore been proposed for angioprevention, the prevention of metastasis through the inhibition of angiogenesis. (wikipedia.org)
  • Tumor growth and metastasis depend on blood supply and blood vessel formation (angiogenesis). (cochrane.org)
  • Angiogenesis is a hallmark of cancer and it is crucial for tumor growth, invasion, and metastasis formation. (frontiersin.org)
  • The fibroblast growth factor receptors (FGFRs) are increasingly considered attractive targets for therapeutic cancer intervention due to their roles in tumor metastasis and angiogenesis. (nature.com)
  • In sum, C11 is a novel selective FGFR1 inhibitor that exhibits potent activity against breast cancer metastasis and angiogenesis. (nature.com)
  • Cancer progression and metastasis depend on recruitment of new capillaries from preexisting vessels, a process known as angiogenesis ( 1 ). (aacrjournals.org)
  • Thus, we identify Hsp90 inhibitors as important regulators of many aspects of tumor angiogenesis (and potentially lymphangiogenesis) and suggest that they may provide therapeutic benefit not only via direct effects on tumor cells but also indirectly by inhibiting the production of angiogenic cytokines and responses of activated endothelial cells that contribute to tumor progression and metastasis. (aacrjournals.org)
  • Publications] Masaki Tamura, Toru Yanase, and kenichi Tanaka: 'Angiogenesis inhibitor and inhibition of metastasis' Hematology and Incology. (nii.ac.jp)
  • Angiogenesis, the process of new blood vessel formation, is critical for tumor progression, invasion, and metastasis in solid tumors. (oncologynurseadvisor.com)
  • Angiogenesis has been shown to be essential for growth and metastasis of solid tumors. (wikidoc.org)
  • In particular, the presence of regional attack, distant metastasis and tumor-induced angiogenesis show highly malignant potential in esophageal carcinoma patients [2]. (acancerjourney.info)
  • Plenty of researches demonstrate that tumor induced angiogenesis is usually required to maintain malignant ESCC growth and metastasis, and constitutes an important hallmark of ESCC progression [3]. (acancerjourney.info)
  • Chemokines and their receptors play important functions in metastasis and tumor growth, however, the role of chemokine receptors in angiogenesis has only recently been discovered [11]. (acancerjourney.info)
  • Withaferin A also inhibits angiogenesis by binding to vimentin and F-actin. (sigmaaldrich.com)
  • One such class of drugs inhibits angiogenesis (the development of new blood vessels), which is essential for tumour growth. (ox.ac.uk)
  • Signal Transduction inhibitors: Imatinib Mesylate (protein-tyrosine kinase inhibitor), Genefitinib (epidermal growth factor receptor tyrosine kinase inhibitor - EGFR-TK), Cetuximab (epidermal growth factor receptor), Lapatinib (epidermal growth factor receptor (EGFR) and human epidermal receptor type 2 (HER2) tyrosine kinase inhibitor. (chemocare.com)
  • Consequently, application of specific strategy, including monoclonal antibody therapeutics and tyrosine kinase inhibitor that may block tumor angiogenesis could prevent the formation of tumor blood vessels and combat ESCC [5]. (acancerjourney.info)
  • Although tumor growth can be stunted by a variety of single angiogenesis inhibitors ( 2 ), combination antiangiogenesis protocols can be more effective than single-agent therapies ( 3 , 4 ). (aacrjournals.org)
  • Therapies that inhibit angiogenesis are attracting fresh interest in combination regimens with immune checkpoint immunotherapy in tumor types such as hepatocellular carcinoma, urothelial carcinoma, and endothelial cancer. (onclive.com)
  • The addition of angiogenesis kinase inhibitors, such as sorafenib, sunitinib, vandetanib, and lenalidomide, to the treatment therapies for patients with advanced non-small cell lung adenocarcinoma improves survival outcomes, a study published in the journal OncoTargets and Therapy has shown. (oncologynurseadvisor.com)
  • Although data have shown that angiogenesis inhibitors significantly improve overall and progression-free survival compared with non-angiogenesis inhibitor-containing therapies, efficacy may be affected by non-small cell lung cancer (NSCLC) histologic subtype. (oncologynurseadvisor.com)
  • HCC is a typical blood vessel-rich tumor, and anti-angiogenesis-related therapies have become the standard treatment for patients with advanced HCC[1-3]. (researchsquare.com)
  • Michele Moschetta, Marta Cesca, Francesca Pretto and Raffaella Giavazzi, " Angiogenesis Inhibitors: Implications for Combination with Conventional Therapies", Current Pharmaceutical Design (2010) 16: 3921. (eurekaselect.com)
  • Targeted therapies involve production of components such as monoclonal antibodies or anti-angiogenesis drugs may best be used in the short term, combination with traditional therapies. (chemocare.com)
  • More research is needed to identify which cancers may be best treated with targeted therapies such as monoclonal antibodies or anti-angiogenesis drugs and to identify additional targets for more types of cancer. (chemocare.com)
  • One of the most recent methods that is being developed for the delivery of anti-angiogenesis factors to tumour regions in cancer sufferers is using genetically modified bacteria that are able to colonize solid tumors in vivo. (wikipedia.org)
  • Scientists have studied the effect of angiogenesis inhibitors on certain kinds of tumors and cells. (hopkinsmedicine.org)
  • An angiogenesis inhibitor medicine, bevacizumab, has been approved by the FDA to aid in the treatment of glioblastoma, colorectal cancer, non-small cell lung cancer, liver (hepatocellular) carcinoma, neuroendocrine tumors, and metastatic renal cell cancer. (hopkinsmedicine.org)
  • A recent method for the delivery of anti-angiogenesis factors to tumor regions in cancer patients uses genetically modified bacteria that are able to colonize solid tumors in vivo, such as Clostridium, Bifidobacteria and Salmonella by adding genes for anti-angiogenic factors such as endostatin or IP10 chemokine and removing any harmful virulence genes. (wikipedia.org)
  • The tumors that did develop from s3f-expressing HEK293 cells developed at a much slower rate and had a significantly lower concentration of tumor-associated blood vessels, indicating that s3f is an inhibitor of tumor angiogenesis. (aacrjournals.org)
  • Therefore, there is a need to develop more selective inhibitors to suppress tumors through selective targeting of FGFRs. (nature.com)
  • Because tumors that are unable to elicit angiogenesis remain in a dormant state and fail to grow beyond a few millimeters in size ( 2 ), the multistep process of angiogenesis has fostered an intense search for agents that might inhibit this process ( 3 ). (aacrjournals.org)
  • The beneficial effects of anti-angiogenesis drugs in the treatment of the deadly brain tumors called glioblastomas appear to result primarily from reduction of edema the swelling of brain tissue and not from any direct anti-tumor effect, according to a study from Massachusetts General Hospital (MGH) researchers. (bio-medicine.org)
  • Angiogenesis is the process whereby new blood vessels form, in response to chemical signals produced by wounded tissue or by tumors. (oasisofhope.com)
  • Axitinib significantly inhibited angiogenesis in rat 9L tumors grown s.c. in scid mice but only moderately delayed tumor growth. (aacrjournals.org)
  • Angiogenesis is crucial for the growth of malignant tumors and metastases ( 1 , 2 ). (aacrjournals.org)
  • Angiogenesis is a crucial element in the development and dissemination of great tumors. (columbiagypsy.net)
  • Anti-angiogenesis agents are types of targeted therapy that use drugs or other substances to stop tumors from making the new blood vessels they need to keep growing. (cancer.org)
  • Tumors that do not produce (or cause other cells to produce) angiogenesis factors can not grow. (cancerquest.org)
  • The invention relates to a combination therapy for the treatment of tumors and tumor metastases comprising administration of receptor tyrosine kinase antagonists/inhibitors, especially ErbB receptor antagonists, more preferably EGF receptor (Her 1) antagonists and anti-angiogenic agents, preferably integrin antagonists, optionally together with agents or therapy forms that have additive or synergistic efficacy when administered together with the combination of antagonists/inhibitors, such as chemotherapeutic agents and or radiation therapy. (patentsencyclopedia.com)
  • However, limits that could affect its use in clinical practice are the need of an intravenous infusion for angiogenesis inhibitors, the increased incidence of treatment associated adverse events, the exclusion of patients with tumors located in central position or at risk of hemorrhage. (explorationpub.com)
  • Angiogenesis is a crucial process for the development of almost all tumors, including non-small-cell lung cancer (NSCLC). (explorationpub.com)
  • Angiogenesis inhibitors were once thought to have potential as a " silver bullet " treatment applicable to many types of cancer , but the limitations of anti-angiogenic therapy have been shown in practice. (wikipedia.org)
  • [1] Nonetheless, inhibitors are used to effectively treat cancer, macular degeneration in the eye, and other diseases that involve a proliferation of blood vessels. (wikipedia.org)
  • [7] Endogenous inhibitors are attractive targets for cancer therapy because they are less toxic and less likely to lead to drug resistance than some exogenous inhibitors. (wikipedia.org)
  • Angiogenesis inhibitors have different side effects from most conventional cancer chemotherapy medicines because they work very differently. (hopkinsmedicine.org)
  • The Foundation promotes angiogenesis research and aiming to improve treatments for patients with angiogenesis related disease (including cancer). (cancerindex.org)
  • Vitamin C therapy can down-regulate angiogenesis and inflammation promoting cytokines in some cancer patients. (greenmedinfo.com)
  • Thus angiogenesis inhibitors have been closely studied for possible cancer treatment. (wikipedia.org)
  • There is currently no reliable evidence from randomized controlled trials demonstrating that the benefits of angiogenesis-inhibitors outweigh their risks in treating advanced thyroid cancer. (cochrane.org)
  • There is currently no reliable evidence available from randomized controlled trials regarding the benefits and harms of the use of angiogenesis-inhibitors for treating advanced thyroid cancer. (cochrane.org)
  • To evaluate the benefits and risks of angiogenesis-inhibitors for metastatic thyroid cancer when given alone, or in combination with chemotherapy or radiotherapy. (cochrane.org)
  • We planned to include randomized controlled trials that compared angiogenesis-inhibitors with other treatments, no treatment, or placebo in participants who had pathologically confirmed advanced thyroid cancer. (cochrane.org)
  • This Research Topic will cover topics related to angiogenesis and tumor related vessels in oral cancer. (frontiersin.org)
  • In order to take advantage of both the COX-dependent and COX-independent benefits of NSAIDs and selective COX-2 inhibitors, will require evaluation of these agents in neoplastic disease settings, using cancer-specific biomarkers. (nih.gov)
  • The reported success of selective COX-2 inhibitors in cancer prevention could be related to angiogenesis inhibition [109]. (nih.gov)
  • Angiogenesis is an important therapeutic target in cancer, and to fully exploit its therapeutic potential, combination chemotherapeutic/antiangiogenic regimens should be optimized and delivered earlier to more patients. (aacrjournals.org)
  • Here, we present the effects of oral rifampicin on human cancer progression and its antiangiogenic properties, which were comparable to the angiogenesis inhibitor endostatin. (aacrjournals.org)
  • Research in angiogenesis has strong implications in cancer therapy as angiogenesis is one of the hallmarks of cancer. (scbt.com)
  • The National Cancer Institute (NCI) will sponsor phase III trials to test the efficacy of AE-941/Neovastat, an angiogenesis inhibitor developed by AEterna Laboratories Inc., a Canadian biotechnology corporation, in the treatment of cancer. (cancernetwork.com)
  • In our work to date with patients, AEterna s AE-941/Neovastat has demonstrated to be an interesting angiogenesis inhibitor for the treatment of cancer. (cancernetwork.com)
  • Angiogenesis plays a crucial role in the growth and spread of cancer. (oasisofhope.com)
  • Agiogenic inhibitors have become an important part of treatment for many type of cancer as they stop tumor from growing their own blood vessels. (oasisofhope.com)
  • The promising but still limited efficacy of angiogenesis inhibitors as monotherapies for cancer treatment indicates a need to integrate these agents into existing therapeutic regimens. (aacrjournals.org)
  • Taken together, these findings clearly support the pharmacological roles of marmesin in regulating angiogenesis, and warrant further evaluation and development as a potential therapeutic agent for the treatment and prevention of angiogenesis-related diseases including cancer. (sigmaaldrich.com)
  • Update on bevacizumab and other angiogenesis inhibitors for brain cancer. (harvard.edu)
  • This phase I, accelerated titration study investigated the maximum tolerated dose, safety, pharmacokinetic profile, and pharmacodynamics of BIBF 1120, a novel, orally available angiokinase inhibitor of vascular endothelial growth factor, platelet-derived growth factor, and fibroblast growth factor receptors, in 61 patients with advanced cancer. (aacrjournals.org)
  • Angiogenesis inhibitors offer a novel approach for cancer therapy ( 5 ). (aacrjournals.org)
  • Cancer Angiogenesis Inhibitor Market Research Report Forecast 20172022 is a valuable source of insightful data for business strategists. (bioportfolio.com)
  • This Cancer Angiogenesis Inhibitor market study provides comprehensive data which enhances the understanding, scope and application of this report. (bioportfolio.com)
  • Are substances that inhibit the growth of new blood vessels (angiogenesis inhibitors), alone or in combination with conventional chemotherapy, likely to improve outcomes for women with ovarian cancer? (cochrane.org)
  • However, there is currently no evidence that angiogenesis inhibitors improve OS, nor is there enough evidence to justify the routine use of angiogenesis inhibitors in treating women with ovarian cancer. (cochrane.org)
  • A. Rossi, P. Maione, M. L. Ferrara, P. C. Sacco, C. Schettino, M. A. Bareschino and C. Gridelli, " Angiogenesis Inhibitors and Vascular Disrupting Agents in Non-Small Cell Lung Cancer", Current Medicinal Chemistry (2009) 16: 3919. (eurekaselect.com)
  • PARP inhibitors are anticipated to be the fastest growing drug class in the ovarian cancer market through the forecast period. (marketresearch.com)
  • We aimed at assessing the overall efficacy of angiogenesis inhibitor (AI)-containing regimens in the treatment of advanced non-small-cell lung cancer (NSCLC) according to histological types. (oncologynurseadvisor.com)
  • Integrin Antagonists and Other Low Molecular Weight Compounds as Inhibitors of Angiogenesis New Drugs in Cancer Therapy. (docme.ru)
  • HIGHLIGHTS Integrin Antagonists and Other Low Molecular Weight Compounds as Inhibitors of Angiogenesis: New Drugs in Cancer Therapy** Athanassios Giannis* and Frank Riibsam Angiogenesis (neovascularization), the process by which new blood capillaries are formed from an already existing blood vessel, is of fundamental importance for a number of physiological and pathological events including embryogenesis, wound healing, chronic inflammation. (docme.ru)
  • Due to the observation that an adequate blood supply is necessary for tumor growth, Folkman postulated in the early 1970s that inhibitors of angiogenesis are of potential use in cancer therapy. (docme.ru)
  • Angiogenesis inhibitors for the treatment of ovarian cancer. (ox.ac.uk)
  • OBJECTIVES: To compare the effectiveness and toxicities of angiogenesis inhibitors in the treatment of ovarian cancer. (ox.ac.uk)
  • SELECTION CRITERIA: Randomised controlled studies comparing angiogenesis inhibitors with either standard chemotherapy or no treatment, in women with ovarian cancer. (ox.ac.uk)
  • We identified five abstracts of completed RCTs of four different angiogenesis-inhibiting agents, with a total of 3701 participants.Meta-analysis of two trials found no statistically significant difference in overall survival (OS) between women with newly-diagnosed advanced ovarian cancer who received concurrent and maintenance bevacizumab compared to those who received chemotherapy (carboplatin and paclitaxel) alone. (ox.ac.uk)
  • Angiogenesis is associated with tumor development and malignancy and is a validated target for cancer treatment. (eurekaselect.com)
  • Tumour angiogenesis and the levels of plasminogen activator inhibitor type I (PAI-I) are both informative prognostic markers in breast cancer. (lu.se)
  • To evaluate the interrelationship of angiogenesis and the PAI-I level in breast cancer, we have evaluated the prognostic value of those factors in a total of 228 patients with primary, unilateral, invasive breast cancer, evaluated at a median follow-up time of 12 years. (lu.se)
  • We conclude that the PAI-I level and the Chalkley count are independent prognostic markers for recurrence-free survival in patients with primary breast cancer, suggesting that the prognostic impact of PAI-I is not only based on its involvement in angiogenesis. (lu.se)
  • Cancer growth inhibitors block certain chemical signals within cells, which slows down or stops the growth of the cancer. (macmillan.org.uk)
  • So it may also be called a cancer growth inhibitor. (macmillan.org.uk)
  • Cancer growth inhibitors make it difficult for cancer cells to receive these signals. (macmillan.org.uk)
  • WO9916755A1 ] The present invention relates to compounds which inhibit tyrosine kinase enzymes, compositions which contain tyrosine kinase inhibiting compounds and methods of using tyrosine kinase inhibitors to treat tyrosine kinase-dependent diseases/conditions such as angiogenesis, cancer, atherosclerosis, diabetic retinopathy or autoimmune diseases, in mammals. (epo.org)
  • Mareedu N, Escalante CP (2017) Angiogenesis Inhibitor Induced Thromboembolism in Cancer Patients. (clinmedjournals.org)
  • But, angiogenesis also plays a crucial role in the promoting the growth and spread of cancer. (oasisofhopecancercenter.com)
  • An important cancer fighting strategy is to inhibit angiogenesis. (oasisofhopecancercenter.com)
  • Angiogenesis inhibitors (AIs) have become established as an effective cancer treatment. (cdc.gov)
  • The National Cancer Institute's Angiogenesis Core Facility seek parties interested in in-licensing a new set of non-cytotoxic antiangiogenic small molecules. (cancer.gov)
  • The National Cancer Institute's Angiogenesis Core Facility is seeking statements of capability or interest from parties interested in collaborative research to further develop, evaluate, or commercialize a new set of non-cytotoxic antiangiogenic small molecules. (cancer.gov)
  • Deregulation of angiogenesis plays a role in many human diseases, including cancer, age-related macular degeneration, diabetic retinopathy, and endometriosis. (cancer.gov)
  • The phase III CONFIRM clinical trials demonstrated that metastatic colorectal cancer patients with elevated serum lactate dehydrogenase (LDH) had improved outcome when the vascular endothelial growth factor receptor (VEGFR) inhibitor PTK/ZK (Vatalanib) was added to FOLFOX4 chemotherapy. (qub.ac.uk)
  • Lenz, H-J. / Intratumoral expression profiling of genes involved in angiogenesis in colorectal cancer patients treated with chemotherapy plus the VEGFR inhibitor PTK787/ZK 222584 (vatalanib) . (qub.ac.uk)
  • Abnormal angiogenesis is not limited to cancer. (cancerquest.org)
  • 5 The process of angiogenesis in cancer is shown in the animation below. (cancerquest.org)
  • The process of blood vessel formation is termed angiogenesis.This process is a very active area of research in cancer treatment for several reasons. (cancerquest.org)
  • Several preclinical studies suggested a potential benefit from combined treatment with inhibitors of epidermal growth factor receptor (EGFR) and angiogenesis, both effective in patients with advanced non-small-cell lung cancer (NSCLC). (explorationpub.com)
  • The complex process of angiogenesis proceeds in the following stages (Figure 1): a) activation of endothelial cells (EC) and pericytes by the growth factors, b) degradation of the basal lamina of the bloodvessel by the action of proteases (collagenases, plasminogen activator), c) migration (and proliferation) of EC and pericytes towards Figure 1. (docme.ru)
  • Because these agents inhibit angiogenesis, they should have at least additive benefit in combination with standard chemotherapy [111] and radiation therapy [24, 112]. (nih.gov)
  • There are known substances that both stimulate angiogenesis and stop, or inhibit, angiogenesis. (chemocare.com)
  • To analyze whether bevacizumab can inhibit inflammatory angiogenesis and lymphangiogenesis in the cornea. (arvojournals.org)
  • Topical or systemic application of bevacizumab inhibits both inflammation-induced angiogenesis and lymphangiogenesis in the cornea. (arvojournals.org)
  • This concept was first proposed by Judah Folkman in the early 1970s, but it wasn't until 2004 that the first angiogenesis inhibitor, bevacizumab (Avastin), was approved. (cancer.org)
  • Endostatin is an endogenous inhibitor of angiogenesis, and in vitro inhibits the migration of endothelial cells. (sigmaaldrich.com)
  • Collagen XVIII is cleaved to form endostatin, and this system might act as the negative control of angiogenesis. (sigmaaldrich.com)
  • The promising clinical trials results of endostatin (an angiogenesis inhibitor) is a good example of this. (frontiersin.org)
  • Furthermore, we found that rifampicin exerts its antiangiogenic effect through inhibition of the expression of angiogenesis-associated genes in a manner comparable to the action of endostatin, an endogenous angiogenesis inhibitor known to down-regulate a variety of growth- and angiogenesis-related genes in a wide range of endothelial lineage cells ( 8 , 9 ). (aacrjournals.org)
  • 1997) Endostatin An Endogenous Inhibitor of Angiogenesis and Tumor Growth. (scirp.org)
  • Aim: To construct the human endostatin gene, which is the angiogenesis inhibitor, into non-fusion expression vector in Escherichia coli. (elsevier.com)
  • Conclusion: The cloned Endostatin gene of 552 bp has almost the same gene sequence with the endostain cDNA of collagen XVIII in GenBank, which indicates that human endostatin gene obtains non-fused expression in Escherichia coli, it lays an experimental methodological foundation for the anti-angiogenesis therapy with endostatin gene. (elsevier.com)
  • Angiogenesis is the formation of new blood vessels. (hopkinsmedicine.org)
  • Angiogenesis inhibitors are substances which prevent this formation of new blood vessels, thereby stopping or slowing the growth or spread of tumours. (cancerindex.org)
  • Anti-angiogenesis is the process of stopping the formation of new blood vessels. (chemocare.com)
  • b) result in the production of eicosanoid products TXA2, PGI2, PGE2 that directly stimulate endothelial cell migration and angiogenesis in vivo, and (c) result in enhanced tumor cell, and possibly, vascular endothelial cell survival by upregulation of the antiapoptotic proteins Bcl-2 and/or activation of PI3K-Akt. (nih.gov)
  • The researchers state that the mTOR inhibitor rapamycin and its analogue temsirolimus both inhibit tumor angiogenesis in vivo and directly inhibit endothelial cell proliferation in vitro. (life-enhancement.com)
  • Finally, we showed for the first time that Hsp90 inhibitors also reduce expression of VEGFR-1 on human vascular endothelial cells, VEGFR-3 on lymphatic endothelial cells in vitro , and all three VEGFRs on mouse vasculature in vivo . (aacrjournals.org)
  • The feasibility of photoacoustic microscopy (PAM) for evaluation of angiogenesis inhibitor was investigated on a chick embryo model in vivo . (osapublishing.org)
  • Here, we investigate the effect of HT on in vitro and in vivo angiogenesis. (elsevier.com)
  • We developed a network walking algorithm to extract connectivity information from the interactome and applied it to simulate the level of network perturbation by three multi-targeted anti-angiogenic kinase inhibitors. (biomedcentral.com)
  • To date, the US Food and Drug Administration has approved 4 oral tyrosine kinase inhibitors (TKIs) and 1 anti-angiogenic antibody for the treatment of advanced HCC[4]. (researchsquare.com)
  • Tyrosine kinase inhibitors and proteasome inhibitors are examples of small-molecule drugs. (cancer.ca)
  • Angiogenesis inhibitor therapy may stabilize the tumor and prevent it from growing further. (hopkinsmedicine.org)
  • However, successful clinical application of angiogenesis inhibitors, irrespective of monotherapy or combination therapy, requires long-term administration, but most of these entering clinical trials are costly, large molecular weight proteins requiring parenteral administration ( 3 , 5 ). (aacrjournals.org)
  • How can I get more information about Angiogenesis Inhibitors Therapy at Oasis of Hope? (oasisofhope.com)
  • She said the hy pothesi s behind combining angiogenesis inhibitors and immunotherapy is that ablation or "reprogramming" the microenvironment might boost the efficacy of anticancer therapy. (onclive.com)
  • However, many key signaling molecules involved in angiogenesis may be deregulated by Hsp90 inhibition, providing an additional benefit of Hsp90-targeted therapy. (aacrjournals.org)
  • This study aimed at confirming whether ACEIs are beneficial in anti-angiogenesis therapy for hepatocellular carcinoma. (researchsquare.com)
  • Preclinical and clinical evidence substantiates the feasibility of combining angiogenesis inhibitors with conventional anticancer therapy. (eurekaselect.com)
  • Modern targeted therapy types include the use of monoclonal antibodies and anti-angiogenesis drugs, both of which are described in greater depth here. (chemocare.com)
  • One form of this therapy uses angiogenesis inhibitors. (medicalnewstoday.com)
  • Therapy with Angiogenesis Inhibitors (AIs) is a newer targeted approach in treating cancers. (clinmedjournals.org)
  • Angiogenesis Inhibitors (AIs) are one of the classes of targeted therapy being used in the treatment of various cancers. (clinmedjournals.org)
  • Interestingly, the expression of angiogenic-stimulating factors such as vascular endothelial growth factor or kinase insert domain receptor were suppressed by FK228, whereas that of angiogenic-inhibiting factors such as von Hippel Lindau and neurofibromin2 were induced, suggesting that a gene-transcription effect was involved in the inhibition of angiogenesis by FK228. (nih.gov)
  • Several of the angiogenesis inhibitors are also effective in treating an eye disease, macular degeneration. (hopkinsmedicine.org)
  • [4] [5] However, the therapeutic use of endogenous inhibitors has disadvantages. (wikipedia.org)
  • Therapeutic potential of selective cyclooxygenase-2 inhibitors in the management of tumor angiogenesis. (nih.gov)
  • Disrupting one or even a few angiogenesis pathways is often insufficient to achieve sustained therapeutic benefits due to the complexity of angiogenesis. (biomedcentral.com)
  • Through increased specificity, potency and ocular permeability, novel SRPK1 inhibitors have potential to reach therapeutic levels in posterior eye segments following eye drop administration and improve treatment for patients with wAMD and DME. (arvojournals.org)
  • Given its high vascularization and immunogenicity, antiangiogenics and immune checkpoint inhibitors (ICI), respectively, are two therapeutic approaches that have shown efficacy in HCC. (biomedcentral.com)
  • We constructed a comprehensive gene functional association network or interactome by transcript profiling an in vitro angiogenesis model, in which human umbilical vein endothelial cells (HUVECs) formed capillary structures when co-cultured with normal human dermal fibroblasts (NHDFs). (biomedcentral.com)
  • We established a comprehensive gene functional association network to model in vitro angiogenesis regulation. (biomedcentral.com)
  • We show that heat treatment of endothelial cells (ECs) affect their differentiation into capillary-like structures in two models of in vitro angiogenesis. (elsevier.com)
  • αPIGF inhibited tumor angiogenesis and lymphangiogenesis, as well as tumor recruitment of proangiogenic macrophages. (sciencemag.org)
  • These studies indicate that semaphorins may perhaps be able to function as modulators of vasculogenesis, angiogenesis, and possibly lymphangiogenesis. (aacrjournals.org)
  • Objective The study was focused on the effect and mechanism of IFN-α and IFN-γ on the proliferation and migration of the lymphatic endothelial cell (LEC), and further discovering the safe, effective and practical inhibitors of lymphangiogenesis.Materials and Methods LECs were taken from the pig thoracic duct. (dissertationtopic.net)
  • Brain-specific angiogenesis inhibitor 2 is a protein that in humans is encoded by the BAI2 gene. (wikipedia.org)
  • BAI1, a p53-target gene, encodes brain-specific angiogenesis inhibitor, a seven-span transmembrane protein and is thought to be a member of the secretin receptor family. (wikipedia.org)
  • BAI1 (brain-specific angiogenesis inhibitor 1) is a member of the so-called adhesion-type family of 7-transmembrane receptors ( 3 ). (pnas.org)
  • There are two other brain-specific angiogenesis inhibitor genes, designated BAI2 and BAI3 which along with BAI1 have similar tissue specificities and structures, however only BAI1 is transcriptionally regulated by p53. (wikidoc.org)
  • Brain-specific angiogenesis inhibitor 1 has been shown to interact with BAIAP3 [4] and MAGI1 . (wikidoc.org)
  • Endogenous inhibitors are found in the body naturally and involved in the day-to-day process of regulating blood vessel formation. (wikipedia.org)
  • During tumor growth, the action of angiogenesis stimulators surpasses the control of angiogenesis inhibitors, allowing for unregulated or less regulated blood vessel growth and formation. (wikipedia.org)
  • To achieve this, tumor cells excrete certain proteins that stimulate blood vessel growth into and around the tumor - a process called angiogenesis. (cancerindex.org)
  • New blood vessel formation, known as angiogenesis, is a fundamental event in the process of tumor growth and metastatic dissemination. (eurekaselect.com)
  • However, when a specific angiogenesis promoter is blocked, some cancers eventually grow blood vessels by using a different angiogenesis promoter. (cancerindex.org)
  • Although new blood vessels can form as part of the body's normal processes, cancers are especially reliant on angiogenesis, as they need a blood supply in order to grow. (cochrane.org)
  • Angiogenesis inhibitors prevent cancers from making new blood vessels. (macmillan.org.uk)
  • In preclinical models, a selective inhibitor of COX-2 was shown to potentiate the beneficial antitumor effects of ionizing radiation with no increase in normal tissue cytotoxicity [113-115]. (nih.gov)
  • Given the safety and tolerability of the selective COX-2 inhibitors, and the potent antiangiogenic properties of these agents, the combination of antiangiogenic chemotherapy with a COX-2 inhibitor warrants clinical evaluation [118, 121, 122]. (nih.gov)
  • The effects of selective COX-2 inhibitors on angiogenesis may also be due, in part, to COX-independent mechanisms [123-125]. (nih.gov)
  • Some of the COX-independent mechanisms for NSAIDs and selective COX-2 inhibitors include activation of protein kinase G, inhibition of NF-kappa B activation, downregulation of the antiapoptotic protein Bcl-XL, inhibition of PPAR delta, and activation of PPAR gamma. (nih.gov)
  • One or more of these COX-independent effects could contribute to the antiangiogenic properties of NSAIDs and selective COX-2 inhibitors. (nih.gov)
  • Here, we identified a new selective FGFR inhibitor, C11, and assessed its antitumor activities. (nature.com)
  • C11 was a selective FGFR1 inhibitor with an IC 50 of 19 nM among a panel of 20 tyrosine kinases. (nature.com)
  • Present FGFR inhibitors can be divided into two groups: nonselective FGFR TKIs and selective FGFR TKIs. (nature.com)
  • The most frequently prescribed antidepressants are in a group called selective serotonin reuptake inhibitors, or SSRIs, according to Mayo Clinic. (reference.com)
  • Endogenous inhibitors are often derived from the extracellular matrix or basement membrane proteins and function by interfering with endothelial cell formation and migration, endothelial tube morphogenesis, and down-regulation of genes expressed in endothelial cells. (wikipedia.org)
  • Antiangiogenic agent, down-regulates the transcription of genes involved in controlling angiogenesis. (sigmaaldrich.com)
  • Experimentally, rifampicin rapidly and markedly down-regulated the expression of a wide spectrum of angiogenesis-associated genes in growing human microvascular endothelial cells, thereby suppressing endothelial cell proliferation and migration. (aacrjournals.org)
  • Developing a global functional association network among angiogenesis-related genes is much needed to facilitate holistic understanding of angiogenesis and to aid the development of more effective anti-angiogenesis therapeutics. (biomedcentral.com)
  • An enrichment test of Biological Processes (BP) of differentially expressed genes (DEG) revealed that angiogenesis related BP categories significantly changed with cell passages. (biomedcentral.com)
  • The interactome includes the involvement of oncogenes and tumor suppressor genes in angiogenesis. (biomedcentral.com)
  • These effects cannot be explained by direct cytotoxicity but are dependent on modulation of angiogenesis-involved genes. (elsevier.com)
  • These are the first data suggesting intratumoral mRNA expression of genes involved in angiogenesis/HIF pathway may predict outcome to VEGFR-inhibitors. (qub.ac.uk)
  • Thus, these compounds would be promising candidates for the development of new anti-angiogenesis therapeutics. (cancer.gov)
  • Development of new anti-angiogenesis therapeutics. (cancer.gov)
  • An angiogenesis inhibitor is a substance that inhibits the growth of new blood vessels ( angiogenesis ). (wikipedia.org)
  • A chemical that interferes with the signals to form new blood vessels is called an angiogenesis inhibitor. (hopkinsmedicine.org)
  • But angiogenesis inhibitors only prevent new blood vessels from forming. (hopkinsmedicine.org)
  • Angiogenesis is the process which forms new blood vessels. (cancerindex.org)
  • Angiogenesis, a process of generation of new blood vessels from the pre-existing vasculature, has been demonstrated to be a basic prerequisite for sustainable growth and proliferation of tumour. (cancerindex.org)
  • Angiogenesis Inhibitors are useful for studying the vascular system, particularly the growth of new blood vessels from existing vessels. (scbt.com)
  • One target is the pathway for angiogenesis: the growth of new blood vessels. (cochrane.org)
  • Anti-angiogenesis drugs target the blood vessels that supply oxygen to the cells, ultimately causing the cells to starve. (chemocare.com)
  • Angiogenesis inhibitors block the chemical signals that cells use to make blood vessels grow. (macmillan.org.uk)
  • Tumor angiogenesis is usually the complex processes by generation of a new network of blood vessels develop from an existing vasculature that penetrates into the neoplastic tissue to supply the nutrients and oxygen required to maintain and enable tumor growth and attack [4]. (acancerjourney.info)
  • Angiogenesis, the growth of new blood vessels from existing vessels, is a normal and vital process in growth and development. (cancer.gov)
  • Biological evaluation of a multi-targeted small molecule inhibitor of tumor-induced angiogenesis. (nih.gov)
  • RO4396686 is a small molecule KDR, FGFR, and PDGFR inhibitor with good pharmacokinetic properties in rodents. (nih.gov)
  • Presently, we investigate the antitumor activity of the small-molecule angiogenesis inhibitor axitinib (AG-013736) and its potential for combination with metronomic cyclophosphamide. (aacrjournals.org)
  • Axitinib (AG-013736) is a potent small-molecule inhibitor of the vascular endothelial growth factor receptor ( 15 ). (aacrjournals.org)
  • Factors such as continued uptake of approved PARP inhibitors owing to their superior efficacy, long treatment duration, and considerable number of treatment opportunities in first-line advanced settings are likely to propel the growth of the drug class. (marketresearch.com)
  • Therefore, researchers sought to evaluate the overall efficacy of angiogenesis inhibitor-containing regimens in the treatment of advanced NSCLC with regard to histologic types. (oncologynurseadvisor.com)
  • This paper is concerned with the bifurcation phenomenon of a free-boundary problem modeling the tumor growth under the action of angiogenesis and inhibitor. (springer.com)
  • In this paper, we study a mathematical model of tumor growth under the action of angiogenesis and inhibitor. (springer.com)
  • Tumor-induced angiogenesis is a process that tumor cells secrete cytokines that stimulate the vascular system to grow toward the tumor. (springer.com)
  • OSCC is a highly vascularized tumor but despite the crucial role of angiogenesis in OSCC, there is no antiangiogenic agent in clinical use and no vascular marker is approved as prognostic marker for this patient population. (frontiersin.org)
  • This antiangiogenic chemotherapy regimen could be enhanced by the concurrent administration of an angiogenesis inhibitor [116-119]. (nih.gov)
  • Tumor growth and progression rely upon angiogenesis, which is regulated by pro- and antiangiogenic factors, including members of the semaphorin family. (jci.org)
  • Brain-specific angiogenesis proteins BAI2 and BAI3 are similar to BAI1 in structure, have similar tissue specificities and may also play a role in angiogenesis. (wikipedia.org)
  • Brain angiogenesis inhibitor 1 (BAI1) is a receptor that recognizes apoptotic cells through its conserved type I thrombospondin repeats and triggers their engulfment through an ELMO1/Dock/Rac1 signaling module. (pnas.org)
  • BAI1 is postulated to be a member of the secretin receptor family, an inhibitor of angiogenesis and a growth suppressor of glioblastomas . (wikidoc.org)
  • Extent of intratumoral angiogenesis, as indicated by microvessel tortuosity and microvessel density, was significantly reduced by paclitaxel in a dose-dependent manner. (nih.gov)
  • In animal studies, high doses of inhibitors were required to prevent tumor growth and the use of endogenous inhibitors would likely be long-term. (wikipedia.org)
  • Biological actions of endogenous inhibitors of angiogenesis. (hindawi.com)
  • Withaferin A is cell permeable and potent angiogenesis inhibitor from the family of withanolides. (agscientific.com)
  • The side effects from angiogenesis inhibitors are generally less and milder than with conventional chemotherapy medicines. (hopkinsmedicine.org)
  • As a result of angiogenesis, the tumor possesses its own vasculature. (springer.com)
  • Assume that the nutrient and the inhibitor are single species consumed by tumor cell through its own vasculature and diffusion from the boundary. (springer.com)
  • Angiogenesis is regulated by the activity of endogenous stimulators and inhibitors. (wikipedia.org)
  • Angiogenesis is controlled by a local balance between stimulators and inhibitors of new vessel growth and is suppressed under normal physiologic conditions. (wikidoc.org)
  • Meanwhile, the combined application of immune checkpoint inhibitors and TKIs is the current clinical research trend, and the results are promising[5, 6]. (researchsquare.com)
  • competitive inhibitor of ATP in other protein kinase reactions. (sigmaaldrich.com)
  • Potent cell-permeable inhibitor of protein kinase C. Induces apoptosis in Jurkat cells. (sigmaaldrich.com)
  • The crystal structure of the human Pg-derived angiogenesis inhibitor, angiostatin, complexed to VEK-30, a peptide from the group A streptococcal surface protein, PAM, was determined and refined to 2.3 A resolution. (rcsb.org)
  • This study investigated the effects of Hsp90 inhibitors on client protein expression and key cellular functions required for tumor angiogenesis. (aacrjournals.org)
  • Known as MET inhibitors, these drugs attack the MET protein, which helps cells grow and spread. (medicalnewstoday.com)
  • Called RET inhibitors, these drugs work by attacking the RET protein. (medicalnewstoday.com)
  • Gene expression profile of ECs subjected to heat shock demonstrates that plasminogen activator inhibitor 1 (PAI-1), a protein involved in the control of extracellular matrix degradation, is specifically up-regulated. (elsevier.com)
  • inhibits endothelial cell proliferation and angiogenesis. (sigmaaldrich.com)
  • 2-Methoxyestradiol (2-ME) is a potent inhibitor of endothelial cell proliferation and angiogenesis. (sigmaaldrich.com)
  • This inhibition suggests that the drug may be useful in inhibiting angiogenesis, which requires endothelial cell proliferation. (life-enhancement.com)
  • C11 inhibited the migration and tube formation of HMEC-1 endothelial cells and inhibited angiogenesis in a CAM assay. (nature.com)
  • Fibroblast growth factor 2 (FGF2) induces endothelial cell migration and angiogenesis through two classes of receptors: receptor tyrosine kinases, such as FGF receptor 1 (FGFR1), and heparan sulfate proteoglycans, such as syndecan 4 (S4). (antibodyassay.com)
  • Angiogenesis needs both EC migration into an angiogenic specific niche market and EC proliferation to be able to type new vascular buildings [2]. (columbiagypsy.net)