AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsHealth Care
Neoplasm InvasivenessPancreatic NeoplasmsNeoplasmsCell Line, TumorCell MovementNeoplasms, Cystic, Mucinous, and SerousSkin NeoplasmsNeoplasm MetastasisGene Expression Regulation, NeoplasticMatrix Metalloproteinase 2ImmunohistochemistryLung NeoplasmsMatrix Metalloproteinase 9Neoplasms, Multiple PrimaryBreast NeoplasmsKidney NeoplasmsTumor Cells, CulturedLiver NeoplasmsThyroid NeoplasmsNeoplasms, Second PrimaryOvarian NeoplasmsNeoplasm ProteinsCarcinoma, Pancreatic DuctalMice, NudeCell ProliferationCadherinsDNA, NeoplasmNeoplasms, ExperimentalNeoplasm TransplantationAdenocarcinoma, MucinousTumor Markers, BiologicalMyeloproliferative DisordersAdenocarcinomaLamininSignal TransductionColonic NeoplasmsCell AdhesionParotid NeoplasmsAdenomaGastrointestinal NeoplasmsCystadenomaNeoplasm StagingNeoplasms, Connective and Soft TissueNeoplasms, Plasma CellReverse Transcriptase Polymerase Chain ReactionCarcinoma, PapillaryCell Transformation, NeoplasticCarcinomaAppendiceal NeoplasmsDrug CombinationsRNA, Small InterferingBone NeoplasmsCystadenoma, MucinousBlotting, WesternEndocrine Gland NeoplasmsUrokinase-Type Plasminogen ActivatorGlioblastomaStomach NeoplasmsTransfectionProstatic NeoplasmsGliomaBile Duct NeoplasmsNeoplasms, Vascular TissueAntigens, NeoplasmEye NeoplasmsNose NeoplasmsProteoglycansRNA, MessengerColorectal NeoplasmsSalivary Gland NeoplasmsMelanomaTrophoblastsNeoplasms, Radiation-InducedAdenocarcinoma, PapillaryMouth NeoplasmsThymus NeoplasmsTesticular NeoplasmsNeoplasms, Muscle TissueNeoplasms, Glandular and EpithelialUrinary Bladder NeoplasmsDisease ProgressionCollagenCystadenocarcinoma, MucinousAntigens, CD82Epithelial CellsReceptors, Urokinase Plasminogen ActivatorUp-RegulationCarcinoma, Squamous CellSoft Tissue NeoplasmsHematologic NeoplasmsUterine NeoplasmsIntestinal NeoplasmsDog DiseasesNeoplasms, Adnexal and Skin AppendageMatrix MetalloproteinasesEpithelial-Mesenchymal TransitionMatrix Metalloproteinase InhibitorsVascular NeoplasmsSweat Gland NeoplasmsCell DivisionLymphomaPrognosisPalatal NeoplasmsDown-RegulationNeoplasms, Complex and MixedRNA InterferenceMandibular NeoplasmsCystadenocarcinomaSplenic NeoplasmsHeart NeoplasmsCystadenoma, SerousMammary Neoplasms, AnimalNeovascularization, PathologicNeoplasm Recurrence, Localbeta CateninBrain NeoplasmsRNA, NeoplasmMaxillary NeoplasmsPhenotypeMatrix Metalloproteinase 14Transplantation, HeterologousAnal Gland NeoplasmsCell LineLiver Neoplasms, ExperimentalNeoplasms, Germ Cell and EmbryonalBone Marrow NeoplasmsVirulenceVimentinAstrocytomaHepatocyte Growth FactorNeoplasms, Adipose TissueHead and Neck NeoplasmsS100 ProteinsMeningeal NeoplasmsDuodenal NeoplasmsMice, SCIDIntroduced SpeciesPituitary NeoplasmsPeritoneal NeoplasmsMutationAdrenal Cortex NeoplasmsGene Expression ProfilingRetrospective StudiesMediastinal NeoplasmsImmunoenzyme TechniquesTomography, X-Ray ComputedProto-Oncogene Proteins c-metTongue NeoplasmsIleal NeoplasmsTissue Inhibitor of Metalloproteinase-2Gene SilencingApoptosisExtracellular MatrixCarcinoma, HepatocellularCarcinoma, Acinar CellSpinal Cord NeoplasmsVaginal NeoplasmsGene Knockdown TechniquesAntineoplastic AgentsAdenoma, OxyphilicNervous System NeoplasmsNeoplasm GradingJanus Kinase 2Muscle NeoplasmsHemangiosarcomaPhosphorylationMatrix Metalloproteinase 7DogsMyelodysplastic-Myeloproliferative DiseasesMammary Neoplasms, ExperimentalPancreatectomyGelatinasesPeripheral Nervous System NeoplasmsTime FactorsCell Growth ProcessesCerebral Ventricle NeoplasmsTissue Inhibitor of Metalloproteinase-1Paranasal Sinus NeoplasmsPleural NeoplasmsTranscription FactorsMice, Inbred BALB CGene ExpressionSarcomaFibrosarcomaCommon Bile Duct NeoplasmsMatrix Metalloproteinases, Membrane-AssociatedMesodermLymphatic MetastasisJaw NeoplasmsFibroblastsEsophageal NeoplasmsOligonucleotide Array Sequence AnalysisOrbital NeoplasmsCarcinogensMetalloendopeptidasesAbdominal NeoplasmsTransforming Growth Factor betaReal-Time Polymerase Chain ReactionCerebellar NeoplasmsCells, CulturedCell Survival
Neoplasm Invasiveness: Ability of neoplasms to infiltrate and actively destroy surrounding tissue.Pancreatic Neoplasms: 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).Neoplasms: 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.Cell Line, Tumor: A cell line derived from cultured tumor cells.Cell Movement: The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.Neoplasms, Cystic, Mucinous, and Serous: Neoplasms containing cyst-like formations or producing mucin or serum.Skin Neoplasms: Tumors or cancer of the SKIN.Neoplasm Metastasis: The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.Gene Expression Regulation, Neoplastic: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.Matrix Metalloproteinase 2: A secreted endopeptidase homologous with INTERSTITIAL COLLAGENASE, but which possesses an additional fibronectin-like domain.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Lung Neoplasms: Tumors or cancer of the LUNG.Matrix Metalloproteinase 9: An endopeptidase that is structurally similar to MATRIX METALLOPROTEINASE 2. It degrades GELATIN types I and V; COLLAGEN TYPE IV; and COLLAGEN TYPE V.Neoplasms, Multiple Primary: Two or more abnormal growths of tissue occurring simultaneously and presumed to be of separate origin. The neoplasms may be histologically the same or different, and may be found in the same or different sites.Breast Neoplasms: Tumors or cancer of the human BREAST.Kidney Neoplasms: Tumors or cancers of the KIDNEY.Tumor Cells, Cultured: 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.Liver Neoplasms: Tumors or cancer of the LIVER.Thyroid Neoplasms: Tumors or cancer of the THYROID GLAND.Neoplasms, Second Primary: Abnormal growths of tissue that follow a previous neoplasm but are not metastases of the latter. The second neoplasm may have the same or different histological type and can occur in the same or different organs as the previous neoplasm but in all cases arises from an independent oncogenic event. The development of the second neoplasm may or may not be related to the treatment for the previous neoplasm since genetic risk or predisposing factors may actually be the cause.Ovarian Neoplasms: Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.Neoplasm Proteins: Proteins whose abnormal expression (gain or loss) are associated with the development, growth, or progression of NEOPLASMS. Some neoplasm proteins are tumor antigens (ANTIGENS, NEOPLASM), i.e. they induce an immune reaction to their tumor. Many neoplasm proteins have been characterized and are used as tumor markers (BIOMARKERS, TUMOR) when they are detectable in cells and body fluids as monitors for the presence or growth of tumors. Abnormal expression of ONCOGENE PROTEINS is involved in neoplastic transformation, whereas the loss of expression of TUMOR SUPPRESSOR PROTEINS is involved with the loss of growth control and progression of the neoplasm.Carcinoma, Pancreatic Ductal: Carcinoma that arises from the PANCREATIC DUCTS. It accounts for the majority of cancers derived from the PANCREAS.Mice, Nude: 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.Cell Proliferation: All of the processes involved in increasing CELL NUMBER including CELL DIVISION.Cadherins: Calcium-dependent cell adhesion proteins. They are important in the formation of ADHERENS JUNCTIONS between cells. Cadherins are classified by their distinct immunological and tissue specificities, either by letters (E- for epithelial, N- for neural, and P- for placental cadherins) or by numbers (cadherin-12 or N-cadherin 2 for brain-cadherin). Cadherins promote cell adhesion via a homophilic mechanism as in the construction of tissues and of the whole animal body.DNA, Neoplasm: DNA present in neoplastic tissue.Neoplasms, Experimental: Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.Neoplasm Transplantation: Experimental transplantation of neoplasms in laboratory animals for research purposes.Adenocarcinoma, Mucinous: An adenocarcinoma producing mucin in significant amounts. (From Dorland, 27th ed)Tumor Markers, Biological: Molecular products metabolized and secreted by neoplastic tissue and characterized biochemically in cells or body fluids. They are indicators of tumor stage and grade as well as useful for monitoring responses to treatment and predicting recurrence. Many chemical groups are represented including hormones, antigens, amino and nucleic acids, enzymes, polyamines, and specific cell membrane proteins and lipids.Myeloproliferative Disorders: Conditions which cause proliferation of hemopoietically active tissue or of tissue which has embryonic hemopoietic potential. They all involve dysregulation of multipotent MYELOID PROGENITOR CELLS, most often caused by a mutation in the JAK2 PROTEIN TYROSINE KINASE.Adenocarcinoma: A malignant epithelial tumor with a glandular organization.Laminin: 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.Signal Transduction: 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.Colonic Neoplasms: Tumors or cancer of the COLON.Cell Adhesion: Adherence of cells to surfaces or to other cells.Parotid Neoplasms: Tumors or cancer of the PAROTID GLAND.Adenoma: A benign epithelial tumor with a glandular organization.Gastrointestinal Neoplasms: Tumors or cancer of the GASTROINTESTINAL TRACT, from the MOUTH to the ANAL CANAL.Cystadenoma: A benign neoplasm derived from glandular epithelium, in which cystic accumulations of retained secretions are formed. In some instances, considerable portions of the neoplasm, or even the entire mass, may be cystic. (Stedman, 25th ed)Neoplasm Staging: Methods which attempt to express in replicable terms the extent of the neoplasm in the patient.Neoplasms, Connective and Soft Tissue: Neoplasms developing from some structure of the connective and subcutaneous tissue. The concept does not refer to neoplasms located in connective or soft tissue.Neoplasms, Plasma Cell: Neoplasms associated with a proliferation of a single clone of PLASMA CELLS and characterized by the secretion of PARAPROTEINS.Reverse Transcriptase Polymerase Chain Reaction: 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.Carcinoma, Papillary: A malignant neoplasm characterized by the formation of numerous, irregular, finger-like projections of fibrous stroma that is covered with a surface layer of neoplastic epithelial cells. (Stedman, 25th ed)Cell Transformation, Neoplastic: Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.Carcinoma: A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm but is often wrongly used as a synonym for "cancer." (From Dorland, 27th ed)Appendiceal Neoplasms: Tumors or cancer of the APPENDIX.Drug Combinations: Single preparations containing two or more active agents, for the purpose of their concurrent administration as a fixed dose mixture.RNA, Small Interfering: 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.Bone Neoplasms: Tumors or cancer located in bone tissue or specific BONES.Cystadenoma, Mucinous: A multilocular tumor with mucin secreting epithelium. They are most often found in the ovary, but are also found in the pancreas, appendix, and rarely, retroperitoneal and in the urinary bladder. They are considered to have low-grade malignant potential.Blotting, Western: 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.Endocrine Gland Neoplasms: Tumors or cancer of the ENDOCRINE GLANDS.Urokinase-Type Plasminogen Activator: A proteolytic enzyme that converts PLASMINOGEN to FIBRINOLYSIN where the preferential cleavage is between ARGININE and VALINE. It was isolated originally from human URINE, but is found in most tissues of most VERTEBRATES.Glioblastoma: 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.Stomach Neoplasms: Tumors or cancer of the STOMACH.Transfection: 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.Prostatic Neoplasms: Tumors or cancer of the PROSTATE.Glioma: 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)Bile Duct Neoplasms: Tumors or cancer of the BILE DUCTS.Neoplasms, Vascular Tissue: Neoplasms composed of vascular tissue. This concept does not refer to neoplasms located in blood vessels.Antigens, Neoplasm: Proteins, glycoprotein, or lipoprotein moieties on surfaces of tumor cells that are usually identified by monoclonal antibodies. Many of these are of either embryonic or viral origin.Eye Neoplasms: Tumors or cancer of the EYE.Nose Neoplasms: Tumors or cancer of the NOSE.Proteoglycans: Glycoproteins which have a very high polysaccharide content.RNA, Messenger: 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.Colorectal Neoplasms: Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.Salivary Gland Neoplasms: Tumors or cancer of the SALIVARY GLANDS.Melanoma: A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body, in the eye, or, rarely, in the mucous membranes of the genitalia, anus, oral cavity, or other sites. It occurs mostly in adults and may originate de novo or from a pigmented nevus or malignant lentigo. Melanomas frequently metastasize widely, and the regional lymph nodes, liver, lungs, and brain are likely to be involved. The incidence of malignant skin melanomas is rising rapidly in all parts of the world. (Stedman, 25th ed; from Rook et al., Textbook of Dermatology, 4th ed, p2445)Trophoblasts: Cells lining the outside of the BLASTOCYST. After binding to the ENDOMETRIUM, trophoblasts develop into two distinct layers, an inner layer of mononuclear cytotrophoblasts and an outer layer of continuous multinuclear cytoplasm, the syncytiotrophoblasts, which form the early fetal-maternal interface (PLACENTA).Neoplasms, Radiation-Induced: Tumors, cancer or other neoplasms produced by exposure to ionizing or non-ionizing radiation.Adenocarcinoma, Papillary: An adenocarcinoma containing finger-like processes of vascular connective tissue covered by neoplastic epithelium, projecting into cysts or the cavity of glands or follicles. It occurs most frequently in the ovary and thyroid gland. (Stedman, 25th ed)Mouth Neoplasms: Tumors or cancer of the MOUTH.Thymus Neoplasms: Tumors or cancer of the THYMUS GLAND.Testicular Neoplasms: Tumors or cancer of the TESTIS. Germ cell tumors (GERMINOMA) of the testis constitute 95% of all testicular neoplasms.Neoplasms, Muscle Tissue: Neoplasms composed of muscle tissue: skeletal, cardiac, or smooth. The concept does not refer to neoplasms located in muscles.Neoplasms, Glandular and Epithelial: Neoplasms composed of glandular tissue, an aggregation of epithelial cells that elaborate secretions, and of any type of epithelium itself. The concept does not refer to neoplasms located in the various glands or in epithelial tissue.Urinary Bladder Neoplasms: Tumors or cancer of the URINARY BLADDER.Disease Progression: 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.Collagen: 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).Cystadenocarcinoma, Mucinous: A malignant cystic or semisolid tumor most often occurring in the ovary. Rarely, one is solid. This tumor may develop from a mucinous cystadenoma, or it may be malignant at the onset. The cysts are lined with tall columnar epithelial cells; in others, the epithelium consists of many layers of cells that have lost normal structure entirely. In the more undifferentiated tumors, one may see sheets and nests of tumor cells that have very little resemblance to the parent structure. (Hughes, Obstetric-Gynecologic Terminology, 1972, p184)Antigens, CD82: A widely expressed transmembrane glycoprotein that functions as a METASTASIS suppressor protein. It is underexpressed in a variety of human NEOPLASMS.Epithelial Cells: Cells that line the inner and outer surfaces of the body by forming cellular layers (EPITHELIUM) or masses. Epithelial cells lining the SKIN; the MOUTH; the NOSE; and the ANAL CANAL derive from ectoderm; those lining the RESPIRATORY SYSTEM and the DIGESTIVE SYSTEM derive from endoderm; others (CARDIOVASCULAR SYSTEM and LYMPHATIC SYSTEM) derive from mesoderm. Epithelial cells can be classified mainly by cell shape and function into squamous, glandular and transitional epithelial cells.Receptors, Urokinase Plasminogen Activator: An extracellular receptor specific for UROKINASE-TYPE PLASMINOGEN ACTIVATOR. It is attached to the cell membrane via a GLYCOSYLPHOSPHATIDYLINOSITOL LINKAGE and plays a role in the co-localization of urokinase-type plasminogen activator with PLASMINOGEN.Up-Regulation: 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.Carcinoma, Squamous Cell: A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)Soft Tissue Neoplasms: Neoplasms of whatever cell type or origin, occurring in the extraskeletal connective tissue framework of the body including the organs of locomotion and their various component structures, such as nerves, blood vessels, lymphatics, etc.Hematologic Neoplasms: Neoplasms located in the blood and blood-forming tissue (the bone marrow and lymphatic tissue). The commonest forms are the various types of LEUKEMIA, of LYMPHOMA, and of the progressive, life-threatening forms of the MYELODYSPLASTIC SYNDROMES.Uterine Neoplasms: Tumors or cancer of the UTERUS.Intestinal Neoplasms: Tumors or cancer of the INTESTINES.Dog Diseases: Diseases of the domestic dog (Canis familiaris). This term does not include diseases of wild dogs, WOLVES; FOXES; and other Canidae for which the heading CARNIVORA is used.Neoplasms, Adnexal and Skin Appendage: Neoplasms composed of sebaceous or sweat gland tissue or tissue of other skin appendages. The concept does not refer to neoplasms located in the sebaceous or sweat glands or in the other skin appendages.Matrix Metalloproteinases: A family of zinc-dependent metalloendopeptidases that is involved in the degradation of EXTRACELLULAR MATRIX components.Epithelial-Mesenchymal Transition: Phenotypic changes of EPITHELIAL CELLS to MESENCHYME type, which increase cell mobility critical in many developmental processes such as NEURAL TUBE development. NEOPLASM METASTASIS and DISEASE PROGRESSION may also induce this transition.Matrix Metalloproteinase Inhibitors: Compounds that inhibit the enzyme activity or activation of MATRIX METALLOPROTEINASES.Vascular Neoplasms: Neoplasms located in the vasculature system, such as ARTERIES and VEINS. They are differentiated from neoplasms of vascular tissue (NEOPLASMS, VASCULAR TISSUE), such as ANGIOFIBROMA or HEMANGIOMA.Sweat Gland NeoplasmsCell Division: The fission of a CELL. It includes CYTOKINESIS, when the CYTOPLASM of a cell is divided, and CELL NUCLEUS DIVISION.Lymphoma: A general term for various neoplastic diseases of the lymphoid tissue.Prognosis: A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.Palatal Neoplasms: Tumors or cancer of the PALATE, including those of the hard palate, soft palate and UVULA.Down-Regulation: 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.Neoplasms, Complex and Mixed: Neoplasms composed of more than one type of neoplastic tissue.RNA Interference: A gene silencing phenomenon whereby specific dsRNAs (RNA, DOUBLE-STRANDED) trigger the degradation of homologous mRNA (RNA, MESSENGER). The specific dsRNAs are processed into SMALL INTERFERING RNA (siRNA) which serves as a guide for cleavage of the homologous mRNA in the RNA-INDUCED SILENCING COMPLEX. DNA METHYLATION may also be triggered during this process.Mandibular Neoplasms: Tumors or cancer of the MANDIBLE.Cystadenocarcinoma: A malignant neoplasm derived from glandular epithelium, in which cystic accumulations of retained secretions are formed. The neoplastic cells manifest varying degrees of anaplasia and invasiveness, and local extension and metastases occur. Cystadenocarcinomas develop frequently in the ovaries, where pseudomucinous and serous types are recognized. (Stedman, 25th ed)Splenic Neoplasms: Tumors or cancer of the SPLEEN.Heart Neoplasms: Tumors in any part of the heart. They include primary cardiac tumors and metastatic tumors to the heart. Their interference with normal cardiac functions can cause a wide variety of symptoms including HEART FAILURE; CARDIAC ARRHYTHMIAS; or EMBOLISM.Cystadenoma, Serous: A cystic tumor of the ovary, containing thin, clear, yellow serous fluid and varying amounts of solid tissue, with a malignant potential several times greater than that of mucinous cystadenoma (CYSTADENOMA, MUCINOUS). It can be unilocular, parvilocular, or multilocular. It is often bilateral and papillary. The cysts may vary greatly in size. (Dorland, 27th ed; from Hughes, Obstetric-Gynecologic Terminology, 1972)Mammary Neoplasms, Animal: Tumors or cancer of the MAMMARY GLAND in animals (MAMMARY GLANDS, ANIMAL).Neovascularization, Pathologic: A pathologic process consisting of the proliferation of blood vessels in abnormal tissues or in abnormal positions.Neoplasm Recurrence, Local: The local recurrence of a neoplasm following treatment. It arises from microscopic cells of the original neoplasm that have escaped therapeutic intervention and later become clinically visible at the original site.beta Catenin: A multi-functional catenin that participates in CELL ADHESION and nuclear signaling. Beta catenin binds CADHERINS and helps link their cytoplasmic tails to the ACTIN in the CYTOSKELETON via ALPHA CATENIN. It also serves as a transcriptional co-activator and downstream component of WNT PROTEIN-mediated SIGNAL TRANSDUCTION PATHWAYS.Brain Neoplasms: 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.RNA, Neoplasm: RNA present in neoplastic tissue.Maxillary Neoplasms: Cancer or tumors of the MAXILLA or upper jaw.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Matrix Metalloproteinase 14: A transmembrane domain-containing matrix metalloproteinase. It is synthesized as an inactive zymogen that is activated by the action of PROPROTEIN CONVERTASES such as FURIN. Matrix metalloproteinase 14 plays a direct role in the cleavage of proteins in the pericellular environment. In addition, it can function indirectly by enzymatically activating the proprotein form of MATRIX METALLOPROTEINASE 15.Transplantation, Heterologous: Transplantation between animals of different species.Anal Gland Neoplasms: Tumors or cancer of the anal gland.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Liver Neoplasms, Experimental: Experimentally induced tumors of the LIVER.Neoplasms, Germ Cell and Embryonal: Neoplasms composed of primordial GERM CELLS of embryonic GONADS or of elements of the germ layers of the EMBRYO, MAMMALIAN. The concept does not refer to neoplasms located in the gonads or present in an embryo or FETUS.Bone Marrow Neoplasms: Neoplasms located in the bone marrow. They are differentiated from neoplasms composed of bone marrow cells, such as MULTIPLE MYELOMA. Most bone marrow neoplasms are metastatic.Virulence: The degree of pathogenicity within a group or species of microorganisms or viruses as indicated by case fatality rates and/or the ability of the organism to invade the tissues of the host. The pathogenic capacity of an organism is determined by its VIRULENCE FACTORS.Vimentin: An intermediate filament protein found in most differentiating cells, in cells grown in tissue culture, and in certain fully differentiated cells. Its insolubility suggests that it serves a structural function in the cytoplasm. MW 52,000.Astrocytoma: Neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors. Fibrillary astrocytomas are the most common type and may be classified in order of increasing malignancy (grades I through IV). In the first two decades of life, astrocytomas tend to originate in the cerebellar hemispheres; in adults, they most frequently arise in the cerebrum and frequently undergo malignant transformation. (From Devita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2013-7; Holland et al., Cancer Medicine, 3d ed, p1082)Hepatocyte Growth Factor: Multifunctional growth factor which regulates both cell growth and cell motility. It exerts a strong mitogenic effect on hepatocytes and primary epithelial cells. Its receptor is PROTO-ONCOGENE PROTEINS C-MET.Neoplasms, Adipose Tissue: Neoplasms composed of fatty tissue or connective tissue made up of fat cells in a meshwork of areolar tissue. The concept does not refer to neoplasms located in adipose tissue.Head and Neck Neoplasms: Soft tissue tumors or cancer arising from the mucosal surfaces of the LIP; oral cavity; PHARYNX; LARYNX; and cervical esophagus. Other sites included are the NOSE and PARANASAL SINUSES; SALIVARY GLANDS; THYROID GLAND and PARATHYROID GLANDS; and MELANOMA and non-melanoma skin cancers of the head and neck. (from Holland et al., Cancer Medicine, 4th ed, p1651)S100 Proteins: A family of highly acidic calcium-binding proteins found in large concentration in the brain and believed to be glial in origin. They are also found in other organs in the body. They have in common the EF-hand motif (EF HAND MOTIFS) found on a number of calcium binding proteins. The name of this family derives from the property of being soluble in a 100% saturated ammonium sulfate solution.Meningeal Neoplasms: Benign and malignant neoplastic processes that arise from or secondarily involve the meningeal coverings of the brain and spinal cord.Duodenal Neoplasms: Tumors or cancer of the DUODENUM.Mice, SCID: 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.Introduced Species: Non-native organisms brought into a region, habitat, or ECOSYSTEM by human activity.Pituitary Neoplasms: Neoplasms which arise from or metastasize to the PITUITARY GLAND. The majority of pituitary neoplasms are adenomas, which are divided into non-secreting and secreting forms. Hormone producing forms are further classified by the type of hormone they secrete. Pituitary adenomas may also be characterized by their staining properties (see ADENOMA, BASOPHIL; ADENOMA, ACIDOPHIL; and ADENOMA, CHROMOPHOBE). Pituitary tumors may compress adjacent structures, including the HYPOTHALAMUS, several CRANIAL NERVES, and the OPTIC CHIASM. Chiasmal compression may result in bitemporal HEMIANOPSIA.Peritoneal Neoplasms: Tumors or cancer of the PERITONEUM.Mutation: Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.Adrenal Cortex Neoplasms: Tumors or cancers of the ADRENAL CORTEX.Gene Expression Profiling: The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.Retrospective Studies: Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.Mediastinal Neoplasms: Tumors or cancer of the MEDIASTINUM.Immunoenzyme Techniques: 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.Tomography, X-Ray Computed: Tomography using x-ray transmission and a computer algorithm to reconstruct the image.Proto-Oncogene Proteins c-met: Cell surface protein-tyrosine kinase receptors for HEPATOCYTE GROWTH FACTOR. They consist of an extracellular alpha chain which is disulfide-linked to the transmembrane beta chain. The cytoplasmic portion contains the catalytic domain and sites critical for the regulation of kinase activity. Mutations of the gene for PROTO-ONCOGENE PROTEINS C-MET are associated with papillary renal carcinoma and other neoplasia.Tongue Neoplasms: Tumors or cancer of the TONGUE.Ileal Neoplasms: Tumors or cancer in the ILEUM region of the small intestine (INTESTINE, SMALL).Tissue Inhibitor of Metalloproteinase-2: A member of the family of TISSUE INHIBITOR OF METALLOPROTEINASES. It is a 21-kDa nonglycosylated protein found in tissue fluid and is secreted as a complex with progelatinase A by human fibroblast and uncomplexed from alveolar macrophages. An overexpression of TIMP-2 has been shown to inhibit invasive and metastatic activity of tumor cells and decrease tumor growth in vivo.Gene Silencing: Interruption or suppression of the expression of a gene at transcriptional or translational levels.Apoptosis: 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.Extracellular Matrix: A meshwork-like substance found within the extracellular space and in association with the basement membrane of the cell surface. It promotes cellular proliferation and provides a supporting structure to which cells or cell lysates in culture dishes adhere.Carcinoma, Hepatocellular: A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.Carcinoma, Acinar Cell: A malignant tumor arising from secreting cells of a racemose gland, particularly the salivary glands. Racemose (Latin racemosus, full of clusters) refers, as does acinar (Latin acinus, grape), to small saclike dilatations in various glands. Acinar cell carcinomas are usually well differentiated and account for about 13% of the cancers arising in the parotid gland. Lymph node metastasis occurs in about 16% of cases. Local recurrences and distant metastases many years after treatment are common. This tumor appears in all age groups and is most common in women. (Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1240; from DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p575)Spinal Cord Neoplasms: Benign and malignant neoplasms which occur within the substance of the spinal cord (intramedullary neoplasms) or in the space between the dura and spinal cord (intradural extramedullary neoplasms). The majority of intramedullary spinal tumors are primary CNS neoplasms including ASTROCYTOMA; EPENDYMOMA; and LIPOMA. Intramedullary neoplasms are often associated with SYRINGOMYELIA. The most frequent histologic types of intradural-extramedullary tumors are MENINGIOMA and NEUROFIBROMA.Vaginal Neoplasms: Tumors or cancer of the VAGINA.Gene Knockdown Techniques: The artificial induction of GENE SILENCING by the use of RNA INTERFERENCE to reduce the expression of a specific gene. It includes the use of DOUBLE-STRANDED RNA, such as SMALL INTERFERING RNA and RNA containing HAIRPIN LOOP SEQUENCE, and ANTI-SENSE OLIGONUCLEOTIDES.Antineoplastic Agents: Substances that inhibit or prevent the proliferation of NEOPLASMS.Adenoma, Oxyphilic: A usually benign glandular tumor composed of oxyphil cells, large cells with small irregular nuclei and dense acidophilic granules due to the presence of abundant MITOCHONDRIA. Oxyphil cells, also known as oncocytes, are found in oncocytomas of the kidney, salivary glands, and endocrine glands. In the thyroid gland, oxyphil cells are known as Hurthle cells and Askanazy cells.Nervous System Neoplasms: Benign and malignant neoplastic processes arising from or involving components of the central, peripheral, and autonomic nervous systems, cranial nerves, and meninges. Included in this category are primary and metastatic nervous system neoplasms.Neoplasm Grading: Methods which attempt to express in replicable terms the level of CELL DIFFERENTIATION in neoplasms as increasing ANAPLASIA correlates with the aggressiveness of the neoplasm.Janus Kinase 2: A Janus kinase subtype that is involved in signaling from GROWTH HORMONE RECEPTORS; PROLACTIN RECEPTORS; and a variety of CYTOKINE RECEPTORS such as ERYTHROPOIETIN RECEPTORS and INTERLEUKIN RECEPTORS. Dysregulation of Janus kinase 2 due to GENETIC TRANSLOCATIONS have been associated with a variety of MYELOPROLIFERATIVE DISORDERS.Muscle Neoplasms: Tumors or cancer located in muscle tissue or specific muscles. They are differentiated from NEOPLASMS, MUSCLE TISSUE which are neoplasms composed of skeletal, cardiac, or smooth muscle tissue, such as MYOSARCOMA or LEIOMYOMA.Hemangiosarcoma: A rare malignant neoplasm characterized by rapidly proliferating, extensively infiltrating, anaplastic cells derived from blood vessels and lining irregular blood-filled or lumpy spaces. (Stedman, 25th ed)Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.Matrix Metalloproteinase 7: The smallest member of the MATRIX METALLOPROTEINASES. It plays a role in tumor progression.Dogs: The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)Myelodysplastic-Myeloproliferative Diseases: Clonal myeloid disorders that possess both dysplastic and proliferative features but are not properly classified as either MYELODYSPLASTIC SYNDROMES or MYELOPROLIFERATIVE DISORDERS.Mammary Neoplasms, Experimental: Experimentally induced mammary neoplasms in animals to provide a model for studying human BREAST NEOPLASMS.Pancreatectomy: Surgical removal of the pancreas. (Dorland, 28th ed)Gelatinases: A class of enzymes that catalyzes the degradation of gelatin by acting on the peptide bonds. EC 3.4.24.-.Peripheral Nervous System Neoplasms: Neoplasms which arise from peripheral nerve tissue. This includes NEUROFIBROMAS; SCHWANNOMAS; GRANULAR CELL TUMORS; and malignant peripheral NERVE SHEATH NEOPLASMS. (From DeVita Jr et al., Cancer: Principles and Practice of Oncology, 5th ed, pp1750-1)Time Factors: Elements of limited time intervals, contributing to particular results or situations.Cell Growth Processes: Processes required for CELL ENLARGEMENT and CELL PROLIFERATION.Cerebral Ventricle Neoplasms: Neoplasms located in the brain ventricles, including the two lateral, the third, and the fourth ventricle. Ventricular tumors may be primary (e.g., CHOROID PLEXUS NEOPLASMS and GLIOMA, SUBEPENDYMAL), metastasize from distant organs, or occur as extensions of locally invasive tumors from adjacent brain structures.Tissue Inhibitor of Metalloproteinase-1: A member of the family of TISSUE INHIBITOR OF METALLOPROTEINASES. It is a N-glycosylated protein, molecular weight 28 kD, produced by a vast range of cell types and found in a variety of tissues and body fluids. It has been shown to suppress metastasis and inhibit tumor invasion in vitro.Paranasal Sinus Neoplasms: Tumors or cancer of the PARANASAL SINUSES.Pleural Neoplasms: Neoplasms of the thin serous membrane that envelopes the lungs and lines the thoracic cavity. Pleural neoplasms are exceedingly rare and are usually not diagnosed until they are advanced because in the early stages they produce no symptoms.Transcription Factors: Endogenous substances, usually proteins, which are effective in the initiation, stimulation, or termination of the genetic transcription process.Mice, Inbred BALB CGene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Sarcoma: A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant.Fibrosarcoma: 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)Common Bile Duct Neoplasms: Tumor or cancer of the COMMON BILE DUCT including the AMPULLA OF VATER and the SPHINCTER OF ODDI.Matrix Metalloproteinases, Membrane-Associated: Matrix metalloproteinases that are associated with the CELL MEMBRANE, either through transmembrane domains or GLYCOSYLPHOSPHATIDYLINOSITOL ANCHORS. Membrane-type matrix metalloproteinases may act within the pericellular environment to influence the process of CELL MIGRATION.Mesoderm: The middle germ layer of an embryo derived from three paired mesenchymal aggregates along the neural tube.Lymphatic Metastasis: Transfer of a neoplasm from its primary site to lymph nodes or to distant parts of the body by way of the lymphatic system.Jaw Neoplasms: Cancers or tumors of the MAXILLA or MANDIBLE unspecified. For neoplasms of the maxilla, MAXILLARY NEOPLASMS is available and of the mandible, MANDIBULAR NEOPLASMS is available.Fibroblasts: Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.Esophageal Neoplasms: Tumors or cancer of the ESOPHAGUS.Oligonucleotide Array Sequence Analysis: Hybridization of a nucleic acid sample to a very large set of OLIGONUCLEOTIDE PROBES, which have been attached individually in columns and rows to a solid support, to determine a BASE SEQUENCE, or to detect variations in a gene sequence, GENE EXPRESSION, or for GENE MAPPING.Orbital Neoplasms: Neoplasms of the bony orbit and contents except the eyeball.Carcinogens: Substances that increase the risk of NEOPLASMS in humans or animals. Both genotoxic chemicals, which affect DNA directly, and nongenotoxic chemicals, which induce neoplasms by other mechanism, are included.Metalloendopeptidases: ENDOPEPTIDASES which use a metal such as ZINC in the catalytic mechanism.Abdominal NeoplasmsTransforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.Real-Time Polymerase Chain Reaction: Methods used for detecting the amplified DNA products from the polymerase chain reaction as they accumulate instead of at the end of the reaction.Cerebellar Neoplasms: Primary or metastatic neoplasms of the CEREBELLUM. Tumors in this location frequently present with ATAXIA or signs of INTRACRANIAL HYPERTENSION due to obstruction of the fourth ventricle. Common primary cerebellar tumors include fibrillary ASTROCYTOMA and cerebellar HEMANGIOBLASTOMA. The cerebellum is a relatively common site for tumor metastases from the lung, breast, and other distant organs. (From Okazaki & Scheithauer, Atlas of Neuropathology, 1988, p86 and p141)Cells, Cultured: 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.Cell Survival: 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.

Immunohistochemical expression of mdm2 and p21WAF1 in invasive cervical cancer: correlation with p53 protein and high risk HPV infection. (1/11529)

AIM: To investigate the immunocytochemical staining pattern of mdm2 and p21WAF1 proteins in invasive cervical cancer and to determine its relation with the expression of p53 and with the high risk HPV infection. METHODS: Immunocytochemistry for p53, mdm2, and p21WAF1 was performed in 31 paraffin embedded sections of invasive cervical cancer. The results were assessed by image analysis, evaluating for each protein the optical density of the immunostained area, scored as percentage of the total nuclear area. The presence of high risk human papillomavirus (HPV) infection was detected by using the polymerase chain reaction. RESULTS: Immunostaining for both mdm2 and p21WAF1 was correlated with p53 expression; however, the correlation between p53 and mdm2 (R = 0.49; p < 0.01) was more significant than between p53 and p21WAF1 (R = 0.31; p < 0.05); the less stringent correlation between p53 and p21WAF1 might reflect the p53 independent mechanisms of p21WAF1 induction. Similar average levels of p53, mdm2, and p21WAF1 immunostaining were found in the presence or absence of high risk HPV-DNA, without significant differences between the two groups. CONCLUSIONS: These data suggest that mdm2 and p21WAF1 proteins are expressed in invasive cervical cancer and that their immunocytochemical staining pattern is not abrogated by the presence of high risk HPV genomic sequences.  (+info)

The alphaE-catenin gene (CTNNA1) acts as an invasion-suppressor gene in human colon cancer cells. (2/11529)

The acquisition of invasiveness is a crucial step in the malignant progression of cancer. In cancers of the colon and of other organs the E-cadherin/catenin complex, which is implicated in homotypic cell-cell adhesion as well as in signal transduction, serves as a powerful inhibitor of invasion. We show here that one allele of the alphaE-catenin (CTNNA1) gene is mutated in the human colon cancer cell family HCT-8, which is identical to HCT-15, DLD-1 and HRT-18. Genetic instability, due to mutations in the HMSH6 (also called GTBP) mismatch repair gene, results in the spontaneous occurrence of invasive variants, all carrying either a mutation or exon skipping in the second alphaE-catenin allele. The alphaE-catenin gene is therefore, an invasion-suppressor gene in accordance with the two-hit model of Knudsen for tumour-suppressor genes.  (+info)

Role of thrombin receptor in breast cancer invasiveness. (3/11529)

Invasion, the ability of an epithelial cancer cell to detach from and move through a basement membrane, is a central process in tumour metastasis. Two components of invasion are proteolysis of extracellular matrix and cellular movement through it. A potential promoter of these two processes is thrombin, the serine proteinase derived from the ubiquitous plasma protein prothrombin. Thrombin promotes the invasion of MDA-MB231 breast tumour cells (a highly aggressive cell line) in an in vitro assay. Invasion by MDA-MB436 and MCF-7 cells, less aggressive cell lines, is not promoted by thrombin. Thrombin, added to the cells, is a stimulator of cellular movement; fibroblast-conditioned medium is the chemotaxin. Thrombin-promoted invasion is inhibited by hirudin. Stimulation of invasion is a receptor-mediated process that is mimicked by a thrombin receptor-activating peptide. Thrombin has no effect on chemotaxis in vitro. Thrombin receptor is detectable on the surface of MDA-MB231 cells, but not on the other two cell lines. Introduction of oestrogen receptors into MDA-MB231 cells by transfection with pHEO had no effect on thrombin receptor expression, in the presence or absence of oestradiol. This paper demonstrates that thrombin increases invasion by the aggressive breast cancer cell line MDA-MB231 by a thrombin receptor-dependent mechanism.  (+info)

Expression of pyrimidine nucleoside phosphorylase mRNA plays an important role in the prognosis of patients with oesophageal cancer. (4/11529)

To clarify the significance of the expression of pyrimidine nucleoside phosphorylase (PyNPase) mRNA as a predictive factor for the prognosis of patients with oesophageal carcinoma, the PyNPase mRNA in the tumours and normal tissues from 55 resected cases of oesophageal carcinoma was examined by a reverse transcription polymerase chain reaction (RT-PCR). As a result, a positive correlation was observed between the tumour/normal (T/N) ratio of the expression of PyNPase mRNA by RT-PCR and that of the enzyme activity of PyNPase based on the findings of an enzyme linked immunosolvent assay (r = 0.594, P = 0.009). The T/N ratio of the expression of PyNPase mRNA was significantly higher in the cases with lymph vessel invasion (P = 0.013), lymph node metastasis (P = 0.0016), and an advanced stage of the disease (P = 0.021) than those without these factors. The patients with a higher T/N ratio of PyNPase mRNA showed significantly worse prognosis than those with a lower T/N ratio (P = 0.023 with log-rank tests). A multivariate analysis for the cumulative survival rates revealed that a high T/N ratio of the expression of PyNPase mRNA was independently related to a poor prognosis. These findings suggested that the determination of PyNPase mRNA by RT-PCR thus appears to be a new useful parameter for identifying both a poor prognosis and a highly malignant potential of oesophageal carcinoma.  (+info)

Low tumour cell proliferation at the invasive margin is associated with a poor prognosis in Dukes' stage B colorectal cancers. (5/11529)

The conflicting results about the prognostic impact of tumour cell proliferation in colorectal cancer might be explained by the heterogeneity observed within these tumours. We have investigated whether a systematic spatial heterogeneity exists between different compartments, and whether the presence of such a systematic heterogeneity has any impact on survival. Fifty-six Dukes' stage B colorectal cancers were carefully morphometrically quantified with respect to the immunohistochemical expression of the proliferative marker Ki-67 at both the luminal border and the invasive margin. The proliferative activity was significantly higher at the luminal border compared with the invasive margin (P<0.001), although the two compartments were also significantly correlated with each other. Tumours with low proliferation at the invasive margin had a significantly poorer prognosis both in univariate (P = 0.014) and in multivariate survival analyses (P = 0.042). We conclude that Dukes' B colorectal cancers exhibit a systematic spatial heterogeneity with respect to proliferation, and tumours with low proliferation at the invasive margin had a poor prognosis. The present data independently confirm recent results from the authors, and provide new insights into the understanding of tumour cell proliferation in colorectal cancer.  (+info)

A possible involvement of aberrant expression of the FHIT gene in the carcinogenesis of squamous cell carcinoma of the uterine cervix. (6/11529)

To investigate involvement of an aberrant expression of the FHIT (fragile histidine triad) gene in the process of carcinogenesis and progression in cervical carcinoma, we examined its expression by the reverse transcriptase polymerase chain reaction (RT-PCR) and cDNA sequence method in 32 cervical invasive carcinomas (25 squamous cell carcinomas and seven adeno- or adenosquamous carcinomas) and 18 of its precursor lesions [four low-grade and 14 high-grade cervical intraepithelial neoplasias (CINs)]. We also examined a link between the occurrence of the aberrant expression and human papillomavirus (HPV). We detected the aberrant FHIT transcripts in 11 of 25 (44%) cervical invasive squamous cell carcinomas and in 5 of 14 (36%) high-grade CINs (CIN 2 or 3), whereas they were not found in seven non-squamous type and four low-grade CINs (CIN 1). The alteration patterns of the FHIT gene expression in high-grade CINs were virtually similar to those found in invasive carcinomas, such that the exons 5-7 were consistently deleted associated or unassociated with loss of the exon 4 and/or 8. The incidence of the aberrant expression was not related to the presence of HPV and its type. These data indicate that the aberrant expression of the FHIT gene is observed in precursor lesions of cervical carcinoma as well as invasive carcinomas, with its incidence not increasing with advance of clinical stage. Given the squamous cell type dominant expression, the aberrant expression may play a critical role in the generation of squamous cell carcinoma of the uterine cervix, but not the consequence of the progression of the cancer.  (+info)

Enhanced tumor growth and invasiveness in vivo by a carboxyl-terminal fragment of alpha1-proteinase inhibitor generated by matrix metalloproteinases: a possible modulatory role in natural killer cytotoxicity. (7/11529)

Matrix metalloproteinases (MMPs) are believed to contribute to the complex process of cancer progression. They also exhibit an alpha1-proteinase inhibitor (alphaPI)-degrading activity generating a carboxyl-terminal fragment of approximately 5 kd (alphaPI-C). This study reports that overexpression of alphaPI-C in S2-020, a cloned subline derived from the human pancreas adenocarcinoma cell line SUIT-2, potentiates the growth capability of the cells in nude mice. After stable transfection of a vector containing a chimeric cDNA encoding a signal peptide sequence of tissue inhibitor of metalloproteinase-1 followed by cDNA for alphaPI-C into S2-020 cells, three clones that stably secrete alphaPI-C were obtained. The ectopic expression of alphaPI-C did not alter in vitro cellular growth. However, subcutaneous injection of the alphaPI-C-secreting clones resulted in tumors that were 1.5 to 3-fold larger than those of control clones with an increased tendency to invasiveness and lymph node metastasis. These effects could be a result of modulation of natural killer (NK) cell-mediated control of tumor growth in nude mice, as the growth advantage of alphaPI-C-secreting clones was not observed in NK-depleted mice, and alphaPI-C-secreting clones showed decreased NK sensitivity in vitro. In addition, production of alphaPI and generation of the cleaved form of alphaPI by MMP were observed in various human tumor cell lines and in a highly metastatic subline of SUIT-2 in vitro. These results provide experimental evidence that the alphaPI-degrading activity of MMPs may play a role in tumor progression not only via the inactivation of alphaPI but also via the generation of alphaPI-C.  (+info)

Collagenase-3 (MMP-13) is expressed by tumor cells in invasive vulvar squamous cell carcinomas. (8/11529)

Collagenase-3 (MMP-13) is a human matrix metalloproteinase specifically expressed by invading tumor cells in squamous cell carcinomas (SCCs) of the head and neck. Here, we have further elucidated the role of MMP-13 in tumor invasion by examining its expression in invasive malignant tumors of the female genital tract. Using in situ hybridization, expression of MMP-13 mRNA was detected in 9 of 12 vulvar SCCs, primarily in tumor cells, but not in intact vulvar epithelium, in cervical SCCs (n = 12), or in endometrial (n = 11) or ovarian adenocarcinomas (n = 8). MMP-13 expression was especially abundant in vulvar carcinomas showing metastasis to lymph nodes and was associated with expression of membrane type 1 MMP by tumor cells and gelatinase-A (MMP-2) by stromal cells, as detected by immunohistochemistry. MMP-13 mRNAs were detected in 9 of 11 cell lines established from vulvar carcinomas and in 4 of 6 cell lines from cervical carcinomas, whereas endometrial (n = 10) and ovarian (n = 9) carcinoma cell lines were negative for MMP-13 mRNA. No correlation was detected between MMP-13 expression and p53 gene mutations in vulvar SCC cell lines. However, MMP-13 expression was detected in 5 of 6 vulvar and cervical SCC cell lines harboring HPV 16 or 68 DNA. These results show that MMP-13 is specifically expressed by malignantly transformed squamous epithelial cells, including vulvar SCC cells, and appears to serve as a marker for their invasive capacity.  (+info)

Relationship between Tumor Cell Invasiveness and Polyploidization - pdf descargarRelationship between Tumor Cell Invasiveness and Polyploidization - pdf descargar
Relationship between Tumor Cell Invasiveness and Polyploidization. . 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.
HS3ST2 modulates breast cancer cell invasiveness via MAP kinase- and Tcf4 (Tcf7l2)-dependent regulation of protease and...HS3ST2 modulates breast cancer cell invasiveness via MAP kinase- and Tcf4 (Tcf7l2)-dependent regulation of protease and...
Heparan sulfate 3-O-sulfotransferase 2 (HS3ST2), an enzyme mediating 3-O-sulfation of heparan sulfate (HS), is silenced by hypermethylation in breast cancer. As HS has an important co-receptor function for numerous signal transduction pathways, the phenotypical changes due to HS3ST2 reexpression were investigated in vitro using high and low invasive breast cancer cell lines. Compared to controls, highly invasive HS3ST2-expressing MDA-MB-231 cells showed enhanced Matrigel invasiveness, transendothelial migration and motility. Affymetrix screening and confirmatory real-time PCR and Western blotting analysis revealed increased expression of several matrix metalloproteinases, cadherin-11, E-cadherin and CEACAM-1, while protease inhibitor and annexin A10 expression were decreased. Low invasive HS3ST2 -expressing MCF-7 cells became even less invasive, with no change in gelatinolytic MMP activity. HS3ST2 expression increased HS-dependent basal and FGF2-specific signaling through the constitutively ...
The Transcriptional Factor Yy1 Upregulates the Novel Invasion Suppressor Hlj1 Expression and Inhibits Cancer Cell Invasion |...The Transcriptional Factor Yy1 Upregulates the Novel Invasion Suppressor Hlj1 Expression and Inhibits Cancer Cell Invasion |...
By using microarray and an invasion/metastasis lung cell line model, we identified the DnaJ-like heat shock protein 40, HLJ1, and found that the expression of HLJ1 correlates negatively with cancer cell invasion ability . Overexpression of HLJ1 can suppress cancer cell invasion in vitro. We further characterize the putative promoter region and investigate the transcriptional regulations of human HLJ1. A serial deletion of the 1.2 kb at the 5′-flanking region of the human HLJ1 gene was subcloned into a vector containing reporter gene and transfected into human lung adenocarcinoma cell line CL1-0, followed by luciferase activity assay. The results indicated that the region from -232 to +176 could drive the basal transcriptional activity of the HLJ1 gene. Sequence analysis of the HLJ1 gene promoter region showed absence of a TATA box, but identified an inverted CCAAT box and four YY1 transcriptional factor-binding sites, which may be important in the regulation of HLJ1 expression. Co- ...
Fluctuations in Tumor u-Organoid Protrusions Govern Lung Cancer Invasiveness: An Organ-on-Chip Approach | 3Bs Research Group...Fluctuations in Tumor u-Organoid Protrusions Govern Lung Cancer Invasiveness: An Organ-on-Chip Approach | 3B's Research Group...
Cancer invasion involves the growth of the tumor and the invasion of cancer cells. During this process, the tumor typically elongates protrusion-like structures, which triggers the invasion of cells into the blood vessel, and thereby, initiate metastasis. Recent evidences using individual cells have identified the key role of membrane protrusion fluctuations in the physicochemical mechanism of directed cell motion]. The exact roles of protrusion fluctuations during tumor growth and invasion have yet not been reported. Different in vitro and in vivo models have been developed to monitor cancer invasion and its mechanistic determinants. These models display certain limitations, which threaten the relevancy of the obtained data. In contrast, organs-on-chip devices can replicate all the key cellular, structural, and rheological properties of solid tumors, contributing to assess the mechanism at work of the disease. In this work, an organ-on-chip approach is used to analyze the important role of ...
MT1-MMP drives cancer cell invasion and intravasation. | Open-iMT1-MMP drives cancer cell invasion and intravasation. | Open-i
MT1-MMP drives cancer cell invasion and intravasation. (A and B) HT-1080 or SCC-1 cells were incubated alone with TIMP-1, TIMP-2, a 21-bp MT1-MMP siRNA, or a 21
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The results of the current study showed the molecular and functional activation of β-catenin by hypoxia in HCC and showed its contribution to hypoxia-induced metastatic phenotypes. The induction of EMT was one of the proinvasive mechanisms augmented by β-catenin during hypoxia. The coexpression of β-catenin and HIF-1α (a marker of hypoxia) in HCC was found to be correlated with metastases and poor prognosis in two independent cohorts of patients. These results confirm the importance of β-catenin in HCC under hypoxic conditions.. Hypoxia plays a critical role in tumor progression (1). Consistent with our previous report (17), it not only facilitated in vitro cell invasion in HCC but also resulted in peritoneal seeding and pulmonary metastasis in an in vivo HAL model. However, the growth of HCC cells and xenografts were suppressed by hypoxia. Further analysis revealed that this could be attributed to the arrest of cell proliferation rather than the induction of apoptosis (Supplementary Fig. ...
ERBB1 and ERBB2 have distinct functions in tumor cell invasion and intravasation - Fingerprint - University of Texas...ERBB1 and ERBB2 have distinct functions in tumor cell invasion and intravasation - Fingerprint - University of Texas...
Fingerprint Dive into the research topics of ERBB1 and ERBB2 have distinct functions in tumor cell invasion and intravasation. Together they form a unique fingerprint. ...
Defining Complementary And Different Medication - KBDefining Complementary And Different Medication - KB
One year of biology and chemistry and physics or equal courses of all three subjects. Obviously, if illness is prevented by pure means earlier than resulting in the breakdown of the immune system which is the bodys mechanism of defence towards illness, severe illnesses equivalent to most cancers and other so-known as incurable diseases can be revented, and so there would be little need for the administration of high-priced conventional drugs since that might be obligatory solely in case of surgery and different traumatic circumstances.. In vitro studies have demonstrated that melatonin induces apoptosis and reduces breast cancer invasiveness and metastasis. The curriculum is designed to permit the scholar to gain the data essential to work in the different medicine setting. But the battle has prevented folks from exercising various medical treatments.. In the event you (or someone you already know) are concerned about finding an appropriate alternative medication university to assist attain ...
Mechanisms of Perineural InvasionMechanisms of Perineural Invasion
Perineural invasion (PNI) is the neoplastic invasion of nerves. PNI is widely recognized as an important adverse pathological feature of many malignancies, including pancreatic, prostate, and head and neck cancers and is associated with a poor prognosis.
Cancer invasion and tissue remodeling--cooperation of protease systems and cell typesCancer invasion and tissue remodeling--cooperation of protease systems and cell types
Proteolytic degradation of the extracellular matrix plays a crucial role in both cancer invasion and non-neoplastic tissue remodeling processes. In human cancers the components of matrix degrading protease systems (uPA, uPAR, PAI-1 and MMPs) can be expressed by either the non-neoplastic stromal cell …
EGF enhances low-invasive cancer cell invasion by promoting IMP-3 expression | SpringerLinkEGF enhances low-invasive cancer cell invasion by promoting IMP-3 expression | SpringerLink
The initiation and progression of cancer is closely associated with the tumor microenvironment. The overexpression of oncogenes during tumor growth and progression by stromal stimuli can affect the...
Vesicle Trafficking in Cancer :: thewileychronicles.comVesicle Trafficking in Cancer :: thewileychronicles.com
Oct 06, 2016 · Malfunction of Rabs-regulating vesicle trafficking could promote cancer invasion. For example, Rab11 is an important component for membrane proteins recycling and proteins transport from TGN to the plasma membrane. Rab11-mediated α6β4 integrin trafficking has been found to contribute to increase cancer cell invasion in breast cancer.
The mode and dynamics of glioblastoma cell invasion into a decellularized tissue-derived extracellular matrix-based three...The mode and dynamics of glioblastoma cell invasion into a decellularized tissue-derived extracellular matrix-based three...
TY - JOUR. T1 - The mode and dynamics of glioblastoma cell invasion into a decellularized tissue-derived extracellular matrix-based three-dimensional tumor model. AU - Koh, Ilkyoo. AU - Cha, Junghwa. AU - Park, Junseong. AU - Choi, Junjeong. AU - Kang, Seok Gu. AU - Kim, Pilnam. PY - 2018/3/1. Y1 - 2018/3/1. N2 - Glioblastoma multiforme (GBM) is the most common brain tumor with very aggressive and infiltrative. Extracellular matrix (ECM) plays pivotal roles in the infiltrative characteristics of GBM. To understand the invasive characteristic of GBM, it is necessary to study cell-ECM interaction in the physiologically relevant biomimetic model that recapitulates the GBM-specific ECM microenvironment. Here, we propose biomimetic GBM-specific ECM microenvironment for studying mode and dynamics of glioblastoma cell invasion. Using tissue decellularization process, we constructed a patient tissue-derived ECM (pdECM)-based three-dimensional in vitro model. In our model, GBM cells exhibited ...
Suppression of PPARβ, and DHA treatment, inhibit NaV1.5 and NHE-1 pro-invasive activities. | DIAL.pr - BOREALSuppression of PPARβ, and DHA treatment, inhibit NaV1.5 and NHE-1 pro-invasive activities. | DIAL.pr - BOREAL
Peroxisome proliferator-activated receptor β (PPARβ) and NaV1.5 voltage-gated sodium channels have independently been shown to regulate human breast cancer cell invasiveness. The n-3 polyunsaturated docosahexaenoic acid (DHA, 22:6n-3), a natural ligand of PPAR, is effective in increasing survival and chemotherapy efficacy in breast cancer patient with metastasis. DHA reduces breast cancer cell invasiveness and it also inhibits PPARβ expression. We have shown previously that NaV1.5 promotes MDA-MB-231 breast cancer cells invasiveness by potentiating the activity of Na(+)/H(+) exchanger type 1 (NHE-1), the major regulator of H(+) efflux in these cells. We report here that DHA inhibited NaV1.5 current and NHE-1 activity in human breast cancer cells, and in turn reduced NaV1.5-dependent cancer cell invasiveness. For the first time, we show that antagonizing PPARβ, or inhibiting its expression, reduced NaV1.5 mRNA and protein expression and NaV1.5 current, as well as NHE-1 activity and cell ...
Activation of phosphoinositide 3-OH kinase by the alpha6beta4 integrin promotes carcinoma invasionActivation of phosphoinositide 3-OH kinase by the alpha6beta4 integrin promotes carcinoma invasion
We demonstrate that the alpha6beta4 integrin promotes carcinoma invasion through a preferential and localized targeting of phosphoinositide-3 OH kinase (PI3K) activity. Stable expression of alpha6beta4 increased carcinoma invasion in a PI3K-dependent manner, and transient expression of a constitutiv …
Invasion Signal | Science SignalingInvasion Signal | Science Signaling
Epidermal growth factor receptor (EGFR), a receptor tyrosine kinase, is implicated in many cancers; however, it is unclear specifically which EGFR pathways are involved in triggering tumor cell invasiveness. The abundance of the small guanosine triphosphatase Arf6, which regulates processes such as membrane trafficking and endocytosis, correlates with the invasiveness of malignant breast cancer cells. In this context, Morishige et al. used small interfering RNA (siRNA) to individually decrease the expression of the 10 genes that encode guanine nucleotide exchange factors (GEFs) that activate Arf family proteins in the invasive human breast cancer cell line MDA-MB-231. GEP100 was the only ArfGEF whose depletion resulted in the inhibition of MDA-MB-231 invasion activity, as measured by an in-gel invasiveness assay. Coimmunoprecipitation studies showed that EGF treatment of MDA-MB-231 cells triggered the association of GEP100 with EGFR. In transfected Cos-7 cells, the authors showed the ...
Cell Invasion Assay (Basement Membrane), 24-well, 8 μm Kit-2313 - Creative BioMartCell Invasion Assay (Basement Membrane), 24-well, 8 μm Kit-2313 - Creative BioMart
Purified Cell Invasion Assay (Basement Membrane), 24-well, 8 μm from Creative Biomart. Cell Invasion Assay (Basement Membrane), 24-well, 8 μm can be used for research.
Tumor volume and lymphovascular space invasion as a prognostic factor in early invasive adenocarcinoma of the cervix<...Tumor volume and lymphovascular space invasion as a prognostic factor in early invasive adenocarcinoma of the cervix<...
TY - JOUR. T1 - Tumor volume and lymphovascular space invasion as a prognostic factor in early invasive adenocarcinoma of the cervix. AU - Murakami, Isao. AU - Fujii, Takuma. AU - Kameyama, Kaori. AU - Iwata, Takashi. AU - Saito, Miyuki. AU - Kubushiro, Kaneyuki. AU - Aoki, Daisuke. PY - 2012/6. Y1 - 2012/6. N2 - Objective: The aim of this study was to investigate the risk and recurrence of early invasive adenocarcinoma of the cervix, and to determine whether non-radical methods of management could be performed. Methods: The medical and histopathological records of 50 patients with early invasive adenocarcinoma of the cervix treated at Keio University Hospital between 1993 and 2005 were reviewed, and compared with the literature. Results: The median follow-up period was 64.3 months. The depth of stromal invasion was ≤3 mm in 33 cases and ,3 mm, but ≤5 mm in 17 cases. The horizontal spread was ≤7 mm in 25 cases and ,7 mm in 25 cases. One of the 33 cases that had tumor volumes of ≤500 mm ...
Leicester Research Archive: Intrinsic genetic characteristics determine tumor-modifying capacity of fibroblasts: Matrix...Leicester Research Archive: Intrinsic genetic characteristics determine tumor-modifying capacity of fibroblasts: Matrix...
Background Stromal fibroblasts can contribute to tumor invasion through the release of matrix metalloproteinases (MMPs). Population studies have suggested that single nucleotide polymorphisms (SNPs) in MMP genes influence levels of expression and may be associated with breast cancer risk and with disease progression. This study directly examined the impact of MMP SNP genotype on the ability of host fibroblasts to promote tumor cell invasion. Methods Primary breast fibroblasts were isolated from patients with (n = 13) or without (n = 19) breast cancer, and their ability to promote breast cancer cell invasion was measured in in vitro invasion assays. Fibroblast invasion-promoting capacity (IPC) was analyzed in relation to donor type (tumor or non-tumor patient), MMP-1, MMP-3, and MMP-9 SNP genotype and MMP activity using independent samples t test and analysis of variance. All statistical tests were two-sided. Results Tumor-derived fibroblasts promoted higher levels of invasion than normal ...
Aspirin and P2Y 12 inhibition attenuate platelet-induced ovarian cancer cell invasion | BMC Cancer | Full TextAspirin and P2Y 12 inhibition attenuate platelet-induced ovarian cancer cell invasion | BMC Cancer | Full Text
Platelet-cancer cell interactions play a key role in successful haematogenous metastasis. Disseminated malignancy is the leading cause of death among ovarian cancer patients. It is unknown why different ovarian cancers have different metastatic phenotypes. To investigate if platelet-cancer cell interactions play a role, we characterized the response of ovarian cancer cell lines to platelets both functionally and at a molecular level. Cell lines 59 M and SK-OV-3 were used as in vitro model systems of metastatic ovarian cancer. Platelet cloaking of each cell line was quantified by flow cytometry. Matrigel invasion chamber assays were used to assess the invasive capacity of the cell lines. The induction of an EMT was assessed by morphology analysis and by gene expression analysis of a panel of 11 EMT markers using TaqMan RT-PCR. SK-OV-3 cells adhered to and activated more platelets than 59 M cells (p = 0.0333). Platelets significantly promoted the ability of only SK-OV-3 cells to invade (p ≤ 0.0001).
Prostaglandin E2 promotes hepatocellular carcinoma cell invasion through upregulation of YB-1 protein expression. | Sigma...Prostaglandin E2 promotes hepatocellular carcinoma cell invasion through upregulation of YB-1 protein expression. | Sigma...
Sigma-Aldrich offers abstracts and full-text articles by [Hai Zhang, Shanyu Cheng, Min Zhang, Xiuping Ma, Li Zhang, Yipin Wang, Rong Rong, Juan Ma, Shukai Xia, Mingzhan Du, Feng Shi, Jie Wang, Qinyi Yang, Xiaoming Bai, Jing Leng].
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4360 Secreted acidic protein rich in cysteine (SPARC) has been suggested as a potential glioma invasion promoting gene. SPARC is highly expressed in human gliomas, promotes glioma invasion, and delays tumor growth in vitro and in vivo. cDNA array reports were performed to determine whether SPARC, which interacts at the cell surface, has an impact on intracellular signaling and downstream gene expression changes that might account for some of its effects on invasion and growth. Additional in vitro studies demonstrated that SPARC delays growth, increases attachment, and modulates migration of tumor cells in extracellular matrix-specific and concentration-dependent manners. It has been reported that SPARC functionally contributes to brain tumor invasion and delays tumor growth in vivo, and that the effects of SPARC are related to the level of SPARC secreted into the extracellular matrix. Thus far, the signaling aspects of glioma migration and invasion are not fully understood. As such, we made an ...
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Furin, a subtilisin/kesin-like proprotein convertase (PC), activates membrane-bound MT1-MMP, which facilitates pro-gelatinase A (MMP2). These activated MT1-MMP and MMP2 are involved in cancer cell invasion and metastasis. In this study, we investigate the contribution of MMP2 activated by furin to cellular invasiveness of cumulatively irradiated cells.. Using previously established AMC-HN3 and AMC-HN8 cell line from laryngeal carcinoma patient, we have generated isogenic model of cumulatively irradiated AMC-HN3R and AMC-HN8R cell line, respectively. AMC-HN3R cells were increased furin expression with upregulation of MT1-MMP/MMP2 and their invasiveness by two fold (p , 0.05) compared to AMC-HN3, while AMC-HN8R cells had no differences compared to AMC-HN8. In case of AMC-HN3R, inhibition of furin activity with the synthetic inhibitor decanoyl-Arg-Val-Lys-Arg-chloromethyl-keton, CMK, showed a significant decrease of MT1-MMP/MMP2 and in vitro cellular invasiveness. Tumors obtained after subcutaneous ...
EGFR-mediated carcinoma cell metastasis mediated by integrin αvβ5 depends on activation of c-Src and cleavage of MUC1<...EGFR-mediated carcinoma cell metastasis mediated by integrin αvβ5 depends on activation of c-Src and cleavage of MUC1<...
TY - JOUR. T1 - EGFR-mediated carcinoma cell metastasis mediated by integrin αvβ5 depends on activation of c-Src and cleavage of MUC1. AU - Lau, Steven K.M.. AU - Shields, David J.. AU - Murphy, Eric A.. AU - Desgrosellier, Jay S.. AU - Anand, Sudarshan. AU - Huang, Miller. AU - Kato, Shumei. AU - Lim, Ssang Taek. AU - Weis, Sara M.. AU - Stupack, Dwayne G.. AU - Schlaepfer, David D.. AU - Cheresh, David A.. PY - 2012/5/7. Y1 - 2012/5/7. N2 - Receptor tyrosine kinases and integrins play an essential role in tumor cell invasion and metastasis. We previously showed that EGF and other growth factors induce human carcinoma cell invasion and metastasis mediated by integrin αvβ5 that is prevented by Src blockade [1]. MUC1, a transmembrane glycoprotein, is expressed in most epithelial tumors as a heterodimer consisting of an extracellular and a transmembrane subunit. The MUC1 cytoplasmic domain of the transmembrane subunit (MUC1.CD) translocates to the nucleus where it promotes the transcription of ...
In silico studies on structure prediction and inhibitory action of selected natural compounds on cell invasion protein SipB...In silico studies on structure prediction and inhibitory action of selected natural compounds on cell invasion protein SipB...
Salmonellosis is one of the most common and widely distributed food borne diseases caused by Salmonella enterica serovar Typhi (S.Typhi). Powerful str..
PTEN inhibits PREX2-catalyzed activation of RAC1 to restrain tumor cell invasion | Science SignalingPTEN inhibits PREX2-catalyzed activation of RAC1 to restrain tumor cell invasion | Science Signaling
Fig. 3 PTENs intact PDZ binding domain is required for antagonism of PREX2-driven invasion, and the PTEN C2-tail is sufficient to suppress invasion.. (A) PREX2 drives invasion. BT549 cells were transfected as indicated and subjected to invasion assays using an FBS gradient or no gradient. (B) PTEN constructs used in invasion assays. (C) PTEN C2-tail, G129E, and C124S block PREX2-driven invasion. BT549 cells were transfected as indicated, and invasion experiments were performed using an FBS gradient. (D) Immunoblots showing PREX2 and PTEN from cells used in invasion assays. Lysates from breast cancer cell lines with endogenous PTEN are shown. (E) C2-tail antagonizes PREX2-driven invasion in SUM149 cells. SUM149 cells were transfected as indicated, and invasion experiments were performed. (F) Coimmunoprecipitation of PTEN constructs and PREX2. BT549 cells were transfected with V5-PREX2 along with the indicated FLAG-PTEN constructs. (G) Schematic showing the binding of the PTEN PDZ binding domain ...
Chinese invasion on Taiwan - Page 21Chinese invasion on Taiwan - Page 21
proteinxx, your post is simply great If there were more bright people like you in control of world, we will get a much better life on this planet. Btw. Tai
Role of CRN2 in glioblastoma cell invasion and characterization of CRN2 deficient mice - Kölner UniversitätsPublikationsServerRole of CRN2 in glioblastoma cell invasion and characterization of CRN2 deficient mice - Kölner UniversitätsPublikationsServer
Die Universität zu Köln ist eine Exzellenzuniversität mit dem klassischen Fächerspektrum einer Volluniversität. Als eine der größen Hochschulen Europas arbeitet sie in Forschung und Lehre auch international auf höchstem Niveau.
The Madeleine Oudin Lab | SacklerThe Madeleine Oudin Lab | Sackler
Chemotherapy is widely used to treat metastatic disease. However, while many patients initially respond, a high percentage of them ultimately relapse. Cells plated in a monolayer respond much better to cytotoxic therapy than the same cells grown in 3D spheroids, or in xenograft tumors in mice, suggesting that the ECM and stromal cells that make up the tumor microenvironment drive drug resistance. While there has been work highlighting mechanisms of resistance derived from the release of cytokines from stromal cells, the role of the ECM in this process remains understudied in 3D in vitro systems or in vivo using mouse models. In addition, how chemotherapy treatment alters the ECM remains unknown. Finally, most studies focus on the effect chemotherapeutics on cell death, while the potentially dangerous effects of these drugs on tumor cell invasion and metastatic capability remain understudied. Our preliminary data show that chemotherapeutics can have different effects on growth and motility in ...
Spying on Cancer Cell Invasion [video] | EurekAlert! Science NewsSpying on Cancer Cell Invasion [video] | EurekAlert! Science News
Celldance 2015: Spying on Cancer Cell Invasion, by Edison Leung with Allison Harney, John Condeelis lab, Albert Einstein College of Medicine.
Most recent papers with the keyword pancreatic cancer neural invasion | Read by QxMDMost recent papers with the keyword pancreatic cancer neural invasion | Read by QxMD
Perineural invasion (PNI) is thought to be one of the factors responsible for the high rate of tumor recurrence after surgery and the pain generation associated with pancreatic cancer. Signaling via the nerve growth factor (NGF) pathway between pancreatic cancer cells and the surrounding nerves has been implicated in PNI, and increased levels of these proteins have been correlated to poor prognosis. In this study, we examine the molecular mechanism of the NGF signaling pathway in PNI in pancreatic cancer. We show that knocking down NGF or its receptors, TRKA and p75NTR, or treatment with GW441756, a TRKA kinase inhibitor, reduces the proliferation and migration of pancreatic cancer cells in vitro ...
Difference between revisions of Hyung-Do Kim - OpenWetWareDifference between revisions of "Hyung-Do Kim" - OpenWetWare
Publications (* co-first): Kim HD*, Sileika TS*, Maniak P, Messersmith PB. Antibacterial performance of polydopamine modified polymer surfaces containing passive and active components. Submitted. 2011 Kim HD, Peyton SR. Bio-inspired materials for parsing matrix physicochemical control of cell migration. Integr Biol. Accepted. 2011 Kim HD*, Hause RJ*, Leung K*, Jones RA. Targeted protein-omic methods are bridging the gap between proteomic and hypothesis-driven protein analysis approaches. Expert Rev Proteomics. Accepted. 2011 Kim HD, Meyer AS, Wagner JP, Alford SK, Wells A, Gertler FB, Lauffenburger DA. Signaling network state predicts Twist-mediated effects on breast cell migration across diverse growth factor contexts. Mol Cell Proteomics. Accepted. 2011 Philippar U, Roussos ET, Oser M, Yamaguchi H, Kim HD, Giampieri S, Wang Y, Goswami S, Wyckoff JB, Lauffenburger DA, Sahai E, Condeelis JS, Gertler FB. A Mena invasion isoform potentiates EGF-induced carcinoma cell invasion and metastasis. Dev ...
Cell Migration or Invasion Assay | BMG LABTECHCell Migration or Invasion Assay | BMG LABTECH
Cell migration & Invasion Assays are important investigate for different cell types and disease states. Read more in this Article.
corrigendum-Isoorientin induces apoptosis, decreases invasiveness, and | OTTcorrigendum-Isoorientin induces apoptosis, decreases invasiveness, and | OTT
Isoorientin induces apoptosis, decreases invasiveness, and downregulates VEGF secretion by activating AMPK signaling in pancreatic cancer cells [Corrigendum] Isoorientin induces apoptosis, decreases invasiveness, and downregulates VEGF secretion by activating AMPK signaling in pancreatic cancer cells [Corrigendum]Ye T, Su J, Huang C, et al. OncoTargets Ther. 2016;9:7481â 7492.The authors have advised that a number of errors were made in some of the figures within their paper.Read the original article
OGT2115 | OGT-2115 | CAS#853929-59-6 | heparanase inhibitor | MedKooOGT2115 | OGT-2115 | CAS#853929-59-6 | heparanase inhibitor | MedKoo
OGT-2115 is a heparanase inhibitor (IC50 = 0.4 μM). Heparanase inhibitors suppress breast cancer cell invasion and migration induced by ER stress, and provide a strong rationale for the development of heparanase-based therapeutics for the prevention of metastasis induced by chemotherapeutic reagents.
Seminar - Pro-invasive tumour-stroma interactions:the key role of cancer associated fibroblasts - The University of NottinghamSeminar - "Pro-invasive tumour-stroma interactions:the key role of cancer associated fibroblasts" - The University of Nottingham
EXTERNAL SPEAKER. Dr Sara Rossana Zanivan, Senior Lecturer, Beatson Institute for Cancer Research, University of Glasgow. "Pro-invasive tumour-stroma interactions:thekey role of cancer associated fibroblasts". Hosted in room C1071 C Floor South Block Queens Medical Centre and dual broadcast to The Staff Room Academic Oncology 1st Floor above South Entrance City Hospital. This forms part of the Division of Cancer & Stem Cells seminar series ...
Control of lung cancer invasion and metastasis by vimentinControl of lung cancer invasion and metastasis by vimentin
Research Topics, Genomes and Genes, Species, Research Grants, Publications about Control of lung cancer invasion and metastasis by vimentin
Effect of TGFβ1 on the phenotype, migratory ability, a | Open-iEffect of TGFβ1 on the phenotype, migratory ability, a | Open-i
Effect of TGFβ1 on the phenotype, migratory ability, and survival of CD16− monocytes. PBMCs were depleted of CD16+ cells using miniMACS magnetic selection. T
Cyclic RNA hsa circ 0091017 inhibits proliferation, migration and invasiveness of bladder cancer cells by binding to microRNA...Cyclic RNA hsa circ 0091017 inhibits proliferation, migration and invasiveness of bladder cancer cells by binding to microRNA...
CONCLUSIONS: The circular RNA hsa_circ_0091017 can inhibit the proliferation, migration and invasiveness of BCa cells by regulating the expression of microRNA-589-5p. PMID: 31957821 [PubMed - in process]...
The decrease chambers were filled with DME medium made up of five% FBS as a chemoattractant | MEK Inhibitor-sgkinhibitor.comThe decrease chambers were filled with DME medium made up of five% FBS as a chemoattractant | MEK Inhibitor-sgkinhibitor.com
Invasion was calculated employing BioCoat MatriGel Invasion Chambers (BD Biosciences) in accordance to the manufacturers recommendations. The upper insert
Cobot Invasion at Japans CEATEC | EE TimesCobot Invasion at Japan's CEATEC | EE Times
Most noticeable on CEATEC Japan for those of us who dont live in Japan was a host of robotic and sensor products programmed to talk, think, and behave like Japanese people, mirroring Japanese sensibilities, preferences, and habits.
Ent survival. However, tumor invasion and metastasis contribute to the great | URAT1 inhibitor urat1inhibitor.comEnt survival. However, tumor invasion and metastasis contribute to the great | URAT1 inhibitor urat1inhibitor.com
Ent survival. However, tumor invasion and metastasis contribute to the great majority of breast Tubastatin A supplier cancer deaths. Our efforts towards the
SCAI (suppressor of cancer cell invasion) - KOMP (Knockout Mouse Project)SCAI (suppressor of cancer cell invasion) - KOMP (Knockout Mouse Project)
The KOMP Repository Collection is located at the MMRRC at the University of California, Davis and Childrens Hospital Oakland Research Institute. Question? Comments? For Mice, Cells, and germplasm please contact us at [email protected], US 1-888-KOMP-MICE or International +1-530-752-KOMP, or for vectors [email protected] or +1-510-450-7917 ...
Automated, Kinetic Imaging of Cell Migration and Invasion Assays using Corning FluoroBlok™ Permeable Supports | October 9, 2014Automated, Kinetic Imaging of Cell Migration and Invasion Assays using Corning FluoroBlok™ Permeable Supports | October 9, 2014
BioTek 应用手册, 10/09 2014, Automated, Kinetic Imaging of Cell Migration and Invasion Assays using Corning FluoroBlok™ Permeable Supports
Save 51% on Invasion: Brain Craving on SteamSave 51% on Invasion: Brain Craving on Steam
Its the zombie-slaying survival game with JRPG elements you didnt know you wanted! Get swarmed by zombies in active-time battles, search for other survivors, eat and most importantly: SURVIVE!
Invasion of the Bunny Snatchers: The Return | Looney Tunes Fanon Wiki | FandomInvasion of the Bunny Snatchers: The Return | Looney Tunes Fanon Wiki | Fandom
Invasion of the Bunny Snatchers: The Return is a 1995 short subject which is directed by Greg Ford, Terry Lennon and Martin Gates. This is a Sequel to Invasion of the Bunny Snatchers.
A proteomic approach to identify endosomal cargoes controlling cancer invasiveness | Journal of Cell ScienceA proteomic approach to identify endosomal cargoes controlling cancer invasiveness | Journal of Cell Science
The available database information concerning Rab17 and its interactors is insufficient to infer potential effectors and pathways through which this GTPase acts to suppress cancer invasiveness and progression. We, therefore, determined the Rab17 interactome and its influence on the cellular proteome in an unbiased manner. The use of high-accuracy MS-based approaches has enabled us to do this and to show that Rab17 has a close physical and functional relationship with the SNARE protein Vamp8. Rab GTPases are known to recruit specific effector proteins that bind to SNAREs, giving specificity to vesicle fusion (Angers and Merz, 2011). Nevertheless, to our knowledge, our study is the first to provide an indication that the stability and cellular levels of a SNARE protein may be controlled by a Rab GTPase. Moreover, because Vamp8 is the only component of the proteome that is significantly altered following Rab17 knockdown, the relationship between this GTPase and Vamp8 stability is likely to be ...
Frontiers | Additive Influence of Extracellular pH, Oxygen Tension, and Pressure on Invasiveness and Survival of Human...Frontiers | Additive Influence of Extracellular pH, Oxygen Tension, and Pressure on Invasiveness and Survival of Human...
BACKGROUND/PURPOSE:The effects of chemical and physical interactions in the microenvironment of solid tumors have not been fully elucidated. We hypothesized that acidosis, hypoxia, and elevated interstitial fluid pressure (eIFP) have additive effects on tumor cell biology and lead to more aggressive behavior during tumor progression. We investigated this phenomenon using 3 human osteosarcoma cell lines and a novel in vitro cell culture apparatus. MATERIALS AND METHODS:U2OS, SaOS, and MG63 cell lines were cultured in media adjusted to various pH levels, oxygen tension (hypoxia 2% O2, normoxia 20% O2), and hydrostatic gauge pressure (0 or 50 mm Hg). Growth rate, apoptosis, cell cycle parameters, and expression of mRNA for proteins associated with invasiveness and tumor microenvironment (CA IX, VEGF-A, HIF-1A, MMP-9, and TIMP-2) were analyzed. Levels of CA IX, HIF-1α, and MMP-9 were measured using immunofluorescence. The effect of pH on invasiveness was evaluated in a Matrigel chamber assay.RESULTS:
Cervical carcinoma with full-thickness stromal invasion: Efficacy of dynamic MR imaging in the assessment of parametrial...Cervical carcinoma with full-thickness stromal invasion: Efficacy of dynamic MR imaging in the assessment of parametrial...
TY - JOUR. T1 - Cervical carcinoma with full-thickness stromal invasion. T2 - Efficacy of dynamic MR imaging in the assessment of parametrial involvement. AU - Iwata, Sumiyo. AU - Joja, Ikuo. AU - Okuno, Keiko. AU - Miyagi, Yasunari. AU - Sakaguchi, Yukiyoshi. AU - Kudo, Takafumi. AU - Hiraki, Yoshio. PY - 2002/9/1. Y1 - 2002/9/1. N2 - The purpose of this study was to investigate the efficacy of dynamic MR imaging in the assessment of parametrial involvement by cervical carcinoma with full-thickness stromal invasion on thinsection oblique axial T2-weighted images. Dynamic MR images of 24 patients with cervical carcinoma with full-thickness stromal invasion on thin-section oblique axial T2-weighted images were evaluated with pathologic correlation. Dynamic MR imaging was performed using a turboFLASH, 3D-FISP, or 2D-FLASH technique. The imaging planes of dynamic MR imaging were oblique axial planes of the uterine cervix. Dynamic MR imaging was performed twice, once for the early phase (40 to 60 ...
JCM | Free Full-Text | Epithelial-to-Mesenchymal Transition and Cancer Invasiveness: What Can We Learn from Cholangiocarcinoma?JCM | Free Full-Text | Epithelial-to-Mesenchymal Transition and Cancer Invasiveness: What Can We Learn from Cholangiocarcinoma?
In addition to its well-established role in embryo development, epithelial-to-mesenchymal transition (EMT) has been proposed as a general mechanism favoring tumor metastatization in several epithelial malignancies. Herein, we review the topic of EMT in cholangiocarcinoma (CCA), a primary liver cancer arising from the epithelial cells lining the bile ducts (cholangiocytes) and characterized by an abundant stromal reaction. CCA carries a dismal prognosis, owing to a pronounced invasiveness and scarce therapeutic opportunities. In CCA, several reports indicate that cancer cells acquire a number of EMT biomarkers and functions. These phenotypic changes are likely induced by both autocrine and paracrine signals released in the tumor microenvironment (cytokines, growth factors, morphogens) and intracellular stimuli (microRNAs, oncogenes, tumor suppressor genes) variably associated with specific disease mechanisms, including chronic inflammation and hypoxia. Nevertheless, evidence supporting a complete EMT of
Coalition for the Reversal of Breast Cancer Mortality in African American WomenCoalition for the Reversal of Breast Cancer Mortality in African American Women
Pancreatic ductal adenocarcinoma (PDAC) and other pancreatic neoplasms exhibited increased SPARCL1 mRNA levels compared to those of the normal pancreas. SPARCL1 mRNA levels were low to absent in microdissected and cultured pancreatic cancer cells, and promoter demethylation increased SPARCL1 levels only slightly in three of eight cell lines. SPARCL1 was observed in small capillaries in areas of inflammation/tumor growth and in some islet cells. In PDAC, 15.4% of vessels were SPARCL1-positive. In contrast, the percentage of SPARCL1-positive vessels was higher in chronic pancreatitis and benign and borderline pancreatic tumors. Recombinant SPARCL1 inhibited pancreatic cancer cell invasion and exerted moderate growth-inhibitory effects. In conclusion, SPARCL1 expression in pancreatic tissues is highly correlated with level of vascularity. Its anti-invasive effects and reduced expression in metastasis indicate tumor-suppressor function ...
The Division of Biology & Biomedical SciencesThe Division of Biology & Biomedical Sciences
Epithelial cell adhesion molecule (EpCAM) is a 40-kD cell-surface glycoprotein that is dramatically overexpressed in the majority of breast cancers. We were the first to demonstrate that EpCAM is directly involved in the regulation of breast cancer migration and invasion. Specifically, in loss-of-function studies we have demonstrated that specific ablation of EpCAM expression: (1) decreases breast cancer invasion in vitro and in vivo; (2) is associated with cytoskeletal rearrangement and alterations in Rho GTPases; and (3) impacts on the expression of transcription factors and genes known to be involved in breast cancer invasion. The hypothesis is that EpCAM plays a central role in the regulation of breast cancer invasion. We are currently exploring this hypothesis in detail using cultured human breast cancer cells, breast cancer xenografts, human breast specimens, and a transgenic mouse model of breast carcinogenesis. Specific aims include (1) Test the hypothesis that EpCAM plays a central role ...
The death receptor CD95 activates the cofilin pathway to stimulate tumour cell invasion | EMBO ReportsThe death receptor CD95 activates the cofilin pathway to stimulate tumour cell invasion | EMBO Reports
Real‐time imaging. Cells were seeded in a Lab‐Tek Chambered #1.0 Borosilicate Coverglass System (Nalgene Nunc International, Rochester, NY, USA) and were mounted on a Zeiss Axiovert 200M microscope for live‐cell imaging (5% CO2; 37°C) for 2-14 h. Phase‐contrast images were captured every 2 min using a Photometics Coolsnap CCD camera (Scientific, Tuscon, AZ, USA). Images were processed using the Metamorph software (Universal imaging, Downington, PA, USA). Several protrusions was scored by off‐line analysis of the generated videos and plotted as means±s.e.m. For real‐time fluorescence imaging, cells were placed on a Leica SP5 inverted microscope equipped with a × 63 1.3NA glycerol objective. Cells were maintained in Leibovitz‐15‐buffered medium (Invitrogen, Breda, The Netherlands) at 37°C in a climate chamber.. Invasion assay. For in vitro invasion assays, 24‐well BioCoat matrigel invasion chambers (#354480, BD Biosciences, Alphen aan den Rijn, The Netherlands) were used ...
Strongylophorine-26, a Rho-dependent inhibitor of tumor cell invasion that reduces actin stress fibers and induces nonpolarized...Strongylophorine-26, a Rho-dependent inhibitor of tumor cell invasion that reduces actin stress fibers and induces nonpolarized...
Strongylophorine-26, a new meroditerpenoid, was recently identified as an inhibitor of cancer cell invasion. This study was undertaken to characterize its mechanism of action. We find that strongylophorine-26 inhibits the motility of MDA-MB-231 breast carcinoma cells on a plastic surface. Upon addition of strongylophorine-26, rapid cell contraction and depolarization occurred, followed by spreading and flattening of the entire cell. Treated cells exhibited increased membrane ruffling throughout and extended lamellipodia in all directions. Strongylophorine-26 induced a decrease in actin stress fibers, a dramatic increase in the size and number of focal adhesions, and the appearance of a dense meshwork of actin filaments around the cell periphery. Strongylophorine-26 caused a transient activation of the small GTPase Rho and treatment with the Rho inhibitor C3 exoenzyme abrogated the anti-invasive activity of strongylophorine-26. These effects are distinct from those of many motility and ...
An essential role for decorin in bladder cancer invasiveness | EMBO Molecular MedicineAn essential role for decorin in bladder cancer invasiveness | EMBO Molecular Medicine
Effective anti‐tumour immune response requires appropriate recruitment and activation of immune cells. However, despite expression of tumour antigens in most tumours, including bladder tumours (Nishiyama et al, 2001; Sharma et al, 2003), escape from T‐cell immunity is more often the rule rather than an exception. In this study, we examined and compared the immune response going on during development of bladder tumours induced by two cell lines: MB49 and its more invasive variant MB49‐I. Our analysis of adaptive immune response during MB49 and MB49‐I development and exploration of molecules secreted by both tumours showed that MB49‐I has developed two mechanisms to acquire invasion properties: loss of putative tumour antigens and overexpression of decorin.. The expression of the male transplantation H‐Y antigens by MB49 was shown to induce an anti‐tumour immune response when injected in female mice (Halak et al, 1999). Our results showed that, in stark contrast to MB49, MB49‐I has ...
Coordination of glioblastoma cell motility by PKCι | Molecular Cancer | Full TextCoordination of glioblastoma cell motility by PKCι | Molecular Cancer | Full Text
Glioblastoma is one of the deadliest forms of cancer, in part because of its highly invasive nature. The tumor suppressor PTEN is frequently mutated in glioblastoma and is known to contribute to the invasive phenotype. However the downstream events that promote invasion are not fully understood. PTEN loss leads to activation of the atypical protein kinase C, PKCι. We have previously shown that PKCι is required for glioblastoma cell invasion, primarily by enhancing cell motility. Here we have used time-lapse videomicroscopy to more precisely define the role of PKCι in glioblastoma. Glioblastoma cells in which PKCι was either depleted by shRNA or inhibited pharmacologically were unable to coordinate the formation of a single leading edge lamellipod. Instead, some cells generated multiple small, short-lived protrusions while others generated a diffuse leading edge that formed around the entire circumference of the cell. Confocal microscopy showed that this behavior was associated with altered behavior
CDH11 | Cancer Genetics WebCDH11 | Cancer Genetics Web
A small subpopulation of highly adaptable breast cancer cells within a vastly heterogeneous population drives cancer metastasis. Here we describe a function-based strategy for selecting rare cancer cells that are highly adaptable and drive malignancy. Although cancer cells are dependent on certain nutrients, e.g., glucose and glutamine, we hypothesized that the adaptable cancer cells that drive malignancy must possess an adaptable metabolic state and that such cells could be identified using a robust selection strategy. As expected, more than 99.99% of cells died upon glutamine withdrawal from the aggressive breast cancer cell line SUM149. The rare cells that survived and proliferated without glutamine were highly adaptable, as judged by additional robust adaptability assays involving prolonged cell culture without glucose or serum. We were successful in isolating rare metabolically plastic glutamine-independent (Gln-ind) variants from several aggressive breast cancer cell lines that we tested. ...
Calpain 2 and PTP1B function in a novel pathway with Src to regulate invadopodia dynamics and breast cancer cell invasion |...Calpain 2 and PTP1B function in a novel pathway with Src to regulate invadopodia dynamics and breast cancer cell invasion |...
The pSUPER.retro (Oligoengine) RNA interference system was used to achieve stable expression of siRNAs. Oligonucleotides targeted to calpain 2 or PTP1B mRNA as well as a nonsilencing control were synthesized by Integrated DNA Technologies, annealed, and cloned into the pSUPER.retro.puro vector according to manufacturers instructions. Retroviral transfection was performed as described previously (Franco et al., 2004a). Wild-type MTLn3 cells were infected at 32°C for 6 h and allowed to recover in growth medium for 24 h before selection with 1 μg/ml puromycin for 4-5 d. Target sequences for calpain 2 in MTLn3 cells: control, 5′-TTCTCCGAACGTGTCACGT-3′; Capn2 si-A, 5′-AGGCCTATGCCAAGATCAA-3′; and Capn2 si-B, 5′-GAATGGCGATTTCTGCATC-3′. Target sequences for PTP1B in MTLn3 cells: PTP1B si-A, 5′-GCTGACACTGATCTCTGAA-3′; and PTP1Bsi-B, 5′-CAGGAGGAGCCTTGGTGTC-3′. Target sequences for human calpain 2 have been described previously (Su et al., 2006). Target sequences for cortactin: ...
Silencing of hyaluronan synthase 2 suppresses the malignant phenotype of invasive breast cancer cellsSilencing of hyaluronan synthase 2 suppresses the malignant phenotype of invasive breast cancer cells
Hyaluronan (HA), a structural component in the extracellular matrix (ECM), has been recognized as a signaling molecule. It is important during various biological activities such as embryogenesis, angiogenesis, wound healing and tumor progression. Increased amount of hyaluronan during embryonic development is necessary for cell migration and differentiation, but the increased production of hyaluronan by tumor cells or tissue fibroblasts is correlated to poor prognosis for tumor progression and chronic inflammation, respectively. Therefore, understanding the mechanisms regulating HA-enriched matrices and the roles of HA in the biological functions is of fundamental biological importance.. Four novel findings are described in this thesis: (1) HA fragments (HA12) and the known angiogenic factor FGF-2 promote endothelial cell differentiation by induction of common but also distinct sets of genes, particularly, upregulation of the chemokine CXCL1/GRO1 gene is necessary for HA12-induced angiogenesis ...
Actions of TGF-beta as tumor suppressor and pro-metastatic factor in human cancerActions of TGF-beta as tumor suppressor and pro-metastatic factor in human cancer
Transforming growth factor-beta (TGF-beta) is a secreted polypeptide that signals via receptor serine/threonine kinases and intracellular Smad effectors. TGF-beta inhibits proliferation and induces apoptosis in various cell types, and accumulation of loss-of-function mutations in the TGF-beta receptor or Smad genes classify the pathway as a tumor suppressor in humans. In addition, various oncogenic pathways directly inactivate the TGF-beta receptor-Smad pathway, thus favoring tumor growth. On the other hand, all human tumors overproduce TGF-beta whose autocrine and paracrine actions promote tumor cell invasiveness and metastasis. Accordingly, TGF-beta induces epithelial-mesenchymal transition, a differentiation switch that is required for transitory invasiveness of carcinoma cells. Tumor-derived TGF-beta acting on stromal fibroblasts remodels the tumor matrix and induces expression of mitogenic signals towards the carcinoma cells, and upon acting on endothelial cells and pericytes, TGF-beta ...
DIGITAL.CSIC: Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating cellsDIGITAL.CSIC: Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating cells
Malignant progression in cancer requires populations of tumor-initiating cells (TICs) endowed with unlimited self renewal, survival under stress, and establishment of distant metastases. Additionally, the acquisition of invasive properties driven by epithelial-mesenchymal transition (EMT) is critical for the evolution of neoplastic cells into fully metastatic populations. Here, we characterize 2 human cellular models derived from prostate and bladder cancer cell lines to better understand the relationship between TIC and EMT programs in local invasiveness and distant metastasis. The model tumor subpopulations that expressed a strong epithelial gene program were enriched in highly metastatic TICs, while a second subpopulation with stable mesenchymal traits was impoverished in TICs. Constitutive overexpression of the transcription factor Snai1 in the epithelial/ TIC-enriched populations engaged a mesenchymal gene program and suppressed their self renewal and metastatic phenotypes. Conversely, ...
Following removal of the primary breast tumour by conservative surgery patients - EGF Prevents the Neuroendocrine...Following removal of the primary breast tumour by conservative surgery patients - EGF Prevents the Neuroendocrine...
Following removal of the primary breast tumour by conservative surgery patients may still have additional malignant foci scattered throughout the breast. which are required to activate the MMP-2 were also increased. Confirming the role of MMP-2 and MT1-MMP radiation enhancement of cancer cell invasion was prevented by an MMP-2 inhibitor and an anti-MT1-MMP antibody. This study also demonstrated that radiation can potentially enhance the invasion ability by inducing the release of pro-invasive factors stored in the Matrigel. Conversely no enhancement of invasiveness was observed with the low metastatic cell line MCF-7. This lack of invasiveness correlated with the absence of the MMP-2 activator MT1-MMP in the MCF-7 cells. Radiotherapy is an efficient modality to treat breast cancer which could be further ABT-751 improved by inhibiting the pro-invasive gene upregulated by radiation. 4 This data also confirmed that proMMP-2 was absent from the FBS-free culture media (Figure 1B lane 2). ProMMP-2 is ...
IJMS | Free Full-Text | The Role of Sialyl-Tn in CancerIJMS | Free Full-Text | The Role of Sialyl-Tn in Cancer
Activation of an aberrant glycosylation pathway in cancer cells can lead to expression of the onco-foetal sialyl-Tn (sTn) antigen. STn is a truncated O-glycan containing a sialic acid α-2,6 linked to GalNAc α-O-Ser/Thr and is associated with an adverse outcome and poor prognosis in cancer patients. The biosynthesis of the sTn antigen has been linked to the expression of the sialytransferase ST6GalNAc1, and also to mutations in and loss of heterozygosity of the COSMC gene. sTn neo- or over-expression occurs in many types of epithelial cancer including gastric, colon, breast, lung, oesophageal, prostate and endometrial cancer. sTn is believed to be carried by a variety of glycoproteins and may influence protein function and be involved in tumour development. This review discusses how the role of sTn in cancer development and tumour cell invasiveness might be organ specific and occur through different mechanisms depending on each cancer type or subtype. As the sTn-antigen is expressed early in
JCI - Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating...JCI - Epithelial-mesenchymal transition can suppress major attributes of human epithelial tumor-initiating...
Malignant progression in cancer requires populations of tumor-initiating cells (TICs) endowed with unlimited self renewal, survival under stress, and establishment of distant metastases. Additionally, the acquisition of invasive properties driven by epithelial-mesenchymal transition (EMT) is critical for the evolution of neoplastic cells into fully metastatic populations. Here, we characterize 2 human cellular models derived from prostate and bladder cancer cell lines to better understand the relationship between TIC and EMT programs in local invasiveness and distant metastasis. The model tumor subpopulations that expressed a strong epithelial gene program were enriched in highly metastatic TICs, while a second subpopulation with stable mesenchymal traits was impoverished in TICs. Constitutive overexpression of the transcription factor Snai1 in the epithelial/TIC-enriched populations engaged a mesenchymal gene program and suppressed their self renewal and metastatic phenotypes. Conversely, ...
RePub, Erasmus University Repository: A microcarrier-based spheroid 3D invasion assay to monitor dynamic cell movement in...RePub, Erasmus University Repository: A microcarrier-based spheroid 3D invasion assay to monitor dynamic cell movement in...
Background: Cell invasion through extracellular matrix (ECM) is a critical step in tumor metastasis. To study cell invasion in vitro, the internal microenvironment can be simulated via the application of 3D models. Results: This study presents a method for 3D invasion examination using microcarrier-based spheroids. Cell invasiveness can be evaluated by quantifying cell dispersion in matrices or tracking cell movement through time-lapse imaging. It allows measuring of cell invasion and monitoring of dynamic cell behavior in three dimensions. Here we show different invasive capacities of several cell types using this method. The content and concentration of matrices can influence cell invasion, which should be optimized before large scale experiments. We also introduce further analysis methods of this 3D invasion assay, including manual measurements and homemade semi-automatic quantification. Finally, our results indicate that the position of spheroids in a matrix has a strong impact on cell ...
E-poster Presentation - ASN EventsE-poster Presentation - ASN Events
Background:. Esophageal cancer (EC) is an aggressive malignancy with increasing incidence and poor outcome (1). New therapeutic strategies are urgently required. The phosphatidylinositol 3-kinase (PI3K)/AKT signal pathway has been documented as a central hub for the malignant behaviors of cancer cells (2). However, the functional role and therapeutic effect of PI3K/AKT inhibitors in esophageal cancer metastasis is underappreciated.. Aim:. We aim to study the clinical significance of PI3K/AKT signaling pathway in EC metastasis and evaluate the therapeutic effect of PI3K/AKT-targeted therapy.. Methods:. A highly invasive cancer cell line (KYSE410-I3) was established by serial selection of the EC cells invading through the matrigel-coated Boyden chamber. Cell migration and invasion were determined using Boyden chamber migration and invasion assays. Western blot and immunohistochemistry were used to detect protein expressions in cell lysates and in a tissue microarray containing 40 pairs of ...
Impact of Multifocality and Lymph Node Metastasis on the Prognosis and Management of Microinvasive Breast Cancer | SpringerLinkImpact of Multifocality and Lymph Node Metastasis on the Prognosis and Management of Microinvasive Breast Cancer | SpringerLink
There are few data on the long-term outcome of patients with microinvasive (T1mi) breast cancer. Moreover, predictors of lym ph node involvement and the im pact of multifocal microinvasion are not wel
Nonpalpable In Situ Ductal Carcinoma of the Breast: Predictors of Multicentricity and Microinvasion and Implications for...Nonpalpable In Situ Ductal Carcinoma of the Breast: Predictors of Multicentricity and Microinvasion and Implications for...
• Fifty breasts with nonpalpable ductal carcinoma in situ (DCIS) were examined for the presence of microinvasion, multicentricity, and number of involved ducts
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Purpose: Head and neck squamous cell carcinoma (HNSCC) is one of the 10 most common cancers with a 50% five-year survival rate, which has remained unchanged for the past three decades. One of the major reasons for the aggressiveness of this cancer is that HNSCCs readily metastasize to cervical lymph nodes that are abundant in the head and neck region. Hence, discovering new molecules controlling the metastatic process as well as understanding their regulation at the molecular level are essential for effective therapeutic strategies.. Experimental Design: Rab25 expression level was analyzed in HNSCC tissue microarray. We used a combination of intravital microscopy in live animals and immunofluorescence in an in vitro invasion assay to study the role of Rab25 in tumor cell migration and invasion.. Results: In this study, we identified the small GTPase Rab25 as a key regulator of HNSCC metastasis. We observed that Rab25 is downregulated in HNSCC patients. Next, we determined that reexpression of ...
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Cancer cell invasion is one of the crucial events in local spreading, growth, and metastasis of tumors. First evidence suggesting an anti-invasive action was published by Nithipatikom et al. (2004) who showed that 2-AG inhibits invasion of androgen-independent prostate cancer cells by a mechanism involving CB1 receptor activation. However, the precise mechanism leading to decreased invasiveness by cannabinoids remained elusive. Recently, several investigations have provided new insight into how cannabinoids could achieve their anti-invasive action.. In this context, several studies suggest a modulation of the MMP system by cannabinoids as part of their anti-invasive action. MMPs belong to a group of enzymes exerting an important function during tumor invasion, metastasis, and angiogenesis through degradation of ECM components (Curran and Murray, 2000; Stamenkovic, 2000). Of all MMPs, particularly MMP-2 and -9, are known to facilitate tumor invasion by proteolytic degradation of major basement ...
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We identified previously that CRMP-1 is an invasion and metastasis suppressor in lung cancer cells (9). CRMP-1 expression is negatively associated with poor overall survival and early postoperative relapse in lung cancer patients (9). The connective tissue growth factor can inhibit lung adenocarcinoma invasion and metastasis by CRMP-1-dependent pathway and mediated through an integrin αvβ3 and αvβ5 regulated signaling (29). However, the detail mechanism of invasion suppressor function of CRMP-1 and its regulation were still not clear.. In this study, we identified a region between nucleotides -100 and -180 containing putative Sp1 and C/EBPα transcriptional regulatory elements as the basal promoter region of the novel invasion suppressor gene, CRMP-1. Overexpression of Sp1 suppressed CRMP-1 promoter activity and CRMP-1 protein expression, whereas overexpression of C/EBPα enhanced expression from the CRMP-1 promoter. Our data also showed that COX-2 overexpression decreased CRMP-1 mRNA and ...
ERK2 drives tumour cell migration in 3D microenvironments by suppressing expression of Rab17 and Liprin-β2 | Journal of Cell...ERK2 drives tumour cell migration in 3D microenvironments by suppressing expression of Rab17 and Liprin-β2 | Journal of Cell...
Upregulation of the extracellular signal-regulated kinase (ERK) pathway has been shown to contribute to tumour invasion and progression. Since the two predominant ERK isoforms (ERK1 and ERK2) are highly homologous and have indistinguishable kinase activities in vitro, both enzymes were believed to be redundant and interchangeable. To challenge this view, here we show that ERK2 silencing inhibits invasive migration of MDA-MB-231 cells, and re-expression of ERK2 but not ERK1 restores the normal invasive phenotype. A detailed quantitative analysis of cell movement on 3D matrices indicates that ERK2 knockdown impairs cellular motility by decreasing the migration velocity as well as increasing the time that cells spend not moving. We used gene expression arrays to identify rab17 and liprin-β2 as genes whose expression was increased by knockdown of ERK2 and restored to normal levels following re-expression of ERK2, but not ERK1. Both Rab17 and Liprin-β2 play inhibitory roles in the invasive ...
Cooperative actions of p21WAF1 and p53 induce Slug protein degradation and suppress cell invasion | EMBO ReportsCooperative actions of p21WAF1 and p53 induce Slug protein degradation and suppress cell invasion | EMBO Reports
We investigated whether p21 cooperates with a p53 mutant. R273H is a naturally occurring mutation that abolishes the DNA binding and thus the trans‐activating activity of p53 [3]. Therefore, in contrast to p53wt expression, p53R273H expression in H1299 cells failed to induce p21 and Mdm2 (Fig 4D, left). Slug protein levels and cellular invasiveness were not markedly altered after expressing p53R273H, but decreased when p53R273H and p21 were co‐expressed. Consistent with this, p53R273H and p21 co‐expression elevated Slug ubiquitination to considerably higher levels than p53R273H expression alone did (Fig 4D, right). These results provide support for the ability of p53R273H to cooperate with p21 in promoting Slug ubiquitination/degradation and thus suppressing cell invasion. Our data also suggest that p53 can contribute to tumor suppression even after the loss of its trans‐activating activity. However, our results are in contrast with a previous report that shRNA‐mediated knockdown of ...
YUAN YUANYUAN YUAN
Hypoxia plays a key role in tumour cell survival, invasion, and metastasis. An increasing number of studies have attemptedto characterize the tumour response to hypoxia and to identify predictive markers of disease. Here we show that hypoxiaincreases tumour cell invasion and migration by the modulation of Rab11, an important molecule for vesicular trafficking.In our study, we found that Rab11, together with the activation of Rac1, could stimulate invasion and migration of cervicalcancer cell lines HeLa/SiHa in hypoxia. Activation of Rac1 activity by hypoxia seems to be central to carcinoma invasion.We also found that these effects could be related to the integrin αvβ3. In addition, we studied the molecular pathway for thisprocess. Our results showed that in cervical cancer cell lines HeLa/SiHa, Rac1 activation in hypoxia could stimulateinvasion and migration, and this process was mediated by integrin αvβ3-mediated FAK and PI3K phosphorylation.Furthermore, hypoxia induced a dramatic increase ...
p53 Target Gene SMAR1 Is Dysregulated in Breast Cancer: Its Role in Cancer Cell Migration and Invasion - pdf descargarp53 Target Gene SMAR1 Is Dysregulated in Breast Cancer: Its Role in Cancer Cell Migration and Invasion - pdf descargar
p53 Target Gene SMAR1 Is Dysregulated in Breast Cancer: Its Role in Cancer Cell Migration and Invasion. . 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.
Cancer Mouse Models | Transgenic Rodents | genOwayCancer Mouse Models | Transgenic Rodents | genOway
Creating genetically modified rodent models to study pathologic conditions for cancer invasiveness, metastasis, DNA repair, cell cycle progression, apoptosis.
Data Availability StatementThe data used to aid the findings of this study are available from your corresponding authors upon...Data Availability StatementThe data used to aid the findings of this study are available from your corresponding authors upon...
Data Availability StatementThe data used to aid the findings of this study are available from your corresponding authors upon request. invasion of HepG2, Hep3B, Huh7, and SMMC-7721 cells. Results of transwell invasion assays of Hep3B, HepG2, Huh7, Rabbit Polyclonal to ELOVL1 and SMMC-7721 cells following treatment with apatinib for 24?h (unique magnification, 200). Quantification of the invasion in Hep3B, HepG2, Huh7, and SMMC-7721 cells (?? shows 0.01 vs. 0? 0.05; Number 3(a)). Western blot analysis showed that apatinib also downregulated the manifestation of the abovementioned MMPs in the protein level (Number 3(b)). Open Ginkgolide C in a separate window Number 3 Real-time PCR and Western blot analysis of manifestation levels of MMP family genes in Hep3B and HepG2 liver cells. (a) Real-time PCR analysis of mRNA levels of MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, MMP-10, MMP-11, and MMP-16. Compared with the control group, the manifestation levels of the mRNAs of MMP-1, MMP-2, MMP-3, MMP-7, MMP-9, ...
MFAP5-mediated ovarian cancer cell motility and invasiveness (Homo sapiens) - WikiPathwaysMFAP5-mediated ovarian cancer cell motility and invasiveness (Homo sapiens) - WikiPathways
Leung CS, Yeung TL, Yip KP, Pradeep S, Balasubramanian L, Liu J, Wong KK, Mangala LS, Armaiz-Pena GN, Lopez-Berestein G, Sood AK, Birrer MJ, Mok SC; Calcium-dependent FAK/CREB/TNNC1 signalling mediates the effect of stromal MFAP5 on ovarian cancer metastatic potential.; Nat Commun, 2014 PubMed Europe PMC Scholia ...
Nose Cancer (Fibrosarcoma) in Dogs | petMDNose Cancer (Fibrosarcoma) in Dogs | petMD
Nasal and paranasal fibrosarcoma is characterized by a malignant tumor based in the connective tissue of the nasal passage or in the surrounding area. A fibrosarcoma specifically refers to the abnormal development of cells. It is typically a slow and invasive process that progresses to a critical state before it is discovered.
Radiogenomic mapping of edema/cellular invasion MRI-phenotypes in glioblastoma multiforme. | The Ferenc Jolesz National Center...Radiogenomic mapping of edema/cellular invasion MRI-phenotypes in glioblastoma multiforme. | The Ferenc Jolesz National Center...
Zinn PO, Mahajan B, Majadan B, Sathyan P, Singh SK, Majumder S, Jolesz FA, Colen RR. Radiogenomic mapping of edema/cellular invasion MRI-phenotypes in glioblastoma multiforme. PLoS One. 2011;6 (10) :e25451.
IL-35 Over-expression is Associated with Genesis of Gastric Cancer -Asian Pacific Journal of Cancer Prevention ...IL-35 Over-expression is Associated with Genesis of Gastric Cancer -Asian Pacific Journal of Cancer Prevention ...
IL-35 Over-expression is Associated with Genesis of Gastric Cancer IL-35;gastric cancer;Ki-67;Bcl-2; Overexpression of interleukin (IL)-35 has been found in a variety of malignancies, but the expression status in gastric cancer has yet to be elucidated clearly. In the present study, positive expression of EBI3 and p35 was 63.3% and 70.0% of cases, respectively. EBI3 expression was strongly related with larger tumor size and invasion depth (P
Radiology Quiz 49777 | Radiopaedia.orgRadiology Quiz 49777 | Radiopaedia.org
poorly enhancing pancreatic tail mass with extension into surrounding fat and direct invasion of the adjacent small bowel loops and left adrenal gland ...
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Inflammation is recognized as a key factor in carcinogenesis; however, the precise mechanisms by which the immune response affects cancer development remain largely unknown. Mutation of the p53 tumor suppressor has been linked to a heightened proinflammatory microenvironment, prompting Di Minin, Bellazzo, and colleagues to study whether activation of inflammatory responses by mutant p53 is involved in driving cancer progression and metastasis. In support of this idea, silencing of mutant p53 in breast cancer cells inhibited cell migration and enhanced apoptosis in response to the proinflammatory cytokine TNFα. Transcriptional profiling revealed a set of TNFα-inducible NFκB target genes with proinvasive and immunogenic functions, which were regulated in a mutant p53-dependent manner. Intriguingly, chemical inhibition of pathways downstream of TNFα showed that, whereas the majority of genes were NFκB-dependent, inhibition of JNK upregulated a subset of genes specifically in cells depleted for ...
EWGBSP CIS vs MIC STUDY 3 - Bács-Kiskun Megyei KórházEWGBSP CIS vs MIC STUDY 3 - Bács-Kiskun Megyei Kórház
The tumour focus/foci must invade into nonspecialized interlobular or interductal stroma (extension of the lesion beyond the confines of a ductolobular unit, development of a desmoplastic stroma). The cells deemed to be invasive must be distributed in a fashion (non-organoid pattern) that does not represent tangential sectioning of a duct or a lobular structure with in-situ carcinoma. Tangentially sectioned in-situ carcinoma foci that simulate microinvasion are distributed in the specialized periductal and intralobular stroma and usually occur as compact groups of tumour cells that have a smooth border surrounded by a circumferential layer of myoepithelial cells and stroma or a thickened basement membrane (29). At sites of microinvasive foci, tumour cells are distributed singly or as small groups that have irregular shapes reminiscent of conventional invasive carcinoma with no particular orientation (29). There is complete absence of surrounding basement membrane and myoepithelial cells: ...
Glucose regulated protein 78 promotes cell invasion via regulation of uPA production and secretion in colon cancer cellsGlucose regulated protein 78 promotes cell invasion via regulation of uPA production and secretion in colon cancer cells
... ;kpubs;kpubs.org
Facts About huge cysts being popped RevealedFacts About huge cysts being popped Revealed
Percutaneous kidney medical procedures is completed for big cysts behind the kidney. This is a minimally invasive process which allows the surgeon to complete endoscopic surgery within the kidney using a modest tract. A tract is an opening created by a small incision in the pores and skin and tissues instantly in to the kidney ...
Paternity Issues in CaliforniaPaternity Issues in California
When paternity is in question, determining a fathers identity can be an invasive process and can result in a man paying financial support for years.
High PARP-1 Expression Is Associated With Tumor Invasion And Poor Prognosis In Gastric Cancer. - ElabscienceHigh PARP-1 Expression Is Associated With Tumor Invasion And Poor Prognosis In Gastric Cancer. - Elabscience
Liu Y, Zhang Y, Zhao Y, et al. High PARP-1 Expression Is Associated With Tumor Invasion And Poor Prognosis In Gastric Cancer[J]. Oncology Letters, 2016, 12(5): 3825-3835.
Epithelial-mesenchymal transition, invasion, and intravision - EMT / Invasion / Intravasation | CourseraEpithelial-mesenchymal transition, invasion, and intravision - EMT / Invasion / Intravasation | Coursera
Video created by Johns Hopkins University for the course Understanding Cancer Metastasis. During this module, well turn our attention to the next steps after the initial primary tumor formation, epithelial to mesenchymal transition of cancer ...
Epithelial-mesenchymal transition, invasion, and intravision - EMT / Invasion / Intravasation | CourseraEpithelial-mesenchymal transition, invasion, and intravision - EMT / Invasion / Intravasation | Coursera
Video created by Johns Hopkins University for the course Understanding Cancer Metastasis. During this module, well turn our attention to the next steps after the initial primary tumor formation, epithelial to mesenchymal transition of cancer ...
Endoscopic submucosal dissectionEndoscopic submucosal dissection
CystadenocarcinomaCystadenocarcinoma
List of MeSH codes (C23)List of MeSH codes (C23)
Brain tumorBrain tumor
MalignancyMalignancy
MalignancyMalignancy
Targeted therapy of lung cancerTargeted therapy of lung cancer
Brain tumorBrain tumor
Brain tumorBrain tumor
DesmoplasiaDesmoplasia
CarcinomaCarcinoma
Mammary tumorMammary tumor
Cathepsin KCathepsin K
Acral lentiginous melanomaAcral lentiginous melanoma
LymphangioleiomyomatosisLymphangioleiomyomatosis
Saliva testingSaliva testing
Neuroendocrine tumorNeuroendocrine tumor
AmeloblastomaAmeloblastoma
Epithelioid sarcomaEpithelioid sarcoma
CarcinomaCarcinoma
GlioblastomaGlioblastoma
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsHealth Care
Neoplasm InvasivenessPancreatic NeoplasmsNeoplasmsCell Line, TumorCell MovementNeoplasms, Cystic, Mucinous, and SerousSkin NeoplasmsNeoplasm MetastasisGene Expression Regulation, NeoplasticMatrix Metalloproteinase 2ImmunohistochemistryLung NeoplasmsMatrix Metalloproteinase 9Neoplasms, Multiple PrimaryBreast NeoplasmsKidney NeoplasmsTumor Cells, CulturedLiver NeoplasmsThyroid NeoplasmsNeoplasms, Second PrimaryOvarian NeoplasmsNeoplasm ProteinsCarcinoma, Pancreatic DuctalMice, NudeCell ProliferationCadherinsDNA, NeoplasmNeoplasms, ExperimentalNeoplasm TransplantationAdenocarcinoma, MucinousTumor Markers, BiologicalMyeloproliferative DisordersAdenocarcinomaLamininSignal TransductionColonic NeoplasmsCell AdhesionParotid NeoplasmsAdenomaGastrointestinal NeoplasmsCystadenomaNeoplasm StagingNeoplasms, Connective and Soft TissueNeoplasms, Plasma CellReverse Transcriptase Polymerase Chain ReactionCarcinoma, PapillaryCell Transformation, NeoplasticCarcinomaAppendiceal NeoplasmsDrug CombinationsRNA, Small InterferingBone NeoplasmsCystadenoma, MucinousBlotting, WesternEndocrine Gland NeoplasmsUrokinase-Type Plasminogen ActivatorGlioblastomaStomach NeoplasmsTransfectionProstatic NeoplasmsGliomaBile Duct NeoplasmsNeoplasms, Vascular TissueAntigens, NeoplasmEye NeoplasmsNose NeoplasmsProteoglycansRNA, MessengerColorectal NeoplasmsSalivary Gland NeoplasmsMelanomaTrophoblastsNeoplasms, Radiation-InducedAdenocarcinoma, PapillaryMouth NeoplasmsThymus NeoplasmsTesticular NeoplasmsNeoplasms, Muscle TissueNeoplasms, Glandular and EpithelialUrinary Bladder NeoplasmsDisease ProgressionCollagenCystadenocarcinoma, MucinousAntigens, CD82Epithelial CellsReceptors, Urokinase Plasminogen ActivatorUp-RegulationCarcinoma, Squamous CellSoft Tissue NeoplasmsHematologic NeoplasmsUterine NeoplasmsIntestinal NeoplasmsDog DiseasesNeoplasms, Adnexal and Skin AppendageMatrix MetalloproteinasesEpithelial-Mesenchymal TransitionMatrix Metalloproteinase InhibitorsVascular NeoplasmsSweat Gland NeoplasmsCell DivisionLymphomaPrognosisPalatal NeoplasmsDown-RegulationNeoplasms, Complex and MixedRNA InterferenceMandibular NeoplasmsCystadenocarcinomaSplenic NeoplasmsHeart NeoplasmsCystadenoma, SerousMammary Neoplasms, AnimalNeovascularization, PathologicNeoplasm Recurrence, Localbeta CateninBrain NeoplasmsRNA, NeoplasmMaxillary NeoplasmsPhenotypeMatrix Metalloproteinase 14Transplantation, HeterologousAnal Gland NeoplasmsCell LineLiver Neoplasms, ExperimentalNeoplasms, Germ Cell and EmbryonalBone Marrow NeoplasmsVirulenceVimentinAstrocytomaHepatocyte Growth FactorNeoplasms, Adipose TissueHead and Neck NeoplasmsS100 ProteinsMeningeal NeoplasmsDuodenal NeoplasmsMice, SCIDIntroduced SpeciesPituitary NeoplasmsPeritoneal NeoplasmsMutationAdrenal Cortex NeoplasmsGene Expression ProfilingRetrospective StudiesMediastinal NeoplasmsImmunoenzyme TechniquesTomography, X-Ray ComputedProto-Oncogene Proteins c-metTongue NeoplasmsIleal NeoplasmsTissue Inhibitor of Metalloproteinase-2Gene SilencingApoptosisExtracellular MatrixCarcinoma, HepatocellularCarcinoma, Acinar CellSpinal Cord NeoplasmsVaginal NeoplasmsGene Knockdown TechniquesAntineoplastic AgentsAdenoma, OxyphilicNervous System NeoplasmsNeoplasm GradingJanus Kinase 2Muscle NeoplasmsHemangiosarcomaPhosphorylationMatrix Metalloproteinase 7DogsMyelodysplastic-Myeloproliferative DiseasesMammary Neoplasms, ExperimentalPancreatectomyGelatinasesPeripheral Nervous System NeoplasmsTime FactorsCell Growth ProcessesCerebral Ventricle NeoplasmsTissue Inhibitor of Metalloproteinase-1Paranasal Sinus NeoplasmsPleural NeoplasmsTranscription FactorsMice, Inbred BALB CGene ExpressionSarcomaFibrosarcomaCommon Bile Duct NeoplasmsMatrix Metalloproteinases, Membrane-AssociatedMesodermLymphatic MetastasisJaw NeoplasmsFibroblastsEsophageal NeoplasmsOligonucleotide Array Sequence AnalysisOrbital NeoplasmsCarcinogensMetalloendopeptidasesAbdominal NeoplasmsTransforming Growth Factor betaReal-Time Polymerase Chain ReactionCerebellar NeoplasmsCells, CulturedCell Survival
Effects of micro-environment- and malignant cell-derived interleukin-1 in carcinogenesis, tumour invasiveness and tumour-host...Effects of micro-environment- and malignant cell-derived interleukin-1 in carcinogenesis, tumour invasiveness and tumour-host...
Effects of small interfering RNA targeting heparanase-1 combined with heparin on invasiveness of mouse hepatocellular carcinoma...Effects of small interfering RNA targeting heparanase-1 combined with heparin on invasiveness of mouse hepatocellular carcinoma...
Stromal Cell Derived factor-1: Its Influence on Invasiveness and Migration of Breast Cancer Cells in Vitro, and Its Association...Stromal Cell Derived factor-1: Its Influence on Invasiveness and Migration of Breast Cancer Cells in Vitro, and Its Association...
Transcriptional repression of MMP-1 by p21SNFT and reduced in vitro invasiveness of hepatocarcinoma cells.Transcriptional repression of MMP-1 by p21SNFT and reduced in vitro invasiveness of hepatocarcinoma cells.
CO2 Pneumoperitoneum Effects on Molecular Markers of Tumor Invasiveness in SH-SY5Y Neuroblastoma CellsCO2 Pneumoperitoneum Effects on Molecular Markers of Tumor Invasiveness in SH-SY5Y Neuroblastoma Cells
RNA Therapeutics - & related info | MendeleyRNA Therapeutics - & related info | Mendeley
Laringectomía total ampliada en carcinoma laríngeo avanzado T4aLaringectomía total ampliada en carcinoma laríngeo avanzado T4a
The natural compound atraric acid is an antagonist of the human androgen receptor inhibiting cellular invasiveness and...The natural compound atraric acid is an antagonist of the human androgen receptor inhibiting cellular invasiveness and...
Endometrial Cancer | Cancer Genetics WebEndometrial Cancer | Cancer Genetics Web
Osteosarcoma | Cancer Genetics WebOsteosarcoma | Cancer Genetics Web
POVEZANOST POJAVE PERITUMORALNIH PUKOTINA U DUKTALNOM INVAZIVNOM KARCINOMU DOJKE S MIOFIBROBLASTIČNOM REAKCIJOM STROMEPOVEZANOST POJAVE PERITUMORALNIH PUKOTINA U DUKTALNOM INVAZIVNOM KARCINOMU DOJKE S MIOFIBROBLASTIČNOM REAKCIJOM STROME
Diagnostic, clinical and therapeutic aspects of primary transitional cell carcinoma of the prostate]. - PubMed - NCBIDiagnostic, clinical and therapeutic aspects of primary transitional cell carcinoma of the prostate]. - PubMed - NCBI
Article abstract | Medical Science MonitorArticle abstract | Medical Science Monitor
Análise da expressão plasmática e tecidual das metaloproteinases de matriz 2 e 9...Análise da expressão plasmática e tecidual das metaloproteinases de matriz 2 e 9...
Article abstract | Medical Science MonitorArticle abstract | Medical Science Monitor
Polo-like kinase 1 is overexpressed in renal cancer and participates in the proliferation and invasion of renal cancer cells. |...Polo-like kinase 1 is overexpressed in renal cancer and participates in the proliferation and invasion of renal cancer cells. |...
Proliferative and Invasive Effects of Progesterone-Induced Blocking Factor in Human Glioblastoma Cells. - NextBio articleProliferative and Invasive Effects of Progesterone-Induced Blocking Factor in Human Glioblastoma Cells. - NextBio article
LncRNA HOXA11-AS promotes proliferation and invasion by targeting miR-124 in human non-small cell lung cancer cells. - NextBio...LncRNA HOXA11-AS promotes proliferation and invasion by targeting miR-124 in human non-small cell lung cancer cells. - NextBio...
Cancer GlossaryCancer Glossary
Early versus deferred androgen suppression therapy for patients with lymph node-positive prostate cancer after local therapy...Early versus deferred androgen suppression therapy for patients with lymph node-positive prostate cancer after local therapy...
Endoscopic submucosal dissection - WikipediaEndoscopic submucosal dissection - Wikipedia
Staging Systems for Musculoskeletal NeoplasmsStaging Systems for Musculoskeletal Neoplasms
Neoplasms 1 Flashcards by Charlie Lefroy | BrainscapeNeoplasms 1 Flashcards by Charlie Lefroy | Brainscape
JUB is highly upregulated in colorectal cancer (CRC) sp | Open-iJUB is highly upregulated in colorectal cancer (CRC) sp | Open-i
MiR-139-5p inhibits CRC invasion via directly targeting | Open-iMiR-139-5p inhibits CRC invasion via directly targeting | Open-i
CIC (capicua transcriptional repressor)CIC (capicua transcriptional repressor)
Cystadenocarcinoma - WikipediaCystadenocarcinoma - Wikipedia
JoVE | Peer Reviewed Scientific Video Journal - Methods and ProtocolsJoVE | Peer Reviewed Scientific Video Journal - Methods and Protocols
Myeloid/Histiocytic Neoplasms Associated with Germ Cell Tumors Harbor Shared Genetic Abnormalities Indicating a Clonal...Myeloid/Histiocytic Neoplasms Associated with Germ Cell Tumors Harbor Shared Genetic Abnormalities Indicating a Clonal...
The Utilization of Imaging Features in the Management of Intraductal Papillary Mucinous NeoplasmsThe Utilization of Imaging Features in the Management of Intraductal Papillary Mucinous Neoplasms
AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsHealth Care
Neoplasm InvasivenessPancreatic NeoplasmsNeoplasmsCell Line, TumorCell MovementNeoplasms, Cystic, Mucinous, and SerousSkin NeoplasmsNeoplasm MetastasisGene Expression Regulation, NeoplasticMatrix Metalloproteinase 2ImmunohistochemistryLung NeoplasmsMatrix Metalloproteinase 9Neoplasms, Multiple PrimaryBreast NeoplasmsKidney NeoplasmsTumor Cells, CulturedLiver NeoplasmsThyroid NeoplasmsNeoplasms, Second PrimaryOvarian NeoplasmsNeoplasm ProteinsCarcinoma, Pancreatic DuctalMice, NudeCell ProliferationCadherinsDNA, NeoplasmNeoplasms, ExperimentalNeoplasm TransplantationAdenocarcinoma, MucinousTumor Markers, BiologicalMyeloproliferative DisordersAdenocarcinomaLamininSignal TransductionColonic NeoplasmsCell AdhesionParotid NeoplasmsAdenomaGastrointestinal NeoplasmsCystadenomaNeoplasm StagingNeoplasms, Connective and Soft TissueNeoplasms, Plasma CellReverse Transcriptase Polymerase Chain ReactionCarcinoma, PapillaryCell Transformation, NeoplasticCarcinomaAppendiceal NeoplasmsDrug CombinationsRNA, Small InterferingBone NeoplasmsCystadenoma, MucinousBlotting, WesternEndocrine Gland NeoplasmsUrokinase-Type Plasminogen ActivatorGlioblastomaStomach NeoplasmsTransfectionProstatic NeoplasmsGliomaBile Duct NeoplasmsNeoplasms, Vascular TissueAntigens, NeoplasmEye NeoplasmsNose NeoplasmsProteoglycansRNA, MessengerColorectal NeoplasmsSalivary Gland NeoplasmsMelanomaTrophoblastsNeoplasms, Radiation-InducedAdenocarcinoma, PapillaryMouth NeoplasmsThymus NeoplasmsTesticular NeoplasmsNeoplasms, Muscle TissueNeoplasms, Glandular and EpithelialUrinary Bladder NeoplasmsDisease ProgressionCollagenCystadenocarcinoma, MucinousAntigens, CD82Epithelial CellsReceptors, Urokinase Plasminogen ActivatorUp-RegulationCarcinoma, Squamous CellSoft Tissue NeoplasmsHematologic NeoplasmsUterine NeoplasmsIntestinal NeoplasmsDog DiseasesNeoplasms, Adnexal and Skin AppendageMatrix MetalloproteinasesEpithelial-Mesenchymal TransitionMatrix Metalloproteinase InhibitorsVascular NeoplasmsSweat Gland NeoplasmsCell DivisionLymphomaPrognosisPalatal NeoplasmsDown-RegulationNeoplasms, Complex and MixedRNA InterferenceMandibular NeoplasmsCystadenocarcinomaSplenic NeoplasmsHeart NeoplasmsCystadenoma, SerousMammary Neoplasms, AnimalNeovascularization, PathologicNeoplasm Recurrence, Localbeta CateninBrain NeoplasmsRNA, NeoplasmMaxillary NeoplasmsPhenotypeMatrix Metalloproteinase 14Transplantation, HeterologousAnal Gland NeoplasmsCell LineLiver Neoplasms, ExperimentalNeoplasms, Germ Cell and EmbryonalBone Marrow NeoplasmsVirulenceVimentinAstrocytomaHepatocyte Growth FactorNeoplasms, Adipose TissueHead and Neck NeoplasmsS100 ProteinsMeningeal NeoplasmsDuodenal NeoplasmsMice, SCIDIntroduced SpeciesPituitary NeoplasmsPeritoneal NeoplasmsMutationAdrenal Cortex NeoplasmsGene Expression ProfilingRetrospective StudiesMediastinal NeoplasmsImmunoenzyme TechniquesTomography, X-Ray ComputedProto-Oncogene Proteins c-metTongue NeoplasmsIleal NeoplasmsTissue Inhibitor of Metalloproteinase-2Gene SilencingApoptosisExtracellular MatrixCarcinoma, HepatocellularCarcinoma, Acinar CellSpinal Cord NeoplasmsVaginal NeoplasmsGene Knockdown TechniquesAntineoplastic AgentsAdenoma, OxyphilicNervous System NeoplasmsNeoplasm GradingJanus Kinase 2Muscle NeoplasmsHemangiosarcomaPhosphorylationMatrix Metalloproteinase 7DogsMyelodysplastic-Myeloproliferative DiseasesMammary Neoplasms, ExperimentalPancreatectomyGelatinasesPeripheral Nervous System NeoplasmsTime FactorsCell Growth ProcessesCerebral Ventricle NeoplasmsTissue Inhibitor of Metalloproteinase-1Paranasal Sinus NeoplasmsPleural NeoplasmsTranscription FactorsMice, Inbred BALB CGene ExpressionSarcomaFibrosarcomaCommon Bile Duct NeoplasmsMatrix Metalloproteinases, Membrane-AssociatedMesodermLymphatic MetastasisJaw NeoplasmsFibroblastsEsophageal NeoplasmsOligonucleotide Array Sequence AnalysisOrbital NeoplasmsCarcinogensMetalloendopeptidasesAbdominal NeoplasmsTransforming Growth Factor betaReal-Time Polymerase Chain ReactionCerebellar NeoplasmsCells, CulturedCell Survival
PathologyCarcinomaColorectal NeoplasmsOvarian NeoplasmsColonic NeoplasmsStomach neoplasmsPapillary mucinousNeoplasticIntraductalPancreatic NeoplasmsRecurrenceProgressionCellsStagingParotid neoplasmsMalignant neoplasm2017TumorsIntracranialPrognosisSalivary gland neoplasmsLocal invasivenessProliferationAdenomaOverexpressionCysticSurvivalApoptosisRare neoplasmCommon neoplasmBenign neoplasmsTumor InvasivenessEpithelial neoplasm
Pathology3
  • We evaluated their molecular and cytogenetic alterations, identifying shared and unique abnormalities, providing evidence of a clonal relationship between these two groups of neoplasms, which traditionally represent different cellular origins.MethodsA search of the pathology database at a major referral center (Memorial Sloan-Kettering Cancer Center) was performed to identify patients diagnosed with GCT between 2012-2018, and had at least 1 prior or subsequent bone marrow biopsy. (medworm.com)
  • In pathology , grading is a measure of the progress of tumors and other neoplasms . (wikidoc.org)
  • Pathology grading systems are used to classify neoplasms in terms of how abnormal the cells appear microscopically and what may be the outcome in terms of rate of growth, invasiveness, and dissemination. (wikidoc.org)
Carcinoma6
Colorectal Neoplasms1
  • Recently, the ESD technique is applied to esophageal or colorectal neoplasms in some institutions, although it is still controversial considering the technical difficulty, associated risks, and favorable outcomes by EMR. (wikipedia.org)
Ovarian Neoplasms1
Colonic Neoplasms1
  • Colonic Neoplasms and 26 others ) and proposed to participate in processes (behavioral fear response, brain development, epithelial cell maturation involved in prostate gland development, learning or memory, negative regulation of androgen receptor signaling pathway and 13 others ). (nrresource.org)
Stomach neoplasms1
Papillary mucinous6
Neoplastic2
Intraductal3
Pancreatic Neoplasms1
  • The term refers to a group of pancreatic neoplasms originating-in papillary form-from the epithelium of the duct system and leading progressively to a dilatation of the duct, which progressively develops a cystic appearance. (hindawi.com)
Recurrence2
Progression1
  • Gliomas comprise a heterogeneous group of neoplasms that differ in location within the central nervous system, in age and sex distribution, in growth potential, in extent of invasiveness, in morphological features, in tendency for progression, and in response to treatments. (medscape.com)
Cells14
Staging1
  • An understanding of the approaches used for staging of musculoskeletal neoplasms requires knowledge of their biologic behavior and natural history. (healio.com)
Parotid neoplasms3
Malignant neoplasm2
20172
  • Rosário, Pedro 2017-11-10 00:00:00 World J Surg (2018) 42:2277-2278 DOI 10.1007/s00268-017-4351-6 LETTE R T O T HE EDI T OR Noninvasive Follicular Thyroid Neoplasm with Papillary-like Nuclear Features (NIFTP): Did We Trade Six for a Half a Dozen? (deepdyve.com)
  • Material y métodos: Se incluyen las resecciones oncológicas de recto en el período 2013-2017. (bvsalud.org)
Tumors8
  • Our results suggest that analysis of the methylation of DNA in mucosal wash fluid may be a good molecular marker for predicting the invasiveness of colorectal tumors. (aacrjournals.org)
  • Recently, narrow-band imaging magnification endoscopy has also been used to predict the invasiveness of colorectal tumors ( 11 ). (aacrjournals.org)
  • As yet, there is no study describing a molecular test for predicting the invasiveness of colorectal tumors. (aacrjournals.org)
  • reported 5% of lymph node ''when defined with strict histopathologic criteria, these metastases and 1% of distant metastases in 102 patients tumors are not expected to show molecular alterations V600E with ''noninvasive follicular thyroid neoplasm with papil- associated with classic PTC, such as BRAF muta- lary-like nuclear features'' (NIFTP). (deepdyve.com)
  • Although researchers have learned much from the study of this diverse group of tumors over the years, the diagnosis and treatment of salivary gland neoplasms remain complex and challenging problems for the head and neck surgeon. (medscape.com)
  • Salivary gland neoplasms make up 6% of all head and neck tumors. (medscape.com)
  • Benign neoplasms occur more frequently in women than in men, but malignant tumors are distributed equally between the sexes. (medscape.com)
  • Almost half of all submandibular gland neoplasms and most sublingual and minor salivary gland tumors are malignant. (medscape.com)
Intracranial1
Prognosis2
  • Our purpose was to ascertain whether the levels of transcript expression of any of 20 genes under study correlated with tumor grade and clinical stage (which even in the year 2000 remain the best overall predictors of prognosis in patients with these three neoplasms). (springer.com)
  • Its role in guiding the treatment of neoplasms, making diagnosis and predicting prognosis has been reported. (oncotarget.com)
Salivary gland neoplasms6
Local invasiveness1
Proliferation2
Adenoma1
Overexpression1
Cystic1
Survival1
  • ABSTRACT: In the treatment of musculoskeletal neoplasms, preservation of limb function and prolongation of survival have improved over the past decade. (healio.com)
Apoptosis1
  • Indeed, deletion of MxA was inversely associated with prostate cancer and MxA regulated cell cycle, invasiveness and docetaxel-induced apoptosis . (termedia.pl)
Rare neoplasm1
  • The Authors report 3 new cases, discussing diagnostic, clinical and therapeutical aspects of this rare neoplasm. (nih.gov)
Common neoplasm1
Benign neoplasms1
Tumor Invasiveness1
  • These contrasting endoscopic technologies not only improve the visualization of early foci missed by conventional endoscopy, but also gain the insight of histopathology and tumor invasiveness, that is so-called optical biopsy. (hindawi.com)
Epithelial neoplasm1
  • A benign epithelial neoplasm characterised by the formation of finger-like projections from the epithelial surface. (brainscape.com)

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