Diminished or failed response of an organism, disease or tissue to the intended effectiveness of a chemical or drug. It should be differentiated from DRUG TOLERANCE which is the progressive diminution of the susceptibility of a human or animal to the effects of a drug, as a result of continued administration.
Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures.
The ability of viruses to resist or to become tolerant to chemotherapeutic agents or antiviral agents. This resistance is acquired through gene mutation.
Simultaneous resistance to several structurally and functionally distinct drugs.
The ability of microorganisms, especially bacteria, to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
The ability of bacteria to resist or to become tolerant to chemotherapeutic agents, antimicrobial agents, or antibiotics. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
The ability of bacteria to resist or to become tolerant to several structurally and functionally distinct drugs simultaneously. This resistance may be acquired through gene mutation or foreign DNA in transmissible plasmids (R FACTORS).
The ability of fungi to resist or to become tolerant to chemotherapeutic agents, antifungal agents, or antibiotics. This resistance may be acquired through gene 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.
Any tests that demonstrate the relative efficacy of different chemotherapeutic agents against specific microorganisms (i.e., bacteria, fungi, viruses).
Substances that reduce the growth or reproduction of BACTERIA.
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.
The capacity of an organism to defend itself against pathological processes or the agents of those processes. This most often involves innate immunity whereby the organism responds to pathogens in a generic way. The term disease resistance is used most frequently when referring to plants.
The ability of viruses to resist or to become tolerant to several structurally and functionally distinct drugs simultaneously. This resistance phenotype may be attributed to multiple gene mutation.
A 170-kDa transmembrane glycoprotein from the superfamily of ATP-BINDING CASSETTE TRANSPORTERS. It serves as an ATP-dependent efflux pump for a variety of chemicals, including many ANTINEOPLASTIC AGENTS. Overexpression of this glycoprotein is associated with multidrug resistance (see DRUG RESISTANCE, MULTIPLE).
The force that opposes the flow of BLOOD through a vascular bed. It is equal to the difference in BLOOD PRESSURE across the vascular bed divided by the CARDIAC OUTPUT.
Drugs used in the treatment of tuberculosis. They are divided into two main classes: "first-line" agents, those with the greatest efficacy and acceptable degrees of toxicity used successfully in the great majority of cases; and "second-line" drugs used in drug-resistant cases or those in which some other patient-related condition has compromised the effectiveness of primary therapy.
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).
Tuberculosis resistant to chemotherapy with two or more ANTITUBERCULAR AGENTS, including at least ISONIAZID and RIFAMPICIN. The problem of resistance is particularly troublesome in tuberculous OPPORTUNISTIC INFECTIONS associated with HIV INFECTIONS. It requires the use of second line drugs which are more toxic than the first line regimens. TB with isolates that have developed further resistance to at least three of the six classes of second line drugs is defined as EXTENSIVELY DRUG-RESISTANT TUBERCULOSIS.
Substances that inhibit or prevent the proliferation of NEOPLASMS.
Agents used to treat AIDS and/or stop the spread of the HIV infection. These do not include drugs used to treat symptoms or opportunistic infections associated with AIDS.
The type species of LENTIVIRUS and the etiologic agent of AIDS. It is characterized by its cytopathic effect and affinity for the T4-lymphocyte.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Agents used in the treatment of malaria. They are usually classified on the basis of their action against plasmodia at different stages in their life cycle in the human. (From AMA, Drug Evaluations Annual, 1992, p1585)
Enzyme of the human immunodeficiency virus that is required for post-translational cleavage of gag and gag-pol precursor polyproteins into functional products needed for viral assembly. HIV protease is an aspartic protease encoded by the amino terminus of the pol gene.
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
A cell line derived from cultured tumor cells.
A sequence-related subfamily of ATP-BINDING CASSETTE TRANSPORTERS that actively transport organic substrates. Although considered organic anion transporters, a subset of proteins in this family have also been shown to convey drug resistance to neutral organic drugs. Their cellular function may have clinical significance for CHEMOTHERAPY in that they transport a variety of ANTINEOPLASTIC AGENTS. Overexpression of proteins in this class by NEOPLASMS is considered a possible mechanism in the development of multidrug resistance (DRUG RESISTANCE, MULTIPLE). Although similar in function to P-GLYCOPROTEINS, the proteins in this class share little sequence homology to the p-glycoprotein family of proteins.
Neoplasms containing cyst-like formations or producing mucin or serum.
Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).
A reverse transcriptase encoded by the POL GENE of HIV. It is a heterodimer of 66 kDa and 51 kDa subunits that are derived from a common precursor protein. The heterodimer also includes an RNAse H activity (RIBONUCLEASE H, HUMAN IMMUNODEFICIENCY VIRUS) that plays an essential role the viral replication process.
A species of gram-positive, aerobic bacteria that produces TUBERCULOSIS in humans, other primates, CATTLE; DOGS; and some other animals which have contact with humans. Growth tends to be in serpentine, cordlike masses in which the bacilli show a parallel orientation.
A class of plasmids that transfer antibiotic resistance from one bacterium to another by conjugation.
A family of MEMBRANE TRANSPORT PROTEINS that require ATP hydrolysis for the transport of substrates across membranes. The protein family derives its name from the ATP-binding domain found on the protein.
Genes for MEMBRANE TRANSPORT PROTEINS that confer resistance to toxic compounds. Several superfamilies of these multidrug export proteins are known and found in both prokaryotes and eukaryotes.
Nonsusceptibility of bacteria to the action of TETRACYCLINE which inhibits aminoacyl-tRNA binding to the 30S ribosomal subunit during protein synthesis.
Antineoplastic antibiotic obtained from Streptomyces peucetius. It is a hydroxy derivative of DAUNORUBICIN.
The ability of fungi to resist or to become tolerant to several structurally and functionally distinct drugs simultaneously. This resistance phenotype may be attributed to multiple gene mutations.
Nonsusceptibility of an organism to the action of penicillins.
An antibiotic produced by the soil actinomycete Streptomyces griseus. It acts by inhibiting the initiation and elongation processes during protein synthesis.
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.
A naphthacene antibiotic that inhibits AMINO ACYL TRNA binding during protein synthesis.
Tumors or cancer of the SKIN.
Inhibitors of reverse transcriptase (RNA-DIRECTED DNA POLYMERASE), an enzyme that synthesizes DNA on an RNA template.
Antibacterial agent used primarily as a tuberculostatic. It remains the treatment of choice for tuberculosis.
A multistage process that includes cloning, physical mapping, subcloning, determination of the DNA SEQUENCE, and information analysis.
The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Proteins found in any species of bacterium.
In vitro method for producing large amounts of specific DNA or RNA fragments of defined length and sequence from small amounts of short oligonucleotide flanking sequences (primers). The essential steps include thermal denaturation of the double-stranded target molecules, annealing of the primers to their complementary sequences, and extension of the annealed primers by enzymatic synthesis with DNA polymerase. The reaction is efficient, specific, and extremely sensitive. Uses for the reaction include disease diagnosis, detection of difficult-to-isolate pathogens, mutation analysis, genetic testing, DNA sequencing, and analyzing evolutionary relationships.
Diseases of plants.
The sequence of PURINES and PYRIMIDINES in nucleic acids and polynucleotides. It is also called nucleotide sequence.
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.
Tumors or cancer of the LUNG.
Tests that demonstrate the relative effectiveness of chemotherapeutic agents against specific parasites.
A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)
A species of protozoa that is the causal agent of falciparum malaria (MALARIA, FALCIPARUM). It is most prevalent in the tropics and subtropics.
Deoxyribonucleic acid that makes up the genetic material of bacteria.
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.
A species of gram-negative, facultatively anaerobic, rod-shaped bacteria (GRAM-NEGATIVE FACULTATIVELY ANAEROBIC RODS) commonly found in the lower part of the intestine of warm-blooded animals. It is usually nonpathogenic, but some strains are known to produce DIARRHEA and pyogenic infections. Pathogenic strains (virotypes) are classified by their specific pathogenic mechanisms such as toxins (ENTEROTOXIGENIC ESCHERICHIA COLI), etc.
Physiologically, the opposition to flow of air caused by the forces of friction. As a part of pulmonary function testing, it is the ratio of driving pressure to the rate of air flow.
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.
A mutation in which a codon is mutated to one directing the incorporation of a different amino acid. This substitution may result in an inactive or unstable product. (From A Dictionary of Genetics, King & Stansfield, 5th ed)
Tumors or cancers of the KIDNEY.
A parasexual process in BACTERIA; ALGAE; FUNGI; and ciliate EUKARYOTA for achieving exchange of chromosome material during fusion of two cells. In bacteria, this is a uni-directional transfer of genetic material; in protozoa it is a bi-directional exchange. In algae and fungi, it is a form of sexual reproduction, with the union of male and female gametes.
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.
One of the FOLIC ACID ANTAGONISTS that is used as an antimalarial or with a sulfonamide to treat toxoplasmosis.
Extrachromosomal, usually CIRCULAR DNA molecules that are self-replicating and transferable from one organism to another. They are found in a variety of bacterial, archaeal, fungal, algal, and plant species. They are used in GENETIC ENGINEERING as CLONING VECTORS.
DNA present in neoplastic tissue.
Elements of limited time intervals, contributing to particular results or situations.
Membrane proteins whose primary function is to facilitate the transport of molecules across a biological membrane. Included in this broad category are proteins involved in active transport (BIOLOGICAL TRANSPORT, ACTIVE), facilitated transport and ION CHANNELS.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control of gene action in neoplastic tissue.
Antibiotic complex produced by Streptomyces kanamyceticus from Japanese soil. Comprises 3 components: kanamycin A, the major component, and kanamycins B and C, the minor components.
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.
Nonsusceptibility of bacteria to the action of the beta-lactam antibiotics. Mechanisms responsible for beta-lactam resistance may be degradation of antibiotics by BETA-LACTAMASES, failure of antibiotics to penetrate, or low-affinity binding of antibiotics to targets.
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
Inhibitors of HIV PROTEASE, an enzyme required for production of proteins needed for viral assembly.
A measure of the quality of health care by assessment of unsuccessful results of management and procedures used in combating disease, in individual cases or series.
A type of strength-building exercise program that requires the body muscle to exert a force against some form of resistance, such as weight, stretch bands, water, or immovable objects. Resistance exercise is a combination of static and dynamic contractions involving shortening and lengthening of skeletal muscles.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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.
Nonsusceptibility of bacteria to the action of CHLORAMPHENICOL, a potent inhibitor of protein synthesis in the 50S ribosomal subunit where amino acids are added to nascent bacterial polypeptides.
Tumors or cancer of the human BREAST.
Tumors or cancer of the LIVER.
The concentration of a compound needed to reduce population growth of organisms, including eukaryotic cells, by 50% in vitro. Though often expressed to denote in vitro antibacterial activity, it is also used as a benchmark for cytotoxicity to eukaryotic cells in culture.
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.
Malaria caused by PLASMODIUM FALCIPARUM. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations.
Tumors or cancer of the THYROID GLAND.
The functional hereditary units of BACTERIA.
An adenocarcinoma producing mucin in significant amounts. (From Dorland, 27th ed)
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
A long acting sulfonamide that is used, usually in combination with other drugs, for respiratory, urinary tract, and malarial infections.
Methods of investigating the effectiveness of anticancer cytotoxic drugs and biologic inhibitors. These include in vitro cell-kill models and cytostatic dye exclusion tests as well as in vivo measurement of tumor growth parameters in laboratory animals.
Nonsusceptibility of a microbe to the action of ampicillin, a penicillin derivative that interferes with cell wall synthesis.
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.
Substances that destroy fungi by suppressing their ability to grow or reproduce. They differ from FUNGICIDES, INDUSTRIAL because they defend against fungi present in human or animal tissues.
Chemical substances, produced by microorganisms, inhibiting or preventing the proliferation of neoplasms.
An enzyme of the oxidoreductase class that catalyzes the reaction 7,8-dihyrofolate and NADPH to yield 5,6,7,8-tetrahydrofolate and NADPH+, producing reduced folate for amino acid metabolism, purine ring synthesis, and the formation of deoxythymidine monophosphate. Methotrexate and other folic acid antagonists used as chemotherapeutic drugs act by inhibiting this enzyme. (Dorland, 27th ed) EC
Proteins encoded by the POL GENE of the HUMAN IMMUNODEFICIENCY VIRUS.
Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly.
Experimentally induced new abnormal growth of TISSUES in animals to provide models for studying human neoplasms.
The capacity of a normal organism to remain unaffected by microorganisms and their toxins. It results from the presence of naturally occurring ANTI-INFECTIVE AGENTS, constitutional factors such as BODY TEMPERATURE and immediate acting immune cells such as NATURAL KILLER CELLS.
An inorganic and water-soluble platinum complex. After undergoing hydrolysis, it reacts with DNA to produce both intra and interstrand crosslinks. These crosslinks appear to impair replication and transcription of DNA. The cytotoxicity of cisplatin correlates with cellular arrest in the G2 phase of the cell cycle.
An antitubercular agent that inhibits the transfer of mycolic acids into the cell wall of the tubercle bacillus. It may also inhibit the synthesis of spermidine in mycobacteria. The action is usually bactericidal, and the drug can penetrate human cell membranes to exert its lethal effect. (From Smith and Reynard, Textbook of Pharmacology, 1992, p863)
The relationship between the dose of an administered drug and the response of the organism to the drug.
Tumors or cancer of the COLON.
Single preparations containing two or more active agents, for the purpose of their concurrent administration as a fixed dose mixture.
A bacteriostatic antibiotic macrolide produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.
A subfamily of transmembrane proteins from the superfamily of ATP-BINDING CASSETTE TRANSPORTERS that are closely related in sequence to P-GLYCOPROTEIN. When overexpressed, they function as ATP-dependent efflux pumps able to extrude lipophilic drugs, especially ANTINEOPLASTIC AGENTS, from cells causing multidrug resistance (DRUG RESISTANCE, MULTIPLE). Although P-Glycoproteins share functional similarities to MULTIDRUG RESISTANCE-ASSOCIATED PROTEINS they are two distinct subclasses of ATP-BINDING CASSETTE TRANSPORTERS, and have little sequence homology.
Five membered rings containing a NITROGEN atom.
Tumors or cancer of the PAROTID GLAND.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
An enzyme that catalyzes the formation of dihydropteroate from p-aminobenzoic acid and dihydropteridine-hydroxymethyl-pyrophosphate. EC
An antibiotic first isolated from cultures of Streptomyces venequelae in 1947 but now produced synthetically. It has a relatively simple structure and was the first broad-spectrum antibiotic to be discovered. It acts by interfering with bacterial protein synthesis and is mainly bacteriostatic. (From Martindale, The Extra Pharmacopoeia, 29th ed, p106)
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.
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)
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 associated with a proliferation of a single clone of PLASMA CELLS and characterized by the secretion of PARAPROTEINS.
Established cell cultures that have the potential to propagate indefinitely.
A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair.
The total number of cases of a given disease in a specified population at a designated time. It is differentiated from INCIDENCE, which refers to the number of new cases in the population at a given time.
Tumors or cancer of the APPENDIX.
Substances that prevent infectious agents or organisms from spreading or kill infectious agents in order to prevent the spread of infection.
The relationships of groups of organisms as reflected by their genetic makeup.
Proteins found in any species of protozoan.
Agents obtained from higher plants that have demonstrable cytostatic or antineoplastic activity.
A unicellular budding fungus which is the principal pathogenic species causing CANDIDIASIS (moniliasis).
Non-susceptibility of a microbe to the action of METHICILLIN, a semi-synthetic penicillin derivative.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
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.
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.
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.
A calcium channel blocker that is a class IV anti-arrhythmia agent.
Short sequences (generally about 10 base pairs) of DNA that are complementary to sequences of messenger RNA and allow reverse transcriptases to start copying the adjacent sequences of mRNA. Primers are used extensively in genetic and molecular biology techniques.
Carcinoma that arises from the PANCREATIC DUCTS. It accounts for the majority of cancers derived from the PANCREAS.
Tumors or cancer of the ENDOCRINE GLANDS.
Tumors or cancer of the GASTROINTESTINAL TRACT, from the MOUTH to the ANAL CANAL.
A general term for various neoplastic diseases of the lymphoid tissue.
All of the processes involved in increasing CELL NUMBER including CELL DIVISION.
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.
The action of a drug in promoting or enhancing the effectiveness of another drug.
A group of SESQUITERPENES and their analogs that contain a peroxide group (PEROXIDES) within an oxepin ring (OXEPINS).
Triazole antifungal agent that is used to treat oropharyngeal CANDIDIASIS and cryptococcal MENINGITIS in AIDS.
Large cytoplasmic ribonucleoprotein particles that have an eight-fold symmetry with a central pore and petal-like structure giving the appearance of an octagonal dome. (The Dictionary of Cell Biology, Lackie and Dow, 2nd ed.)
Therapy with two or more separate preparations given for a combined effect.
MYCOBACTERIUM infections of the lung.
Any of the infectious diseases of man and other animals caused by species of MYCOBACTERIUM.
Tumors or cancer located in bone tissue or specific BONES.
Enzymes found in many bacteria which catalyze the hydrolysis of the amide bond in the beta-lactam ring. Well known antibiotics destroyed by these enzymes are penicillins and cephalosporins.
Vertical transmission of hereditary characters by DNA from cytoplasmic organelles such as MITOCHONDRIA; CHLOROPLASTS; and PLASTIDS, or from PLASMIDS or viral episomal DNA.
Nonsusceptibility of bacteria to the action of VANCOMYCIN, an inhibitor of cell wall synthesis.
Agents that inhibit PROTEIN KINASES.
Tumors or cancer of the UTERUS.
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.
Potentially pathogenic bacteria found in nasal membranes, skin, hair follicles, and perineum of warm-blooded animals. They may cause a wide range of infections and intoxications.
Methods which attempt to express in replicable terms the extent of the neoplasm in the patient.
Tumors or cancer of the EYE.
A bacterial DNA topoisomerase II that catalyzes ATP-dependent breakage of both strands of DNA, passage of the unbroken strands through the breaks, and rejoining of the broken strands. Gyrase binds to DNA as a heterotetramer consisting of two A and two B subunits. In the presence of ATP, gyrase is able to convert the relaxed circular DNA duplex into a superhelix. In the absence of ATP, supercoiled DNA is relaxed by DNA gyrase.
Genotypic differences observed among individuals in a population.
A group of often glycosylated macrocyclic compounds formed by chain extension of multiple PROPIONATES cyclized into a large (typically 12, 14, or 16)-membered lactone. Macrolides belong to the POLYKETIDES class of natural products, and many members exhibit ANTIBIOTIC properties.
A family of 6-membered heterocyclic compounds occurring in nature in a wide variety of forms. They include several nucleic acid constituents (CYTOSINE; THYMINE; and URACIL) and form the basic structure of the barbiturates.
Neoplasms composed of vascular tissue. This concept does not refer to neoplasms located in blood vessels.
A 51-amino acid pancreatic hormone that plays a major role in the regulation of glucose metabolism, directly by suppressing endogenous glucose production (GLYCOGENOLYSIS; GLUCONEOGENESIS) and indirectly by suppressing GLUCAGON secretion and LIPOLYSIS. Native insulin is a globular protein comprised of a zinc-coordinated hexamer. Each insulin monomer containing two chains, A (21 residues) and B (30 residues), linked by two disulfide bonds. Insulin is used as a drug to control insulin-dependent diabetes mellitus (DIABETES MELLITUS, TYPE 1).
A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
The quantity of measurable virus in a body fluid. Change in viral load, measured in plasma, is sometimes used as a SURROGATE MARKER in disease progression.
Ability of neoplasms to infiltrate and actively destroy surrounding tissue.
Tumors or cancer of the NOSE.
Semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic.
Tumors, cancer or other neoplasms produced by exposure to ionizing or non-ionizing radiation.
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.
Highly proliferative, self-renewing, and colony-forming stem cells which give rise to NEOPLASMS.
A protozoan disease caused in humans by four species of the PLASMODIUM genus: PLASMODIUM FALCIPARUM; PLASMODIUM VIVAX; PLASMODIUM OVALE; and PLASMODIUM MALARIAE; and transmitted by the bite of an infected female mosquito of the genus ANOPHELES. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high FEVER; SWEATING; shaking CHILLS; and ANEMIA. Malaria in ANIMALS is caused by other species of plasmodia.
The insertion of recombinant DNA molecules from prokaryotic and/or eukaryotic sources into a replicating vehicle, such as a plasmid or virus vector, and the introduction of the resultant hybrid molecules into recipient cells without altering the viability of those cells.
Non-susceptibility of an organism to the action of the cephalosporins.
Drug regimens, for patients with HIV INFECTIONS, that aggressively suppress HIV replication. The regimens usually involve administration of three or more different drugs including a protease inhibitor.
A group of QUINOLONES with at least one fluorine atom and a piperazinyl group.
Tumors or cancer of the SALIVARY GLANDS.
Tumors or cancer of the TESTIS. Germ cell tumors (GERMINOMA) of the testis constitute 95% of all testicular neoplasms.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
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.
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)
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)
An antitumor alkaloid isolated from VINCA ROSEA. (Merck, 11th ed.)
Discrete segments of DNA which can excise and reintegrate to another site in the genome. Most are inactive, i.e., have not been found to exist outside the integrated state. DNA transposable elements include bacterial IS (insertion sequence) elements, Tn elements, the maize controlling elements Ac and Ds, Drosophila P, gypsy, and pogo elements, the human Tigger elements and the Tc and mariner elements which are found throughout the animal kingdom.
A potent, non-nucleoside reverse transcriptase inhibitor used in combination with nucleoside analogues for treatment of HIV INFECTIONS and AIDS.
A benign epithelial tumor with a glandular organization.
Tuberculosis resistant to ISONIAZID and RIFAMPIN and at least three of the six main classes of second-line drugs (AMINOGLYCOSIDES; polypeptide agents; FLUOROQUINOLONES; THIOAMIDES; CYCLOSERINE; and PARA-AMINOSALICYLIC ACID) as defined by the CDC.
Nonsusceptibility of bacteria to the antibiotic KANAMYCIN, which can bind to their 70S ribosomes and cause misreading of messenger RNA.
Diminished or failed response of PLANTS to HERBICIDES.
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
Neoplasms composed of muscle tissue: skeletal, cardiac, or smooth. The concept does not refer to neoplasms located in muscles.
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.
A selective increase in the number of copies of a gene coding for a specific protein without a proportional increase in other genes. It occurs naturally via the excision of a copy of the repeating sequence from the chromosome and its extrachromosomal replication in a plasmid, or via the production of an RNA transcript of the entire repeating sequence of ribosomal RNA followed by the reverse transcription of the molecule to produce an additional copy of the original DNA sequence. Laboratory techniques have been introduced for inducing disproportional replication by unequal crossing over, uptake of DNA from lysed cells, or generation of extrachromosomal sequences from rolling circle replication.
Substances that are destructive to protozoans.
Human immunodeficiency virus. A non-taxonomic and historical term referring to any of two species, specifically HIV-1 and/or HIV-2. Prior to 1986, this was called human T-lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV). From 1986-1990, it was an official species called HIV. Since 1991, HIV was no longer considered an official species name; the two species were designated HIV-1 and HIV-2.
A group of compounds that contain the structure SO2NH2.
Inhibitors of the enzyme, dihydrofolate reductase (TETRAHYDROFOLATE DEHYDROGENASE), which converts dihydrofolate (FH2) to tetrahydrofolate (FH4). They are frequently used in cancer chemotherapy. (From AMA, Drug Evaluations Annual, 1994, p2033)
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.

Interleukin-6 dependent induction of the cyclin dependent kinase inhibitor p21WAF1/CIP1 is lost during progression of human malignant melanoma. (1/9539)

Human melanoma cell lines derived from early stage primary tumors are particularly sensitive to growth arrest induced by interleukin-6 (IL-6). This response is lost in cell lines derived from advanced lesions, a phenomenon which may contribute to tumor aggressiveness. We sought to determine whether resistance to growth inhibition by IL-6 can be explained by oncogenic alterations in cell cycle regulators or relevant components of intracellular signaling. Our results show that IL-6 treatment of early stage melanoma cell lines caused G1 arrest, which could not be explained by changes in levels of G1 cyclins (D1, E), cdks (cdk4, cdk2) or by loss of cyclin/cdk complex formation. Instead, IL-6 caused a marked induction of the cdk inhibitor p21WAF1/CIP1 in three different IL-6 sensitive cell lines, two of which also showed a marked accumulation of the cdk inhibitor p27Kip1. In contrast, IL-6 failed to induce p21WAF1/CIP1 transcript and did not increase p21WAF1/CIP1 or p27kip1 proteins in any of the resistant lines. In fact, of five IL-6 resistant cell lines, only two expressed detectable levels of p21WAF1/CIP1 mRNA and protein, while in three other lines, p21WAF1/CIP1 was undetectable. IL-6 dependent upregulation of p21WAF1/CIP1 was associated with binding of both STAT3 and STAT1 to the p21WAF1/CIP1 promoter. Surprisingly, however, IL-6 stimulated STAT binding to this promoter in both sensitive and resistant cell lines (with one exception), suggesting that gross deregulation of this event is not the unifying cause of the defect in p21WAF1/CIP1 induction in IL-6 resistant cells. In somatic cell hybrids of IL-6 sensitive and resistant cell lines, the resistant phenotype was dominant and IL-6 failed to induce p21WAF1/CIP1. Thus, our results suggest that in early stage human melanoma cells, IL-6 induced growth inhibition involves induction of p21WAF1/CIP1 which is lost in the course of tumor progression presumably as a result of a dominant oncogenic event.  (+info)

Retinoic acid, but not arsenic trioxide, degrades the PLZF/RARalpha fusion protein, without inducing terminal differentiation or apoptosis, in a RA-therapy resistant t(11;17)(q23;q21) APL patient. (2/9539)

Primary blasts of a t(11;17)(q23;q21) acute promyelocytic leukaemia (APL) patient were analysed with respect to retinoic acid (RA) and arsenic trioxide (As2O3) sensitivity as well as PLZF/RARalpha status. Although RA induced partial monocytic differentiation ex vivo, but not in vivo, As203 failed to induce apoptosis in culture, contrasting with t(15;17) APL and arguing against the clinical use of As203 in t(11;17)(q23;q21) APL. Prior to cell culture, PLZF/RARalpha was found to exactly co-localize with PML onto PML nuclear bodies. However upon cell culture, it quickly shifted towards microspeckles, its localization found in transfection experiments. Arsenic trioxide, known to induce aggregation of PML nuclear bodies, left the microspeckled PLZF/RARalpha localization completely unaffected. RA treatment led to PLZF/RARalpha degradation. However, this complete PLZF/RARalpha degradation was not accompanied by differentiation or apoptosis, which could suggest a contribution of the reciprocal RARalpha/PLZF fusion product in leukaemogenesis or the existence of irreversible changes induced by the chimera.  (+info)

Overexpression of the multidrug resistance-associated protein (MRP1) in human heavy metal-selected tumor cells. (3/9539)

Cellular and molecular mechanisms involved in the resistance to cytotoxic heavy metals remain largely to be characterized in mammalian cells. To this end, we have analyzed a metal-resistant variant of the human lung cancer GLC4 cell line that we have selected by a step-wise procedure in potassium antimony tartrate. Antimony-selected cells, termed GLC4/Sb30 cells, poorly accumulated antimony through an enhanced cellular efflux of metal, thus suggesting up-regulation of a membrane export system in these cells. Indeed, GLC4/Sb30 cells were found to display a functional overexpression of the multidrug resistance-associated protein MRP1, a drug export pump, as demonstrated by Western blotting, reverse transcriptase-polymerase chain reaction and calcein accumulation assays. Moreover, MK571, a potent inhibitor of MRP1 activity, was found to markedly down-modulate resistance of GLC4/Sb30 cells to antimony and to decrease cellular export of the metal. Taken together, our data support the conclusion that overexpression of functional MRP1 likely represents one major mechanism by which human cells can escape the cytotoxic effects of heavy metals.  (+info)

Differential regulation of specific genes in MCF-7 and the ICI 182780-resistant cell line MCF-7/182R-6. (4/9539)

To elucidate the mechanisms involved in anti-oestrogen resistance, two human breast cancer cell lines MCF-7 and the ICI 182780-resistant cell line, MCF-7/182R-6, have been compared with regard to oestrogen receptor (ER) expression, ER function, ER regulation, growth requirements and differentially expressed gene products. MCF-7/182R-6 cells express a reduced level of ER protein. The ER protein is functional with respect to binding of oestradiol and the anti-oestrogens tamoxifen, 4-hydroxy-tamoxifen and ICI 182780, whereas expression and oestrogen induction of the progesterone receptor is lost in MCF-7/182R-6 cells. The ER protein and the ER mRNA are regulated similarly in the two cell lines when subjected to treatment with oestradiol or ICI 182780. Oestradiol down-regulates ER mRNA and ER protein expression. ICI 182780 has no initial effect on ER mRNA expression whereas the ER protein level decreases rapidly in cells treated with ICI 182780, indicating a severely decreased stability of the ER protein when bound to ICI 182780. In vitro growth experiments revealed that the ICI 182780-resistant cell line had evolved to an oestradiol-independent phenotype, able to grow with close to maximal growth rate both in the absence of oestradiol and in the presence of ICI 182780. Comparison of gene expression between the two cell lines revealed relatively few differences, indicating that a limited number of changes is involved in the development of anti-oestrogen resistance. Identification of the differentially expressed gene products are currently in progress.  (+info)

p53 status of newly established acute myeloid leukaemia cell lines. (5/9539)

We analysed the status of the p53 gene and protein in eight newly established acute myeloid leukaemia (AML) cell lines representing blast cells of either de novo leukaemia patients in first remission or patients with relapsed and chemotherapy-resistant disease causing their death. There were no mutations in the p53 gene in any of the cell lines as analysed by single-strand conformation polymorphism of amplified exons 5-8. However, the p53 protein was clearly and consistently expressed in all of these cell lines, as shown by immunohistochemistry, Western blotting and flow cytometry. The consistently expressed p53 protein was located in both the nucleus and the cytoplasm of all the cell lines and, as shown by flow cytometry, it was mostly in a conformation typical of the mutated protein. These AML cell lines offer a tool for studying the production and function of the p53 protein and its possible role in cell cycle regulation and chemoresistance as well as in the regulation of apoptosis in AML.  (+info)

Profound variation in dihydropyrimidine dehydrogenase activity in human blood cells: major implications for the detection of partly deficient patients. (6/9539)

Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5FU), thereby limiting the efficacy of the therapy. To identify patients suffering from a complete or partial DPD deficiency, the activity of DPD is usually determined in peripheral blood mononuclear cells (PBM cells). In this study, we demonstrated that the highest activity of DPD was found in monocytes followed by that of lymphocytes, granulocytes and platelets, whereas no significant activity of DPD could be detected in erythrocytes. The activity of DPD in PBM cells proved to be intermediate compared with the DPD activity observed in monocytes and lymphocytes. The mean percentage of monocytes in the PBM cells obtained from cancer patients proved to be significantly higher than that observed in PBM cells obtained from healthy volunteers. Moreover, a profound positive correlation was observed between the DPD activity of PBM cells and the percentage of monocytes, thus introducing a large inter- and intrapatient variability in the activity of DPD and hindering the detection of patients with a partial DPD deficiency.  (+info)

SDZ PSC 833, the cyclosporine A analogue and multidrug resistance modulator, activates ceramide synthesis and increases vinblastine sensitivity in drug-sensitive and drug-resistant cancer cells. (7/9539)

Resistance to chemotherapy is the major cause of cancer treatment failure. Insight into the mechanism of action of agents that modulate multidrug resistance (MDR) is instrumental for the design of more effective treatment modalities. Here we show, using KB-V-1 MDR human epidermoid carcinoma cells and [3H]palmitic acid as metabolic tracer, that the MDR modulator SDZ PSC 833 (PSC 833) activates ceramide synthesis. In a short time course experiment, ceramide was generated as early as 15 min (40% increase) after the addition of PSC 833 (5.0 microM), and by 3 h, [3H]ceramide was >3-fold that of control cells. A 24-h dose-response experiment showed that at 1.0 and 10 microM PSC 833, ceramide levels were 2.5- and 13.6-fold higher, respectively, than in untreated cells. Concomitant with the increase in cellular ceramide was a progressive decrease in cell survival, suggesting that ceramide elicited a cytotoxic response. Analysis of DNA in cells treated with PSC 833 showed oligonucleosomal DNA fragmentation, characteristic of apoptosis. The inclusion of fumonisin B1, a ceramide synthase inhibitor, blocked PSC 833-induced ceramide generation. Assessment of ceramide mass by TLC lipid charring confirmed that PSC 833 markedly enhanced ceramide synthesis, not only in KB-V-1 cells but also in wild-type KB-3-1 cells. The capacity of PSC 833 to reverse drug resistance was demonstrated with vinblastine. Whereas each agent at a concentration of 1.0 microM reduced cell survival by approximately 20%, when PSC 833 and vinblastine were coadministered, cell viability fell to zero. In parallel experiments measuring ceramide metabolism, it was shown that the PSC 833/vinblastine combination synergistically increased cellular ceramide levels. Vinblastine toxicity, also intensified by PSC 833 in wild-type KB-3-1 cells, was as well accompanied by enhanced ceramide formation. These data demonstrate that PSC 833 has mechanisms of action in addition to P-glycoprotein chemotherapy efflux pumping.  (+info)

Modulation of the cytotoxicity of 3'-azido-3'-deoxythymidine and methotrexate after transduction of folate receptor cDNA into human cervical carcinoma: identification of a correlation between folate receptor expression and thymidine kinase activity. (8/9539)

Cervical carcinoma is an AIDS-defining illness. The expression of folate receptors (FRs) in cervical carcinoma (HeLa-IU1) cells was modulated by stable transduction of FR cDNA encapsidated in recombinant adeno-associated virus-2 in the sense and antisense orientation (sense and antisense cells, respectively). Although sense cells proliferated slower than antisense or untransduced cells in vivo and in vitro in 2% (but not 10%) FCS, [methyl-3H]thymidine incorporation into DNA was significantly increased in sense cells in 10% serum; therefore, the basis for this discrepancy was investigated. The activity of thymidine kinase (TK) was subsequently directly correlated with the extent of FR expression in single cell-derived clones of transduced cells. This elevated TK activity was not a result of recruitment of the salvage pathway based on the presence of adequate dTTP pools, normal thymidylate synthase (TS) activity, persistence of increased thymidine incorporation despite the exogenous provision of excess 5,10-methylene-tetrahydrofolate, and documentation of adequate folates in sense cells. The increase in TK activity conferred significant biological properties to sense cells (but not antisense or untransduced cells) as demonstrated by augmented phosphorylation of 3'-azido-3'-deoxythymidine (AZT) and concomitantly greater sensitivity to the cytotoxic effects of AZT. Conversely, sense cells were highly resistant to methotrexate, but this was reversed by the addition of AZT. The direct correlation of FR expression and TK activity indicates a previously unrecognized consequence of FR overexpression.  (+info)

Role of the Drug Transporter ABCC3 in Breast Cancer Chemoresistance. . 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.
Supplementary test information for BCR-ABL1 Mutation Analysis for Tyrosine Kinase Inhibitor Resistance such as test interpretation, additional tests to consider, and other technical data.
Despite the tremendous efforts for improving therapeutics of lung cancer patients, its prognosis remains disappointing. This can be largely attributed to the lack of comprehensive understanding of drug resistance leading to insufficient development of effective therapeutics in clinic. Based on the current progresses of lung cancer research, we classify drug resistance mechanisms into three different levels: molecular, cellular and pathological level. All these three levels have significantly contributed to the acquisition and evolution of drug resistance in clinic. Our understanding on drug resistance mechanisms has begun to change the way of clinical practice and improve patient prognosis. In this review, we focus on discussing the pathological changes linking to drug resistance as this has been largely overlooked in the past decades.
How to deal with cancer drug resistance - posted in Research Idea, Design and Collaboration: Anybody has a good idea on how to solve cancer drug resistance issues. Many new drugs are designed to block one or more signal transduction pathways in order to block cancer cell proliferation. But cancer cell can bypass the blocked pathway and survives later in the treatment cycles. Combination or coktail of multiple drugs can have serious side-effects. What other general ideas can provide better...
Cancer Drug Resistance is an open access journal, focusing on pharmacological aspects of drug resistance and its reversal, molecular mechanisms of drug resistance and drug classes, etc. Both clinical and experimental aspects of drug resistance in cancer are included.
Free Online Library: Research and Markets: This Essential Report on Cancer Drug Resistance is Available Now. by Business Wire; Business, international Antimitotic agents Market research Reports Antineoplastic agents Care and treatment Drug therapy Cancer research Cancer treatment Drug resistance in microorganisms Microbial drug resistance Oncology, Experimental Pharmaceutical industry
TY - JOUR. T1 - Induction of apoptosis and suppression of tumor growth by Nur77-derived Bcl-2 converting peptide in chemoresistant lung cancer cells. AU - Pearce, Martin C.. AU - Gamble, John T.. AU - Kopparapu, Prasad R.. AU - ODonnell, Edmond F.. AU - Mueller, Monica J.. AU - Jang, Hyo Sang. AU - Greenwood, Julie A.. AU - Satterthwait, Arnold C.. AU - Tanguay, Robert L.. AU - Zhang, Xiao Kun. AU - Kolluri, Siva Kumar. PY - 2018. Y1 - 2018. N2 - Resistance to chemotherapy is a major cause of treatment failure and poor overall survival in patients with lung cancer. Identification of molecular targets present in resistant cancer cells is essential for addressing therapeutic resistance and prolonging lung cancer patient survival. Members of the B-cell lymphoma 2 (Bcl-2) family of proteins are associated with chemotherapeutic resistance. In this study, we found that pro-survival protein Bcl-2 is upregulated in paclitaxel resistant cells, potentially contributing to chemotherapy resistance. To ...
Drug resistance remains a great challenge in the treatment of gastric cancer. The goal of this study was to explore the anti-tumor effects and mechanism of cytokine-induced killer (CIK) cell combined with oxaliplatin (L-OHP) in human oxaliplatin-resistant gastric cancer cells. After producing oxaliplatin-resistant gastric cancer cells, cell morphology, growth and doubling time were observed, followed by detection of cell cycle distribution and apoptosis, drug sensitivity (e.g., L-OHP) and expression of P-gp and livin. MTT assay, in vivo pharmacodynamics and pathomorphology experiments were used to detect killing activities of CIK combined with L-OHP. Compared with parental gastric cancer cells, oxaliplatin-resistant gastric cancer cells in S phase were reduced and cell apoptosis rate was increased (P < 0.05), the inhibition rate of 10 chemotherapeutics on oxaliplatin-resistant gastric cancer cells was significantly lower and the expression of P-gp was significantly higher (P < 0.05). However, there was
The dose-limiting toxicity of chemotherapeutics, heterogeneity and drug resistance of cancer cells, and difficulties of targeted delivery to tumors all pose daunting challenges to effective cancer therapy. We report that small interfering RNA (siRNA) duplexes readily penetrate intact bacterially derived minicells previously shown to cause tumor stabilization and regression when packaged with chemotherapeutics. When targeted via antibodies to tumor-cell-surface receptors, minicells can specifically and sequentially deliver to tumor xenografts first siRNAs or short hairpin RNA (shRNA)-encoding plasmids to compromise drug resistance by knocking down a multidrug resistance protein. Subsequent administration of targeted minicells containing cytotoxic drugs eliminate formerly drug-resistant tumors. The two waves of treatment, involving minicells loaded with both types of payload, enable complete survival without toxicity in mice with tumor xenografts, while involving several thousandfold less drug, ...
Drug resistance is a major obstacle in curing ovarian cancer but new research from the Centenary Institute has discovered a treatment that kills ovarian cancer cells in a new way that
The molecular mechanism by which cancer-associated fibroblasts (CAFs) confer chemoresistance in ovarian cancer is poorly understood. The purpose of the present study was to evaluate the roles of CAFs in modulating tumor vasculature, chemoresistance, and disease progression. Here, we found that CAFs upregulated the lipoma-preferred partner (LPP) gene in microvascular endothelial cells (MECs) and that LPP expression levels in intratumoral MECs correlated with survival and chemoresistance in patients with ovarian cancer. Mechanistically, LPP increased focal adhesion and stress fiber formation to promote endothelial cell motility and permeability. siRNA-mediated LPP silencing in ovarian tumor-bearing mice improved paclitaxel delivery to cancer cells by decreasing intratumoral microvessel leakiness. Further studies showed that CAFs regulate endothelial LPP via a calcium-dependent signaling pathway involving microfibrillar-associated protein 5 (MFAP5), focal adhesion kinase (FAK), ERK, and LPP. Thus, ...
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Read up on the latest developments in several important areas of cancer research emerging from the 2019 American Association for Cancer Research annual meeting.
Drug resistance may emerge de novo when beneficial peptides are expressed by bacteria using completely random, noncoding DNA sequences
Hello: We have a drug resistant cell (murine) line that routinely is grown in presence of the drug. When these cell were grown in absence of the drug the phenotype changed to sensible after 90 passages (we compare levels of accumulation of drug in WT and resistant cell, the resistant accumulate less). Can we conclude that there may be single mutation event involved in the generation of resistance and that after 90 passages in absence of selection pressure reverted? Or is it just matter of regulation of expression of genes under that stress? And that in absence of drug everything goes back to normal levels? Is 90 passages too long to restore normal levels of expressions and actually it is a mutation? How to calculate the mutation frequency and number of passages necessary for the expression of a mutation? Thanks for your help! Nancy ...
Bacteria in tumors make cancer resistant to chemotherapy. Wait, what? That’s right. According to Ravid Straussman at the Weizmann Institute, Gammapro
{loadposition article-preamble} Hi Everyone, Lauren Miller had spectacular success using EFT for her stage 3 cancer. She shares her story (and EFT methods) in this article. Please note that while only one successful EFT session launched this remarkab...
The findings presented here support a model linking Pgrmc1 to cancer progression. Pgrmc1 is overexpressed in breast tumors (Crudden et al., 2005), is induced by chemotherapy (Mallory et al., 2005b), and promotes chemotherapy resistance in breast cancer cells (Crudden et al., 2006). In separate papers, Peluso et al. subsequently showed that Pgrmc1 is overexpressed in ovarian cancer, where it contributes to chemotherapy resistance (Peluso et al., 2008a) and suppresses apoptosis (Peluso et al., 2008b). However, many tumors express Pgrmc1 before chemotherapy, suggesting a function for Pgrmc1 other than drug resistance. Indeed, Pgrmc1 is induced by carcinogens in vivo, suggesting a role in the early stages of tumorigenesis (Selmin et al., 1996). In the present study, we present evidence that Pgrmc1 promotes tumor growth in vivo. We inhibited Pgrmc1 expression by using a sequence-specific shRNA that had been previously characterized in human kidney cells (Hughes et al., 2007) and used two separate in ...
Researchers now able to use a 3D computer model to helps screen millions of chemo drugs, giving researchers a view of the structure of a protein believed played a crucial role in chemotherapy failure.
In cancer chemotherapy, multidrug resistance (MDR) is a major clinical problem which occurs by an influential mechanism and which leads to the failure of cancer chemotherapy and/or a relapse of the cancer. In this study ...
A protein that enables cancer cells to grow, invade tissues and eventually resist chemotherapy and has lethal consequences for patients was found by researchers.
Active drug efflux by the adenosine triphosphate-binding cassette (ABC) transporter ABCG2 is one of the common mechanisms causing multiple drug resistance in various human cancers. In the intrinsic drug resistance of hepatocellular carcinoma (HCC), the role of ABCG2 is closely associated with side population (SP), a minor subset of cancer stem-like cells with unique capacity to extrude lipophilic dye Hoechst 33342 and many chemotherapeutic agents. In this study, we showed that ABCG2 was intrinsically expressed in a subgroup of HCC tissues and its expression pattern significantly influenced the levels of drug efflux from HCC cell lines. In MHCC-97L HCC cell line with intrinsic ABCG2 expression, we confirmed the importance of SP cells to the drug efflux-related chemotherapy resistance and found that the SP analysis provided an efficient method to evaluate the functional activity of ABCG2 transporter. In this cell line, we discovered that the SP proportion was modulated by the treatments of Akt ...
Cisplatin-based chemotherapy is recommended as the primary treatment for advanced bladder cancer (BC) with unresectable or metastatic disease. However, the benefits are limited due to the acquisition of drug resistance. The mechanisms of resistance remain unclear. Although there are some reports that some molecules are associated with cisplatin resistance in advanced BC, those reports have not been fully investigated. Therefore, we undertook a new search for cisplatin resistance-related genes targeted by tumor suppressive microRNAs as well as genes that were downregulated in cisplatin-resistant BC cells and clinical BC tissues. First, we established cisplatin-resistant BOY and T24 BC cell lines (CDDP-R-BOY, CDDP-R-T24). Then, Next Generation Sequence analysis was performed with parental and cisplatin-resistant cell lines to search for the microRNAs responsible for cisplatin resistance. We conducted gain-of-function analysis of microRNAs and their effects on cisplatin resistance, and we searched target
Therapy resistance can arise within tumor cells because of genetic or phenotypic changes (intrinsic resistance), or it can be the result of an interaction with the tumor microenvironment (extrinsic resistance). Exosomes are membranous vesicles 40 to 100 nm in diameter constitutively released by almost all cell types, and mediate cell-to-cell communication by transferring mRNAs, miRNAs, DNAs and proteins causing extrinsic therapy resistance. They transfer therapy resistance by anti-apoptotic signalling, increased DNA-repair or delivering ABC transporters to drug sensitive cells. As functional mediators of tumor-stroma interaction and of epithelial to mesenchymal transition, exosomes also promote environment-mediated therapy resistance. Exosomes may be used in anticancer therapy exploiting their delivery function. They may effectively transfer anticancer drugs or RNAs in the context of gene therapy reducing immune stimulatory effects of these drugs and hydrophilic qualities facilitating crossing of cell
The estrogen receptor (ER) is expressed in approximately 70% of the breast carcinomas. In general, for these patients anti-hormonal therapy is the therapy of first choice. Despite good responses in 50-60% of the patients, unfortunately all patients develop (acquired) resistance. Patients with acquired anti-hormonal resistance can be subdivided into three different groups: (1) patients that have lost ER-expression (~25%), (2) patients with preserved ER-expression (~55%) and (3) patients with enhanced ER-expression (~30%). Several studies suggest different treatment strategies for these three different ER-phenotypes in antihormonal resistant breast cancer. In patients with acquired anti-hormonal resistance, ~30% of the patients still respond to hormone-additive therapy with estrogens. In vitro studies have shown estrogen-induced apoptosis in long-treated estrogen deprived cells (simulating aromatase inhibitor resistance). It is suggested that this estrogen-hypersensitivity is accompanied by ...
TY - JOUR. T1 - Overcoming cancer cell resistance to Smac mimetic induced apoptosis by modulating cIAP-2 expression. AU - Petersen, Sean L.. AU - Peyton, Michael. AU - Minna, John D.. AU - Wang, Xiaodong. PY - 2010/6/29. Y1 - 2010/6/29. N2 - Smac mimetics target cancer cells in a TNFα-dependent manner, partly via proteasome degradation of cellular inhibitor of apoptosis 1 (cIAP1) and cIAP2. Degradation of cIAPs triggers the release of receptor interacting protein kinase (RIPK1) from TNF receptor I (TNFR1) to form a caspase-8 activating complex together with the adaptor protein Fas-associated death domain (FADD). We report here a means through which cancer cells mediate resistance to Smac mimetic/TNFα-induced apoptosis and corresponding strategies to overcome such resistance. These human cancer cell lines evades Smac mimetic-induced apoptosis by up-regulation of cIAP2, which although initially degraded, rebounds and is refractory to subsequent degradation. cIAP2 is induced by TNFα via NF-κB ...
For decades, natural products represent a significant source of diverse and unique bioactive lead compounds in drug discovery field. In Clinical oncology, complete tumors remission is hampered by the development of drug-resistance. Therefore, development of cytotoxic agents that may overcome drug resistance is urgently needed. Here, the natural benzophenanthridine alkaloid sanguinarine has been studied for its cytotoxic activity against multidrug resistance (MDR) cancer cells. We investigated the role of the ATP-binding cassette (ABC) transporters BCRP/ABCG2, P-glycoprotein/ABCB1 and its close relative ABCB5 in drug resistance. Further drug resistance mechanisms analyzed in this study were the tumor suppressor TP53 and the epidermal growth factor receptor (EGFR). Multidrug resistant cells overexpressing BCRP, ABCB5 and mutated ∆EGFR were not cross-resistant towards sanguinarine. Interestingly, P-gp overexpressing cells were hypersensitive to sanguinarine. Doxorubicin uptake assay carried by flow
Defining the molecular transcriptomic profile for predicting the clinical outcome of anthracycline resistant breast cancers. Defining metastases in relation with the primary tumor. BREAST-OMICS
TY - JOUR. T1 - Molecular determinants of sensitivity or resistance of cancer cells toward sanguinarine. AU - Saeed, Mohamed E.M.. AU - Mahmoud, Nuha. AU - Sugimoto, Yoshikazu. AU - Efferth, Thomas. AU - Abdel-Aziz, Heba. PY - 2018/2/26. Y1 - 2018/2/26. N2 - For decades, natural products represented a significant source of diverse and unique bioactive lead compounds in drug discovery field. In Clinical oncology, complete tumors remission is hampered by the development of drug-resistance. Therefore, development of cytotoxic agents that may overcome drug resistance is urgently needed. Here, the natural benzophenanthridine alkaloid sanguinarine has been studied for its cytotoxic activity against multidrug resistance (MDR) cancer cells. We investigated the role of the ATP-binding cassette (ABC) transporters BCRP/ABCG2, P-glycoprotein/ABCB1 and its close relative ABCB5 in drug resistance. Further drug resistance mechanisms analyzed in this study were the tumor suppressor TP53 and the epidermal growth ...
Two recent in vitro studies conducted in the U.S. and Europe raise a provocative question: Can FDA-approved human immunodeficiency virus (HIV) drugs be used to treat chemoresistant ovarian cancer? Both studies were based upon the fact that HIV patients taking antiretroviral inhibitors have a lower incidence of infection-associated malignancies. Based upon that fact, the researchers…
Pancreatic ductal adenocarcinoma (PDAC) has a five-year survival rate of only 9%. Acquired drug resistance is a major factor that limits the effectiveness of chemotherapy. Exosomes, secreted
Italian and German scientists have designed peptides to target the protein-protein interface of a key enzyme in DNA synthesis crucial for cancer growth. The peptides act by a novel inhibitory mechanism and curb cancer cell growth in drug resistant ovarian cancer cells. The interdisciplinary research project was led by the University of Modena and Reggio Emilia (UNIMORE) and the Heidelberg Institute for Theoretical Studies (HITS).
TY - JOUR. T1 - Gene expression profile associated with docetaxel resistance in breast cancer cells. AU - Brown, Iain. AU - Heys, Steven Darryll. AU - Schofield, Andrew Craig. PY - 2007/9. Y1 - 2007/9. U2 - 10.1016/S1359-6349(07)71737-8. DO - 10.1016/S1359-6349(07)71737-8. M3 - Abstract. VL - 5. SP - 15. EP - 15. JO - European Journal of Cancer. Supplement. JF - European Journal of Cancer. Supplement. SN - 1359-6349. IS - 3. ER - ...
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This cisplatin-resistant cell line has been developed by chronic exposure of the parent cisplatin-sensitive A2780 cell line (ECACC No. 93112519) to increasing concentrations of cisplatin. A2780cis is cross-resistant to melphalan, adriamycin and irradiation. An increased ability to repair DNA damage as well as cytogenetic abnormalities has been observed. In order to retain resistance cisplatinum has to be added to the media every 2-3 passages. In addition to this matched pair of drug-sensitive/resistant cell lines an adriamycin-resistant cell line, A2780adr (ECACC No. 93112520), has been isolated from the same parental line A2780 ...
Osimertinib binds tightly to a protein, epidermal growth factor receptor (EGFR), which is overexpressed in many tumours.. EGFR is involved in a pathway that signals for cell proliferation, and so is a target for drugs. Blocking the action of EGFR (inhibiting it) can switch it off, and so is a good way to treat the disease.. Osimertinib is an effective anticancer drug that works in this way. It is used to treat non-small-cell lung cancer (NSCLC), in cases where the cancer cells have a particular (T790M) mutant form of EGFR.. It is a so-called third-generation EGFR inhibitor, which was approved as a cancer treatment in 2017. Osimertinib is a covalent inhibitor: as such, it binds irreversibly to EGFR by forming a chemical bond with it.. Although patients generally respond well to osimertinib, most acquire drug resistance within one year of treatment, so the drug stops working.. Drug resistance arises because the EGFR protein mutates, so that the drug binds less tightly.. One such mutation, called ...
Chemoresistant tumor cells pose a threat to the efficacy of treatment and severely worsen the prognosis for the treated animal due to relapse. Understanding the mechanism of resistance is the first step leading to circumvention of the resistance and development of more efficient therapies. The chemotherapeutic doxorubicin was used to ... read more treat canine MelT4 melanoma, and POS and HMPOS osteosarcoma cells. The survival of cells was determined by cell count as well as MTT essay, and the mRNA of surviving cells isolated. PCR and electrophoresis were used to visualize the presence of mRNA coding for drug efflux pumps MDR, ABCB5 and ABCG2 as well as transcription factors NANOG, Oct-4 and SOX-2. The presence of cell surface marker CD-133 was also determined. Western Blots were performed for ABCB5 and ABCG2 to determine eventual translation of the results on an mRNA level to a protein level. A non-treated cell population equal to the surviving population was used as reference in all ...
Cancer Drug Resistance is an open access journal, focusing on pharmacological aspects of drug resistance and its reversal, molecular mechanisms of drug resistance and drug classes, etc. Both clinical and experimental aspects of drug resistance in cancer are included.
Model of tumor cell resistance to antineoplastic therapy through angiopoietin-like protein 2 (ANGPTL2) expression. Tumor cell-secreted ANGPTL2 induces spleen ty
The Ras/MEK/ERK and PI3K/Akt/mTor pathways play a central role in the regulation of normal cell growth, division and differentiation. Dysregulation of these signaling pathways driven by oncogenic mutations/activation leading to elevated kinase activity has been demonstrated in many human cancers. Strong evidence suggests the existence of a feedback loop with crosstalk between these two signaling cascades leading to redundancy in survival pathways. Consequently, monotherapy targeting a single cascade may be insufficient to induce tumor cell death due to drug resistance mechanisms. Initial biological results are presented from a series of novel small molecule kinase inhibitors specifically designed to simultaneously target both MEK1 and PI3K. Structural analogs of the ATP-competitive PI3K inhibitor ZSTK474 and the ATP-noncompetitive class of MEK inhibitors PD0325901, respectively, were covalently combined to provide single compound dual inhibitors. Inhibitors showed potent MEK1 inhibition (0.015 , ...
Health, ...German researchers have identified an unexpected molecular marker that...Triple-negative breast cancers --which do not express the genes for es...At the IMPAKT Breast Cancer Conference in Brussels PhD student Caroli...The researchers undertook their study in three steps. First they condu...,Gene,expression,predicts,chemotherapy,sensitivity,,of,triple-negative,breast,cancer,medicine,medical news today,latest medical news,medical newsletters,current medical news,latest medicine news
Background: Among several chemotherapeutic agents, 5-Fluorouracil (5-FU) has been widely used as a key drug in adjuvant chemotherapy for gastric cancer. However, no reliable marker, which predicts the response to 5-FU in an adjuvant setting, has been identified. Hypoxia-induced drug resistance, via up-regulation of hypoxia-inducible factor (HIF) -1α, is a major obstacle in the development of effective cancer therapy. Despite the numerous investigations, few clinical studies have so far assessed the relationship between the HIF-1α expression and the chemo-resistance of gastric cancer patients in an adjuvant setting.. Objective: To determine whether the expression of HIF-1α predicts the relapse of gastric cancer patients who underwent curative surgery followed by adjuvant 5-FU chemotherapy.. Materials and Methods: Two HIF-1α knockdown gastric cancer cell lines were established in order to clarify the role of HIF-1α in chemo-resistance against 5-FU. The sensitivity to 5-FU was evaluated by MTT ...
The development of targeted therapies has provided new options for the personalized management of patients with advanced solid tumors. mAbs directed against the EGFR, such as cetuximab and panitumumab, have emerged as important therapeutic agents in the treatment of metastatic colorectal cancer patients. However, their use is substantially limited by intrinsic and acquired cancer cell resistance. Several hypotheses have been developed to explain why resistant cancer cell arises and how it is possible to overcome it. One possibility is cancer intrinsic genetic heterogeneity, which could be more prominent in the metastatic setting (28, 29). Heterogeneous genetic alterations in genes involved in the EGFR pathways have been hypothesized to play a role in resistance to anti-EGFR drugs in colorectal cancer, including activating mutations in KRAS, NRAS, B-RAF, and PIK3CA, and loss of expression of PTEN (13). The overall scenario is complicated by presence of additional genetic mechanisms able to ...
TY - JOUR. T1 - Molecular determinants of chemotherapy resistance in ovarian cancer. AU - Cooley, Megan. AU - Fang, Pingping. AU - Fang, Fang. AU - Nephew, Kenneth. AU - Chien, Jeremy. PY - 2015/11/1. Y1 - 2015/11/1. KW - cancer genomics. KW - chemotherapy. KW - functional genomics. KW - heterogeneity. KW - intra-tumor. KW - ovarian cancer. KW - resistance. UR - http://www.scopus.com/inward/record.url?scp=84947967812&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=84947967812&partnerID=8YFLogxK. U2 - 10.2217/pgs.15.130. DO - 10.2217/pgs.15.130. M3 - Article. C2 - 26554863. AN - SCOPUS:84947967812. VL - 16. SP - 1763. EP - 1767. JO - Pharmacogenomics. JF - Pharmacogenomics. SN - 1462-2416. IS - 16. ER - ...
New research using mathematical models of different types of cancer-including melanoma, pancreatic, and colorectal-to determine the evolutionary dynamics of lesions in response to treatment is revealing why and how cancer cells resist targeted therapies. The study by Ivana Bozic, PhD, from the Department of Mathematics at Harvard University, and colleagues was published online in eLife.. Study Details. The investigators, a team of mathematicians and oncologists from a variety of academic centers, designed a mathematical model to predict the effects of combination targeted therapies on tumors based on data obtained from 20 melanoma patients receiving vemurafenib (Zelboraf). They then applied their model to an independent set of pancreatic, colorectal, and melanoma cancer patients with metastatic disease. Their findings showed that when dual therapy is used, most patients experience longer-term disease control as long as there were no single cell mutations that caused cross-resistance to both ...
It is in this setting that emerging molecular analyses of blood specimens, so-called liquid biopsies, are poised to revolutionize cancer screening (5). Circulating cell-free DNA (cfDNA) in the blood consists of small fragments of DNA that are approximately 150 nucleotides in length. cfDNA is primarily derived from normal tissues, but a small fraction may be derived from tumor cells in individuals who have cancer. This circulating tumor DNA (ctDNA) may be identified by the presence of characteristic mutations in cancer genes or by variations in chromosome copy numbers (6). Recent studies have established the reliability of ctDNA genotyping for monitoring treatment response and identifying drug resistance mechanisms in patients with advanced cancer (7, 8). However, the much lower amount of ctDNA in the plasma of patients who have a localized tumor poses a challenge for early cancer screening, as does the absence of knowledge about which mutation to look for. Furthermore, some background ...
Background] Most NSCLC patients harboring activating EGFR mutations benefit from treatment with EGFR-TKIs, but the final clinical efficacy of EGFR-TKIs varies because of development of tumor resistant to EGFR-TKIs. Multiple kinase-targeted 2nd generation TKIs such as afatinib have been developed to overcome drug resistance to the 1st generation TKIs. Afatinib is an irreversible multitargeted TKI targeting EGFR including T790M, HER2 and HER4. To develop further personalized therapeutics and drug resistance modifiers, we should understand the molecular based mechanism of drug resistance to 2nd as well as 3rd generation TKIs. In our present study, we present a novel finding that acquisition of cancer stem-like cells properties accompanying with activation of residual Src family kinase (SFK)/focal adhesion kinase (FAK) is responsible for the survival of afatinib-resistant lung cancer cells when expression of targeted EGFR, HER2 and HER4 is abraded.. [Materials and methods] We have established ...
Keywords: daunorubicin cytarabine Bcl2 p27Kip1 cell adhesion-mediated medication resistance Launch Hematological malignancy of severe myeloid leukemia (AML) type is normally extremely heterogeneous with a higher incidence of relapse averaging 30%-50% in under 5 years because of drug resistance despite the fact that 70%-80% patients go through remission pursuing induction chemotherapy.1-3 Inability to apparent the complete population of AML cells subsequent drug treatment continues to be related to the microenvironmental cell adhesion-mediated drug-resistance (CAMDR) cues supplied by the bone tissue marrow 3-D structure to AML cells.4 Differential connections of AML cells with neighboring cells or with extracellular matrix (ECM) proteins in the bone tissue marrow microenvironment have already been proven to impart CAMDR to AML cells.5-10 Within this essential situation the interaction of very past due antigen 4 (VLA 4) portrayed by AML cells with stromal fibronectin (FN) has a major function in ...
They will use the funds to develop software tools for designing and testing site-specific CRISPR systems that target drug resistance mechanisms in cancer cells.
Affiliation (Current):東北大学,農学研究科,教授, Research Field:Applied microbiology,Biological Sciences,Science and Engineering,Applied molecular and cellular biology,応用微生物学・応用生物化学, Keywords:糸状菌,転写因子,トランスポーター,シグナル伝達,麹菌,菌類,発現制御,アミラーゼ生産,ヒスチジンキナーゼ,転写制御因子, # of Research Projects:19, # of Research Products:127, Ongoing Project:Elucidation of drug resistance mechanisms in filamentous fungi by functional analyses of transcription factors
(Medical Xpress) -- A new study by TCD researchers investigates drug-resistant ovarian cancer cells. The findings which have been recently published in the international publication, PLoS One will increase understanding of molecular markers in drug-resistant ovarian cancer with a view to improving clinical treatment.
New cancer research from The Jackson Laboratory is providing a better understanding of the processes underlying cell-to-cell differences within glioblastoma tumors - a crucial finding because these differences contribute to therapy resistance.
PerProGlio Project aims to identify individual parameters that determine recurrence and therapy resistance in Glioblastoma (GBM) with possible therapeutic implications.
The drug resistant cell line MOR/0.2R has been derived from the parent line, MOR, by continuous exposure to increasing concentrations of doxorubicin (also known as adriamycin). MOR/0.2R accumulate lower levels of doxorubicin than the parent line and have been shown to overexpress multi drug resistance associated protein (MRP). Expression of a 190kDa membrane protein associated with the degree of drug-resistance has been indicated. Cells grow as easily detaching aggregates ...
The expanding spectrum of both established and candidate oncogenic driver mutations identified in non-small-cell lung cancer (NSCLC), coupled with the increasing number of clinically available signal transduction pathway inhibitors targeting these driver mutations, offers a tremendous opportunity to enhance patient outcomes. Despite these molecular advances, advanced-stage NSCLC remains largely incurable due to therapeutic resistance. In this Review, we discuss alterations in the targeted oncogene (on-target resistance) and in other downstream and parallel pathways (off-target resistance) leading to resistance to targeted therapies in NSCLC, and we provide an overview of the current understanding of the bidirectional interactions with the tumour microenvironment that promote therapeutic resistance. We highlight common mechanistic themes underpinning resistance to targeted therapies that are shared by NSCLC subtypes, including those with oncogenic alterations in epidermal growth factor ...
Our observations identify NM23-H1 as the archetype of a metastasis suppressor gene acting as repressor of the early stages of the invasive program in primary tumors. We propose that NM23-H1 functions as a barrier against the conversion of in situ carcinoma into invasive carcinoma. Our data support the notion that NM23-H1 silencing induces an invasive phenotype linked to partial EMT associated with the β-catenin nuclear translocation and upregulation of TCF/LEF-1-mediated transcription, a molecular signature of the Wnt pathway (32). EMT is a major switch to exacerbate the metastatic behavior by generating migratory and invasive signals, as well as anticancer drug resistance phenotypes (33). We found that NM23-H1 is reduced at the invasive front of human primary tumors concomitantly with reduced membrane-bound E-cadherin, further supporting the biological significance of our experimental data. Collectively, our data identify NM23-H1 as a critical regulator of E-cadherin-mediated intercellular ...
The total number of patients enrolled in this clinical trial will be 55 subjects. This trial utilized a standard 3 + 3 dose escalation design, until the MTD or the maximum specified dose was been reached. In Phase 2, additional patients with GBM were treated at the MTD (or other selected optimum Phase 2 dose) to measure tumor responses to treatment.. ...
Fingerprint Dive into the research topics of Reversal of cisplatin resistance in vivo by an anti-fos ribozyme. Together they form a unique fingerprint. ...
During the third situation, we were unable to make a definitive determination. Other cases with acquired mutations of uncertain significance integrated two cancers with ,-catenin mutations, the two of which occurred concomitantly with the EGFR T790M mutation. Fifteen posttreatment biopsies did not reveal any new mutations as assessed from the SNaPshot assay, nor MET or EGFR amplification. Two sufferers on this group had inadequate posttreatment tissue for EGFR and MET gene copy amount analyses. Between the 15 individuals without having an recognized genetic resistance mechanism, only 2 patients had stopped EGFR TKI treatment for more than two weeks in the time of biopsy. Each of the drug-resistant tumor specimens underwent routine pathological analyses, and in some instances, sizeable alterations from the predominant histology of the resistant tumors have been observed. To our surprise, 5 patients were found to have a diagnosis of smaller cell lung cancer inside their drug-resistant tumor ...
The failure of chemotherapeutic drugs in treatment of various cancers is attributed to the acquisition of drug resistance. However, the migration mechanisms of drug-resistant cancer cells remain incom...
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The emergence of clinical drug resistance continues to be an obstacle for the successful treatment of cancer. Our current understanding of mechanisms associated with drug resistance has been ascertained by investigating drug-resistant models created by exposing a parental population to increasing co …
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Gefitinib level of resistance remains a main issue in the treatment of lung adenocarcinoma. Inhibition of pAKT by LY294002 or inhibition of pMET by PHA-665752 considerably inhibited SL 0101-1 the …. ...
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This proposal outlines a 5 year program designed to develop the principal investigator into an independent translational researcher and investigate the role of...
Colorectal cancer is the third most common cancer among men and women. It is a major clinical problem worldwide, considering a high number of positive-diagnosed patients and death rate among them....
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TEHRAN (Tasnim) - Investigators have discovered a novel non-genetic cause of resistance to the targeted anti-cancer therapy cetuximab. Their findings suggest a strategy for overcoming this resistance.
Learning is about pushing the boundaries of what we know and stepping outside of our comfort zones, which causes resistance. If take the time to notice what you
... targeted cancer therapies would be capable of improving the therapeutic perspective among patients with drug resistance. ...
Primary or acquired drug resistance to this drug is very rare. Additional adjuvant chemotherapy may be necessary if a patients ... This continuous signaling, it is presumed, leads to the development of myeloid and/or lymphoid neoplasms that commonly include ... The drug often causes long-term complete hematological and cytogenic remissions as doses well below those used to treat chronic ... The disease is treated with a chemotherapy drug, lenalidomide. Human chromosome translocations between the PDGFRB gene and at ...
... lymphoid neoplasms, or features of both types of neoplasms. Most commonly, the present with features of myeloid neoplasms with ... This resistance is linked to the occurrence of a S601P mutation in PDGFRA. Acquired resistance to imatinib have in most cases ... That is, many types of these disorders are remarkably susceptible to relatively non-toxic drugs. Hematopoietic stem cells give ... Like the latter neoplasm, hematologic neoplasms cause by ETV6-JAK2 and BCR-JAK2 are aggressive and progress rapidly. Too few ...
Sequential application of drugs can lead to the sequential evolution of resistance mutations to each drug in turn. Gleevec is ... which may be benign neoplasms) or else a malignant neoplasm (cancer). These neoplasms are also indicated, in the diagram below ... However, most patients' tumors eventually become resistant to these drugs. Two major mechanisms of acquired resistance have ... Schimke RT (May 1984). "Gene amplification, drug resistance, and cancer". Cancer Research. 44 (5): 1735-1742. PMID 6713376. ...
... and for histiocytic neoplasms in 2021. Acquired resistance to BRAF inhibitors, such as vemurafenib and dabrafenib, commonly ... "Cobimetinib Orphan Drug Designations and Approvals". U.S. Food and Drug Administration (FDA). 26 April 2021. Retrieved 4 July ... "Drug Trials Snapshots: Cotellic". U.S. Food and Drug Administration (FDA). 30 July 2020. Retrieved 21 September 2021. This ... "Cobimetinib Orphan Drug Designations and Approvals". U.S. Food and Drug Administration (FDA). 31 January 2014. Retrieved 4 July ...
Creative Peptides, Eli Lilly, and Cebix all had drug development programs for a C-peptide product. Cebix had the only ongoing ... C-peptide may be used for determining the possibility of gastrinomas associated with Multiple Endocrine Neoplasm syndromes (MEN ... to help determine degree of insulin resistance. Therapeutic use of C-peptide has been explored in small clinical trials in ... Bigelow BV (23 February 2015). "Cebix Shuts Down Following Mid-Stage Trial of C-Peptide Drug". Xconomy. Garde D (February 24, ...
Abrogating drug resistance in malignant peripheral nerve sheath tumors by disrupting hyaluronan-CD44 interactions with small ... A nerve sheath tumor is a type of tumor of the nervous system (nervous system neoplasm) which is made up primarily of the ... From benign tumors like schwannoma to high grade malignant neoplasms known as malignant peripheral nerve sheath tumors, ... PubMed: 6310227] Carroll S. Molecular mechanisms promoting the pathogenesis of Schwann cell neoplasms. Acta Neuropathol. 2012 ...
Spaans JN, Goss GD (August 2014). "Trials to Overcome Drug Resistance to EGFR and ALK Targeted Therapies - Past, Present, and ... Recurrence of lung cancer Horn L, Lovly CM (2018). "Chapter 74: Neoplasms of the lung". In Jameson JL, Fauci AS, Kasper DL, ... Clinical trials are underway to evaluate how well these drugs kill lung cancer cells in humans. Several drugs that target ... Targeting these tags with drugs can kill cancer cells. Early-stage research in NSCLC using drugs aimed at epigenetic ...
"Researchers Uncover Drug-Resistance Mechanisms in BRAF Melanoma". Genetic Engineering & Biotechnology News. November 25, 2010. ... a rare type of histiocytic neoplasm. Vemurafenib causes programmed cell death in melanoma cell lines. Vemurafenib interrupts ... Drug has EMA link, Antineoplastic and immunomodulating drugs, B-Raf inhibitors, Chloroarenes, Fluoroarenes, Sulfonamides, ... "Drug hope for advanced melanoma". BBC News. 2009-06-02. Retrieved 2009-06-07. Harmon, Amy (2010-02-21). "A Roller Coaster Chase ...
... drug resistance, multiple, viral MeSH G12.392.395 - drug resistance, neoplasm MeSH G12.392.491 - insecticide resistance MeSH ... drug resistance, fungal MeSH G12.392.269.383.500 - drug resistance, multiple, fungal MeSH G12.392.269.420 - drug resistance, ... drug resistance, multiple, viral MeSH G12.392.300 - drug resistance, multiple MeSH G12.392.300.500 - drug resistance, multiple ... herb-drug interactions MeSH G12.392.269 - drug resistance, microbial MeSH G12.392.269.347 - drug resistance, bacterial MeSH ...
Metastasis and drug resistance are distinguishable. Access to methylation profiling is important to cancer research because: ... caused by accumulation of DNA mutations and epigenetic alterations leading to unrestrained cell proliferation and neoplasm ... Drug therapies can inhibit PIK3CA. Another example is the BRAF gene, one of the first to be implicated in melanomas. BRAF ... Some anticancer drugs target mtDNA and have shown positive results in killing tumor cells. Research has used mitochondrial ...
Dou QP, Li B (August 1999). "Proteasome inhibitors as potential novel anticancer agents". Drug Resistance Updates. 2 (4): 215- ... Kales SC, Ryan PE, Nau MM, Lipkowitz S (June 2010). "Cbl and human myeloid neoplasms: the Cbl oncogene comes of age". Cancer ... Vries EG, Verweij J (2000). "Clinical Cancer Research 2000: New Agents and Therapies". Drug Resistance Updates. 3 (4): 197-201 ... Drug Resistance Updates. 5 (6): 249-58. doi:10.1016/s1368-7646(02)00121-8. PMID 12531181. Clifford SC, Cockman ME, Smallwood AC ...
Chen HY, Shao CJ, Chen FR, Kwan AL, Chen ZP (2010). "Role of ERCC1 promoter hypermethylation in drug resistance to cisplatin in ... Such mutations and epigenetic alterations can give rise to cancer (see malignant neoplasms). Thus, CpG island hyper/hypo- ...
Active targeting strategies aim to increase drug transport into cells to improve efficacy and counter multidrug resistance. In ... Bone defects or fractures can occur in a number of ways, including trauma, neoplasm, osteoporosis, or congenital disorders. ... increasing concentration of the drug at the site of action and decreasing drug concentration elsewhere, thereby increasing the ... clinical use and new drugs". Nature Reviews Drug Discovery. 15 (3): 173-183. doi:10.1038/nrd.2015.10. PMC 4890615. PMID ...
Cysts also may be present due to intraductal papillary mucinous neoplasm. Pancreas divisum is a malformation in which the ... Type 2 diabetes mellitus, which begins with insulin resistance, is characterized by the ultimate failure of pancreatic β cells ... Less frequent but important causes are hypertriglyceridemia, drugs, infections. Chronic pancreatitis is a long-standing ... Pancreatic tumors (masses) including pancreatic cancer Serous cystadenoma of the pancreas Solid pseudopapillary neoplasm ...
... drug resistance, viral MeSH G04.185.515.286.420.500 - drug resistance, multiple, viral MeSH G04.185.515.329 - drug resistance, ... neoplasm regression, spontaneous MeSH G04.335.119.260 - erythrocyte aging MeSH G04.335.122.100 - autocrine communication MeSH ... vancomycin resistance MeSH G04.185.515.286.383 - drug resistance, fungal MeSH G04.185.515.286.383.500 - drug resistance, ... drug resistance, multiple, fungal MeSH G04.185.515.329.750 - drug resistance, multiple, viral MeSH G04.185.515.372 - germ-free ...
Axitinib, a drug used to treat renal cell carcinoma, has been shown to be effective at inhibiting the Abl kinase activity in ... JAK2 mutations have been shown to be central to myeloproliferative neoplasms and JAK kinases play a central role in driving ... Combination therapies with nilotinib and ruxolitnib have also shown success in suppressing resistance by targeting the JAK-STAT ... In apoptotic inhibition, BCR-ABL cells have been shown to be resistant to drug-induced apoptosis but also have a proapoptotic ...
This is the more common process of insulin resistance, which leads to adult-onset diabetes. Another example can be seen in ... This occurs, for instance, during drug addiction or progression to cancer. All living cells have the ability to receive and ... Such mutations and epigenetic alterations can give rise to cancer (see malignant neoplasms).[verification needed] Investigation ... The disequilibrium caused by these changes often causes withdrawal when the long-term use of a drug is discontinued. ...
Mock, Beverly A.; Nacy, C. A. (December 1988). "Hormonal modulation of sex differences in resistance to Leishmania major ... "Interleukin 6 is essential for in vivo development of B lineage neoplasms". Journal of Experimental Medicine. 182 (1): 243-248 ... traits associated with cancer initiation and progression in an effort to develop strategies for identifying and analyzing drug ...
Combining multiple chemotherapeutic drugs into one treatment helps overcome the problem of drug resistance. Furthermore, ... McKay, Lorraine I.; Cidlowski, John A. (2003). "Corticosteroids in the Treatment of Neoplasms". {{cite journal}}: Cite journal ... Drug Resistance Updates: Reviews and Commentaries in Antimicrobial and Anticancer Chemotherapy. 15 (5-6): 249-257. doi:10.1016/ ... Vincristine is a drug isolated from the Madagascar periwinkle, first discovered by the Eli Lilly company in 1958 in a search ...
February 2013). "Modelling vemurafenib resistance in melanoma reveals a strategy to forestall drug resistance". Nature. 494 ( ... a benign but locally infiltrative odontogenic neoplasm. The V600E mutation may also be linked, as a single-driver mutation (a ... In spite of the drug's high efficacy, 20% of tumors still develop resistance to the treatment. In mice, 20% of tumors become ... Drugs that treat cancers driven by BRAF mutations have been developed. Two of these drugs, vemurafenib and dabrafenib are ...
... lymphoproliferative neoplasms, malnutrition, and use of immunosuppressive drugs. People with recurrent boils are as well more ... It may occur following antibiotic use due to the development of resistance to the antibiotics used. An associated skin disease ... Knowledge of the antimicrobial resistance of S. aureus is important in the selection of antimicrobials for treatment. Nodule ( ... Laube S, Farrell M (2002). "Bacterial skin infection in the elderly: diagnosis and treatment". Drugs & Aging. 19 (5): 331-42. ...
The main problem with pathogenic drug treatments in the modern world is drug resistance. Many patients don't take the full ... "Integrated pan-cancer map of EBV-associated neoplasms reveals functional host-virus interactions". Cancer Research. 79 (23): ... only the bacteria which have developed genetic mutations to combat the drug can survive. This reduces drug effectiveness and ... These drugs are specifically designed to kill microbes or inhibit further growth within the host environment. Multiple terms ...
Studies have shown that the high levels of insulin resulting from insulin resistance might enhance insulin resistance. Studies ... Hyperinsulinemia can be seen in a variety of conditions including diabetes mellitus type 2, in neonates and in drug-induced ... Neoplasm Carbohydrate malabsorption Pancreatic cancer Polycystic ovary syndrome (PCOS) Trans fats Since hyperinsulinemia and ... Shanik, M.H.; Yuping, X.; Skrha, J.; Danker, R.; Zick, Y.; Roth, J. (2008). "Insulin Resistance and Hyperinsulinemia". Diabetes ...
Curiously, mutant revertant MCF-7/AdrVp cells that lost their multidrug resistance and became drug-sensitive also lost H19 ... In contrast to most other cancers, adrenocortical neoplasms appear to have decreased expression of H19. To determine a possible ... Drug-resistant MCF-AdrVp cells do not overexpress P-glycoprotein, a cell membrane efflux pump commonly found in multidrug ... p95, or NCA-90, is related to carcinoembryonic antigens, which have been found to reduce drug toxicity by Kawaharata et al. NCI ...
"A set of miRNAs that involve in the pathways of drug resistance and leukemic stem-cell differentiation is associated with the ... "miR-28 is a thrombopoietin receptor targeting microRNA detected in a fraction of myeloproliferative neoplasm patient platelets ...
Acquired resistance to Gleevec is uncommon but has been observed in patients whose mutated cells develop a T674I or D842V ... This drug, also known as Gleevec, has been a FDA-approved and most successful treatment for Philadelphia chromosome-positive ... Vega F, Medeiros LJ, Bueso-Ramos CE, Arboleda P, Miranda RN (2015). "Hematolymphoid neoplasms associated with rearrangements of ... While the success of Gleevec in treating the myeloproliferative neoplasm/myeloblastic leukemia or T-lymphoblastic leukemia/ ...
... can occur which prevent the drugs from binding to the protein, leading to resistance to these types of drugs. Drugs used in ... Survivors of childhood cancer are more than 13 times as likely to get a secondary neoplasm during the 30 years after treatment ... Resistance is a major cause of treatment failure in chemotherapeutic drugs. There are a few possible causes of resistance in ... drug-to-drug interactions, genetics, and obesity, which have major impacts on the actual concentration of the drug in the ...
... and colon neoplasms. PELP1 signaling contributes to hormonal therapy resistance. Altered localization of PLP1 contributes to ... Since PELP1 lacks known enzymatic activity, drugs that target PELP1 interactions with other proteins should have clinical ... AR, PELP1 and Src form constitutive complexes in prostate neoplasms model cells that exhibit androgen independence. Cytoplasmic ... Since PELP1 interacts with histone modifications and epigenetic enzymes, drugs targeting epigenetic modifier enzymes may be ...
"Counteracting Drug Resistance in Melanoma". 2015. Archived from the original on 2015-02-04. "Bristol drug cuts death risk in ... Melanoma is a type of neuroectodermal neoplasm. There are four main types of melanoma: Other histopathologic types are: Mucosal ... "GSK melanoma drugs add to tally of U.S. drug approvals". Reuters. May 30, 2013. Archived from the original on September 24, ... Rebecca, Vito W.; Herlyn, Meenhard (2020). "Nongenetic Mechanisms of Drug Resistance in Melanoma". Annual Review of Cancer ...
ISBN 978-0-7817-5007-3. Frequency of lymphoid neoplasms. (Source: Modified from WHO Blue Book on Tumour of Hematopoietic and ... Based on this study, the Food and Drug Administration approved ibrutinib for use in Waldenström macroglobulinemia in 2015. ... When primary or secondary resistance invariably develops, salvage therapy is considered. Allogeneic stem cell transplantation ... "FDA approves zanubrutinib for Waldenström's macroglobulinemia". U.S. Food and Drug Administration (FDA). 1 September 2021. ...
"Drug resistance in metastatic castration-resistant prostate cancer". Nature Reviews. Clinical Oncology. 8 (1): 12-23. doi: ... "Male Genitals - Prostate Neoplasms". Pathology study images. University of Virginia School of Medicine. Archived from the ... "FDA approves new drug for advanced prostate cancer" (Press release). Food and Drug Administration. 15 May 2013. Archived from ... based National Prostate Cancer Coalition stated that prostate cancer drugs were outnumbered seven to one by breast cancer drugs ...
It may be beneficial to limit the use of systemic drugs, since bacteria can develop antimicrobial resistance and some specific ... induced Genetic/developmental disorders Specific infections Inflammatory and immune conditions Reactive processes Neoplasms ... Local drug deliveries in periodontology has gained acceptance and popularity compared to systemic drugs due to decreased risk ... Systemic drug delivery in conjunction with non-surgical therapy may be used as a means to reduce the percentage of the ...
A third technique is to enhance the radiosensitivity of the cancer by giving certain drugs during a course of radiation therapy ... Daly MJ (March 2009). "A new perspective on radiation resistance based on Deinococcus radiodurans". Nature Reviews. ... Hypopituitarism commonly develops after radiation therapy for sellar and parasellar neoplasms, extrasellar brain tumours, head ... Examples of radiosensitizing drugs include cisplatin, nimorazole, and cetuximab. The impact of radiotherapy varies between ...
... drug-induced lichen planus, lichenoid drug eruption) Drug-induced lupus erythematosus Drug-induced nail changes Drug-induced ... neoplasms, and cysts are skin lesions that develop from the epidermal layer of the skin. Aberrant basal cell carcinoma ... Electrical burn Equestrian perniosis Erythema ab igne (fire stains, toasted skin syndrome) Erythrocyanosis crurum Favre- ... Chemotherapy-induced hyperpigmentation Drug-induced acne Drug-induced angioedema Drug-related gingival hyperplasia Drug-induced ...
... but by using different drugs concurrently it would be more difficult for the tumor to develop resistance to the combination. ... A study of 93 patients with incurable neoplasms". J Natl Med Assoc. 43 (4): 211-240. PMC 2616951. PMID 14850976. Li, MC; Hertz ... Farber met resistance to conducting his studies at a time when the commonly held medical belief was that leukemia was incurable ... This drug was pivotal in the cure of testicular cancer. Subsequently, Eve Wiltshaw and others at the Institute of Cancer ...
As proton-pump inhibition can suppress infection, any treatment with this class of drug should be ceased 2 weeks prior to ... ISBN 0-7817-5007-5. Frequency of lymphoid neoplasms. (Source: Modified from WHO Blue Book on Tumour of Hematopoietic and ... "Resistance of t(11;18) positive gastric mucosa-associated lymphoid tissue lymphoma to Helicobacter pylori eradication therapy ... or a combination of all three drugs. The final results of this study, including the later addition of a rituximab-alone arm, ...
Drug Discovery. 6 (12): 975-90. doi:10.1038/nrd2422. PMC 7097588. PMID 18049472. S2CID 583709. Albini A, Marchisone C, Del ... There are multiple explanations for such resistance. Not all cancer cells have cell entry receptors for the virus and not all ... Its expression is also increased in a wide range of other malignant neoplasms. Factor X (F10) is frequently expressed in normal ... Simon AY, Moritoh K, Torigoe D, Asano A, Sasaki N, Agui T (December 2009). "Multigenic control of resistance to Sendai virus ...
Aldoxorubicin is a new version of doxorubicin that is designed to safely deliver a higher dose of the drug directly to the ... Cancer stem cells are a small population of tumor cells characterized by general chemo-resistance, the ability to self-renew, ... a distinctive aggressive neoplasm showing rhabdoid features. Clinicopathologic, immunohistochemical, and ultrastructural study ... Two of these inhibitory proteins that have been studied recently are CTLA-4 and PD1, and drugs targeting these proteins are in ...
January 2002). "Augmented expression of P-gp/multi-drug resistance gene by all-trans retinoic acid in monocytic leukemic cells ... Misago N, Narisawa Y (September 2006). "Cytokeratin 15 expression in neoplasms with sebaceous differentiation". Journal of ... December 2003). "The multidrug resistance-associated protein 3 (MRP3) is associated with a poor outcome in childhood ALL and ... Staud F, Pavek P (April 2005). "Breast cancer resistance protein (BCRP/ABCG2)". The International Journal of Biochemistry & ...
Bernatsky S, Clarke AE, Suissa S (February 2008). "Hematologic malignant neoplasms after drug exposure in rheumatoid arthritis ... Hall AG, Tilby MJ (September 1992). "Mechanisms of action of, and modes of resistance to, alkylating agents used in the ... 2010), "Oxazaphosphorines: new therapeutic strategies for an old class of drugs", Expert Opin Drug Metab Toxicol, 6 (8): 919- ... increasing both pharmacologic and toxic effects of the drug; alternatively, drugs that inhibit hepatic microsomal enzymes (e.g ...
... which is a strong risk factor for insulin resistance, although insulin resistance is a common finding among women with PCOS in ... Rasgon N (June 2004). "The relationship between polycystic ovary syndrome and antiepileptic drugs: a review of the evidence". ... androgen-secreting neoplasms, and other pituitary or adrenal disorders, should be investigated. History-taking, specifically ... Insulin resistance can be observed in both normal weight and overweight people, although it is more common in the latter (and ...
Examples include neoplasms of the gingival or alveolar mucosa (usually squamous cell carcinoma),: 299 conditions which cause ... An estimated 10% of all antibiotic prescriptions are made by dentists, a major factor in antibiotic resistance. They are often ... Since many cases of toothache are inflammatory in nature, over the counter non-steroidal anti-inflammatory drugs (NSAIDs) may ... Consequently, acute or chronic maxillary sinusitis can be perceived as maxillary toothache, and neoplasms of the sinus (such as ...
... neither dasatinib nor nilotinib could overcome drug resistance caused by one particular mutation found to occur in the ... May 2016). "The 2016 revision to the World Health Organization classification of myeloid neoplasms and acute leukemia". Blood. ... The first of this new class of drugs was imatinib mesylate (marketed as Gleevec or Glivec), approved by the US Food and Drug ... "FDA approves new orphan drug for chronic myelogenous leukemia" (Press release). US Food and Drug Administration. September 4, ...
"Drugs@FDA: FDA-Approved Drugs". Michael Oettel; Ekkehard Schillinger (6 December 2012). Estrogens and Antiestrogens II: ... This is due to its synthetic nature and its resistance to metabolism in certain tissues such as the intestines, liver, and ... "Pharmacology and Clinical Utility of Hormones in Hormone Related Neoplasms". In Alan C. Sartorelli, David G. Johns (eds.). ... Velayudham LS, Farrell GC (2003). "Drug-induced cholestasis". Expert Opin Drug Saf. 2 (3): 287-304. doi:10.1517/eods.2.3. ...
April 2002). "Risk of renal and colonic neoplasms and spontaneous pneumothorax in the Birt-Hogg-Dubé syndrome". Cancer ... June 2016). "The FNIP co-chaperones decelerate the Hsp90 chaperone cycle and enhance drug binding". Nature Communications. 7: ... "Loss of the Birt-Hogg-Dubé tumor suppressor results in apoptotic resistance due to aberrant TGFβ-mediated transcription". ... cosegregation of kidney neoplasms with BHD cutaneous lesions was observed in 3 families with a family history of kidney tumors ...
Unlisted Drugs. Pharmaceutical Section, Special Libraries Association. 1965. Bakke OM, Wardell WM, Lasagna L (May 1984). "Drug ... The improved potency of MGA compared to medroxyprogesterone acetate may be due to increased resistance to metabolism of MGA ... Frick J, Marberger H, Swoboda HP (May 1971). "[Hormone therapy of prostatic neoplasms]". Urologe (in German). 10 (3): 117-9. ... Drugs with unknown mechanisms of action, Glucocorticoids, Hormonal antineoplastic drugs, Hormonal contraception, Pregnanes, ...
Particularly, resistance to conventional therapeutics and high propensity to metastasize were taken into account when choosing ... This represents the conditio sine qua non for the finding of drugs that can be effective against PDAC. The most promising ... have close to no impact on the course of this aggressive neoplasm. Therefore, virtually all of the patients diagnosed with PC ... strong proof-of-concept activity of any of these compounds will be a green light for proceeding to an Investigational New Drug ...
Infobox drug articles with non-default infobox title, Infobox drug articles without a structure image, Chemical articles ... malignant neoplasms, acute renal failure, age under 18 years (no clinical study data available). It should also be used with ... increasing resistance to denaturation and the action of inhibitors while preserving the enzymes native structure and activity, ... CS1 errors: missing periodical, Orphaned articles from May 2021, All orphaned articles, Drugs with non-standard legal status, ...
Drug Resistance, Neoplasm * E2F1 Transcription Factor / biosynthesis * E2F1 Transcription Factor / deficiency * E2F1 ... which in turn activated the phosphoinositide-3-kinase/Akt pathway to resist drug-induced apoptosis. Moreover, E2F1 directly ...
Drug Resistance, Neoplasm. *Gene Expression Regulation, Neoplastic. *MAP Kinase Signaling System. *Melanoma ...
Keywords: Leukemia, myelogenous, chronic, BCR-ABL positive/drug therapy; Drug resistance; Drug monitoring, neoplasm; Receptor ... Leukemia, myelogenous, chronic, BCR-ABL positive; Drug resistance; Drug monitoring, neoplasm; Receptor Protein-Tyrosine Kinases ... Imatinib resistance is generally due to the appearance of clones expressing mutated forms of BCR-ABL, in which the amino acid ... Some imatinib resistance mechanisms may be overcome by dose escalation.(41,42) A retrospective analysis was carried out for ...
Keywords: Ovarian Neoplasms, Multicellular Spheroids, CDC25A, Drug Resistance, Cell Cycle, and Molecular Targeted Therapy ... Loss-of-function studies showed that CDC25A promoted cisplatin-resistance and paclitaxel-resistance and inhibited the drug- ... Sun Y, Li S, Yang L, Zhang D, Zhao Z, Gao J, Liu L. CDC25A Facilitates Chemo-resistance in Ovarian Cancer Multicellular ... Sun Y, Li S, Yang L, Zhang D, Zhao Z, Gao J, Liu L. CDC25A Facilitates Chemo-resistance in Ovarian Cancer Multicellular ...
Drug Resistance, Neoplasm. Parasramka MA, Ho E, Williams DE, Dashwood RH. 2012. MicroRNAs, diet, and cancer: new mechanistic ... Colonic Neoplasms. Parasramka MA, W Dashwood M, Wang R, Abdelli A, Bailey GS, Williams DE, Ho E, Dashwood RH. 2012. MicroRNA ... Neoplasms. Parasramka MA, Ho E, Williams DE, Dashwood RH. 2012. MicroRNAs, diet, and cancer: new mechanistic insights on the ...
... lung neoplasms; lungs; multiple drug resistance; neoplasm cells. Abstract:. ... Lung adenocarcinomas exhibit chemoresistance ... induced resistance; leaves; necrosis; pathogens; tobacco; tomatoes; transgenic plants. Abstract:. ... Nonhost resistance as a ... Herb-induced liver injury is a leading cause of drug-induced liver injury in China and its incidence is also increasing ... Egcg maintained nrf2-mediated redox homeostasis and minimized etoposide resistance in lung cancer cells ...
Neoplasm Staging. dc.subject. Prognosis. dc.subject. Immunohistochemistry. dc.subject. Drug Resistance, Neoplasm. ... Circulating Biomarkers and Resistance to Endocrine Therapy in Metastatic Breast Cancers: Correlative Results from AZD9496 Oral ... PURPOSE: Common resistance mechanisms to endocrine therapy (ET) in estrogen receptor (ER)-positive metastatic breast cancers ... Circulating Biomarkers and Resistance to Endocrine Therapy in Metastatic Breast Cancers: Correlative Results from AZD9496 Oral ...
Current work in my lab is focused on understanding the role of the bone marrow microenvironment in leukemia drug resistance, ... My scientific focus is leukemia, specifically myeloproliferative neoplasms (MPN) including CML, chronic myelomonocytic leukemia ... drug resistance and new molecular therapies in leukemia. My work describing the selective effects of imatinib on CML cells ...
... also may occur during suppression of host resistance by neoplasms, by cytotoxic drugs, and, possibly, by radiation therapy. ... Percutaneous electrical nerve stimulation: an alternative to antiviral drugs for acute herpes zoster. Anesth Analg. 1998 Oct. ... Strasfeld L, Chou S. Antiviral drug resistance: mechanisms and clinical implications. Infect Dis Clin North Am. 2010 Sep. 24(3 ... Degreef H. Famciclovir, a new oral antiherpes drug: results of the first controlled clinical study demonstrating its efficacy ...
5 Drug Resistance, Neoplasm * 4 Antineoplastic Agents * 4 Cell-Derived Microparticles * 4 Neoplasms ... Microparticles derived from drug-resistant cells regulate miR-503 and PYK2 to promote migration and invasion in breast cancer. ... Inhibition of the multidrug resistance P-glycoprotein: Time for a change of strategy?. Callaghan, R; Luk, F; Bebawy, M. ... Microparticles mediate MRP1 intercellular transfer and the re-templating of intrinsic resistance pathways. Lu, JF; Luk, F; Gong ...
Neoplasms Medicine & Life Sciences 24% * Oligonucleotide Array Sequence Analysis Medicine & Life Sciences 11% ... Drug resistance can occur at many levels, including increased drug efflux, drug inactivation, alterations in drug target, ... Drug resistance can occur at many levels, including increased drug efflux, drug inactivation, alterations in drug target, ... Drug resistance can occur at many levels, including increased drug efflux, drug inactivation, alterations in drug target, ...
Drug Resistance, Neoplasm Humans Neoplasms Substances Antimetabolites, Antineoplastic Cytarabine Deoxycytidine Kinase Cytidine ... The acquired resistance in U937R cells was followed by increase in cytidine deaminase (CDA) activity, decrease in DCK activity ... 1.3 microM). The resistance in carcinomas was associated with higher CDA activity and lower influx when compared to araC ... Impact of cytidine deaminase activity on intrinsic resistance to cytarabine in carcinoma cells. Takuya Ohta, Hiroki Hori, ...
Taken together, our study illuminates that high level of GGT5 in CAFs contributes to cancer cell survival and drug resistance, ... Moreover, high expression of GGT5 in CAFs enhanced the drug resistance of cancer cells by increasing intracellular glutathione ... Lung cancer is a highly aggressive neoplasm with an unfavorable survival [1]. Non-small cell lung cancer (NSCLC) is the most ... Figure 4. Increased GGT5 in CAFs promotes the drug resistance of LUAD cells. (A) Apoptosis cells of A549 and LAC1 cells treated ...
... and blastic plasmacytoid dendritic cell neoplasm (BPDCN) sometimes become resistant to the targeted drug tagraxofusp. Cancer, ... An account of the discovery of the true source of resistance to the drug - and the identification of a drug that may overcome ... After uncovering cause of drug resistance in leukemia, researchers find a way to overcome it ... After uncovering cause of drug resistance in leukemia, researchers find way to overcome it. ...
Drug Resistance, Antineoplastic Neoplasm Drug Resistance Resistance, Antineoplastic Agent Resistance, Antineoplastic Drug NLM ... Drug Resistance [G07.690.773.984] * Drug Resistance, Microbial [G07.690.773.984.269] * Drug Resistance, Multiple [G07.690. ... DRUG RESISTANCE NEOPL. Entry Term(s). Antibiotic Resistance, Neoplasm Antineoplastic Agent Resistance Antineoplastic Drug ... Drug Resistance, Neoplasm Preferred Concept UI. M0028386. Scope Note. Resistance or diminished response of a neoplasm to an ...
NMS-E973, a novel synthetic inhibitor of Hsp90 with activity against multiple models of drug resistance to targeted agents, ... Prediction of drug penetration in tuberculosis lesions. Sarathy, J. P., Zuccotto, F., Hsinpin, H., Sandberg, L., Via, L. E., ... The anti-tubercular drug delamanid as a potential oral treatment for visceral leishmaniasis. Patterson, S., Wyllie, S., Norval ... Activation of bicyclic nitro-drugs by a novel nitroreductase (NTR2) in Leishmania. Wyllie, S., Roberts, A. J., Norval, S., ...
Previously, we derived two drug-resistant breast cancer sublines (tamoxifen- and fulvestrant-resistant cell lines) from the ... In the current study, to further define molecular characteristics of acquired antiestrogen resistance we constructed an ... performed genome-wide mRNA and microRNA profiling to identify differential molecular pathways underlying acquired resistance to ... However, employing a systems biology approach to better understand the complexities underlying drug resistance phenotypes in ...
USP24 promotes drug resistance during cancer therapy. Wang, S. A., Young, M. J., Wang, Y. C., Chen, S. H., Liu, C. Y., Lo, Y. A ... Differential Impact of the rpoB Mutant on Rifampin and Rifabutin Resistance Signatures of Mycobacterium tuberculosis Is ...
in Breast Cancer Metastasis and Drug Resistance, 2nd Edition (A. Ahmad, ed.) Springer Medical Publishers, New York. ... He also provides lectures for sessions on Molecular Diagnostics, Immunology, Haematology, Haematological Neoplasms, and ... Guo, B., Tam, A., Santi, S.A., Parissenti, A.M. (2016) Role of autophagy and lysosomal drugsequestration in acquired resistance ... His research expertise is in the area of molecular pharmacology, with a particular emphasis on chemotherapy drug resistance in ...
Investigation of circulating lncRNAs in B-cell neoplasms. Clin Chim Acta. 2014;431:255-9. ... Have been identified as mediators of drug resistance, the exact mechanisms of drug resistance, cross-talk among different ... CircPAN3 mediates drug resistance in acute myeloid leukemia through the miR-153-5p/miR-183-5p-XIAP axis. Exp Hematol. 2019;70: ... CircPAN3 contributes to drug resistance in acute myeloid leukemia through regulation of autophagy. Leuk Res. 2019;85:106198. ...
New aspects of clinical drug resistance: the role of gene amplification and the reversal of resistance in drug refractory ... Glutathione S-transferases and drug resistance. Morrow, C. S. & Cowan, K. H., 1990, In: Cancer Cells. 2, 1, p. 15-22 8 p.. ... Glutathione S-transferase and drug resistance.. Cazenave, L. A., Moscow, J. A., Myers, C. E. & Cowan, K. H., 1989, In: Cancer ... The phenomenon of pleiotropic drug resistance.. Myers, C., Cowan, K., Sinha, B. & Chabner, B., 1987, In: Important advances in ...
KCNQ1OT1 polymorphism rs35622507 and methylation status of KCNQ1OT1 promoter influence the drug resistance to L-OHP. Aging 2022 ... Query Trace: Neoplasms and KCNQ1OT1[original query] ...
Investigating immune cell "macrophage" driven drug resistance in Acute Myeloid Leukaemia. Williams, M., Guzman, M. & Wheadon, H ... MACRESIST: Investigating immune cell "macrophage" driven drug resistance in Acute Myeloid Leukaemia. Williams, M. ... Macrophage driven therapy resistance in AML: from macrophage subset characterisation to the potential for therapeutic ...
Neoplasms 29% * Drug Resistance 10% * F-Box Proteins 8% * Ubiquitin-Conjugating Enzymes 8% ...
TUMOR SPECIFIC DELIVERY OF VERTICILLIN A OVERCOMES EPIGENETIC SILENCING RESPONSIBLE FOR DRUG RESISTANCE. Liu, K., Colson, Y., ... Neoplasms 12% * Tumor Hypoxia: Molecular Studies and Clinical Exploitation. Terris, D. J., GIACCIA, A., BLOCH, D., Bouley, D., ... Understanding Mechanisms of Resistance to Anti-angiogenic Treatments. Arbab, A. S. & ARBAB, A. S. ...
Neoplasms 9% * Drug Resistance 8% * Cell Survival 7% * Growth 4% Powered by Pure, Scopus & Elsevier Fingerprint Engine™ © 2022 ...
Drug Resistance 47% * Neoplasms 41% * Crystallography 37% * Proto-Oncogenes 30% 62 Scopus citations ... Burke, A. C., Swords, R. T., Kelly, K. & Giles, F. J., Mar 2011, In: Expert Opinion on Emerging Drugs. 16, 1, p. 85-103 19 p.. ... Mahalingam, D., Mita, A., Sankhala, K., Swords, R., Kelly, K., Giles, F. & Mita, M. M., 2009, In: Current Drug Targets. 10, 10 ... Apostolidou, E., Swords, R., Alvarado, Y. & Giles, F. J., 2007, In: Drugs. 67, 15, p. 2153-2171 19 p.. Research output: ...
Anti-Bacterial Agents, Bacteremia, Child, Drug Resistance, Multiple, Bacterial, Febrile Neutropenia, Gram-Negative Bacteria, ...
  • It inhibits DNA methyltransferase to re-activate silent genes, limiting METASTASIS and NEOPLASM DRUG RESISTANCE . (bvsalud.org)
  • Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures. (nih.gov)
  • Sun Y, Li S, Yang L, Zhang D, Zhao Z, Gao J, Liu L. CDC25A Facilitates Chemo-resistance in Ovarian Cancer Multicellular Spheroids by Promoting E-cadherin Expression and Arresting Cell Cycles. (jcancer.org)
  • Loss-of-function studies showed that CDC25A promoted cisplatin-resistance and paclitaxel-resistance and inhibited the drug-induced apoptosis in ovarian cancer MCS. (jcancer.org)
  • Resistance to chemotherapy limits the effectiveness of anti-cancer drug treatment. (qub.ac.uk)
  • Resistance to chemotherapy is believed to cause treatment failure in over 90% of patients with metastatic cancer, and resistant micrometastic tumour cells may also reduce the effectiveness of chemotherapy in the adjuvant setting. (qub.ac.uk)
  • This review focuses on molecular mechanisms of drug resistance that operate to reduce drug sensitivity in cancer cells. (qub.ac.uk)
  • Moreover, high expression of GGT5 in CAFs enhanced the drug resistance of cancer cells by increasing intracellular glutathione and reducing the intracellular reactive oxygen species in cancer cells. (aging-us.com)
  • Taken together, our study illuminates that high level of GGT5 in CAFs contributes to cancer cell survival and drug resistance, indicating that GGT5 may be a promising therapeutic target in lung adenocarcinoma. (aging-us.com)
  • Lung cancer is a highly aggressive neoplasm with an unfavorable survival [ 1 ]. (aging-us.com)
  • The drug works like a guided missile with a poison payload: The IL3 portion carries the toxin to cancer cells and essentially gives them a case of diphtheria. (statnews.com)
  • However, employing a systems biology approach to better understand the complexities underlying drug resistance phenotypes in cancer continues to represent a significant challenge to the field. (biomedcentral.com)
  • Previously, we derived two drug-resistant breast cancer sublines (tamoxifen- and fulvestrant-resistant cell lines) from the MCF7 breast cancer cell line and performed genome-wide mRNA and microRNA profiling to identify differential molecular pathways underlying acquired resistance to these important antiestrogens. (biomedcentral.com)
  • By integrating miRNA-related network, gene/miRNA expression and text-mining, the current study provides a computational-based systems biology approach for further investigating the molecular mechanism underlying antiestrogen resistance in breast cancer cells. (biomedcentral.com)
  • Unfortunately, tumor cells often develop resistance to endocrine therapy [ 1 ], representing a major obstacle limiting the success of breast cancer treatment. (biomedcentral.com)
  • In breast cancer, alterations in expression of miRNAs appear to play important roles in drug resistance [ 7 , 8 ] and thus may represent new therapeutic targets. (biomedcentral.com)
  • His research expertise is in the area of molecular pharmacology, with a particular emphasis on chemotherapy drug resistance in breast and ovarian cancer. (laurentian.ca)
  • Deciphering the evolution of cancer cells under therapeutic pressure is a crucial step to understand the mechanisms that lead to treatment resistance. (researchgate.net)
  • Methods: Methylation differences between the drug-resistance cervical cancer cell, SiHa, and its derived oxaliplatinresistant S3 cells were detected by methylation specific microarray. (ncku.edu.tw)
  • Conclusions: These results suggest that global methylation is associated with the development of drug resistance and could serve as a biomarker and therapeutic target for drug resistance in cervical cancer. (ncku.edu.tw)
  • Recognizing resistance or susceptibility to the current standard cisplatin and paclitaxel treatment could improve therapeutic outcomes of metastatic or recurrent cervical cancer. (biomedcentral.com)
  • Class III tubulin is a common target for taxane chemotherapy and its overexpression has been associated with resistance in patients with NSCLC, breast cancer and gastric cancer treated with tubulin binding agents [ 13 ]. (biomedcentral.com)
  • Cancer drugs often fail due to the emergence of clinical resistance. (oncotarget.com)
  • Hyaluronic acid-modified multifunctional Q-graphene for targeted killing of drug-resistant lung cancer cells. (cdc.gov)
  • Considering the urgent need to explore multifunctional drug delivery system for overcoming multidrug resistance, we prepared a new nanocarbon material Q-Graphene as a nanocarrier for killing drug-resistant lung cancer cells. (cdc.gov)
  • Overall, a highly promising multifunctional nanoplatform was developed for tracking and monitoring targeted drug delivery for efficiently killing drug-resistant cancer cells. (cdc.gov)
  • The model organism D. melanogaster is studied to find ground-breaking research in neurology, sleep, cancer, and drug discovery. (cram.com)
  • In the context of public health, oral cancer represents one of the most aggravating conditions of oral health, representing 5% of all neoplasms. (bvsalud.org)
  • The detailed structure may guide the development of new drugs that modify JAK activity, amplifying or dampening cell responses, with potential applications in cancer therapies. (edu.au)
  • Above: The structure of SOCS1 (red) bound to a JAK protein (beige) could inform the development of new drugs to treat cancer. (edu.au)
  • In particular, overactive JAK signalling is linked to the development of cancer-like conditions called myeloproliferative neoplasms (MPNs) - which include polycythemia vera, essential thrombocythemia and primary myelofibrosis - as well as certain acute childhood leukaemias . (edu.au)
  • If we could design a drug that inhibits SOCS1, this might boost anti-cancer immune responses, potentially improving anti-cancer immunotherapies. (edu.au)
  • Clearly, if drug resistance could be overcome, the impact on survival would be highly significant. (qub.ac.uk)
  • The incidence, mortality, and survival of leukemia depends on the diagnosis, prognosis, as well as natural history of neoplasms arising from the malignant transformation of hemopoietic stem cells or progenitor cells in the bone marrow [ 3 ]. (biomedcentral.com)
  • Background The presence of resistance to chemotherapy is associated with poor tumor response and patient survival in a variety of tumors. (utmb.edu)
  • While checkpoint inhibitors have demonstrated survival benefit and are currently approved in the front-line and second-line settings, primary and secondary resistance is common. (port.ac.uk)
  • Methods Using a nude rat human xenograft model of extremity melanoma,we analyzed tumors for glutathione (GSH), the main protein in the melphalan resistance pathway. (utmb.edu)
  • As a clinician-scientist with a translational research focus I am heading an extramurally funded research laboratory that is dedicated to the study of signaling pathways, drug resistance and new molecular therapies in leukemia. (utah.edu)
  • We demonstrated that dramatically different molecular mechanisms underlie progression to resistance to tamoxifen (henceforth, MCF7-T) and fulvestrant (henceforth, MCF7-F) and also identified specific genes and biochemical pathways associated with SERM- and SERD-resistance. (biomedcentral.com)
  • Endometriosis is characterized by progesterone resistance and hyperactivity of the AKT and MAPK pathways. (webpediatrica.com)
  • The atomic-level structure of SOCS1 binding to its partner protein JAK could guide the development of drugs that alter disease-causing cell signalling pathways, and may have applications for treating some blood cancers, including leukaemias . (edu.au)
  • Although most patients respond well to imatinib therapy, the literature shows that one third develops resistance or intolerance. (scielo.br)
  • Circulating Biomarkers and Resistance to Endocrine Therapy in Metastatic Breast Cancers: Correlative Results from AZD9496 Oral SERD Phase I Trial. (cam.ac.uk)
  • PURPOSE: Common resistance mechanisms to endocrine therapy (ET) in estrogen receptor (ER)-positive metastatic breast cancers include, among others, ER loss and acquired activating mutations in the ligand-binding domain of the ER gene (ESR1LBDm). (cam.ac.uk)
  • Combined detection and genotyp- performed before antimicrobial drug vey to assess the impact of chikungu- ing of Chikungunya virus by a specifi c therapy based on amoxicillin/clavu- nya fever and Aede s infestation levels. (cdc.gov)
  • Currently, the three classes of commonly used drugs for adjuvant endocrine therapy are selective estrogen receptor modulators (SERMs, e.g., tamoxifein), selective estrogen receptor down-regulators (SERDs, e.g., fulvestrant), and aromatase inhibitors (AIs). (biomedcentral.com)
  • Attempts to modulate resistance in conjunction with systemic chemotherapy have been limited by the toxicity of combined therapy, particularly gastrointestinal or hematopoetic toxicity. (utmb.edu)
  • This study explored systemic modulation of resistance in conjunction with intra-arterial regional therapy to determine if tumor responses to melphalan could be improved with acceptable toxicity. (utmb.edu)
  • BCR-ABL kinase domain mutation analysis, evaluation of drug interactions, and compliance to therapy are recommended before the start of second-line TKI therapy. (medscape.com)
  • OBJECTIVES OF THE ASSESSMENT: The Ministère de la Santé et des Services sociaux (MSSS) asked the Agence d'évaluation des technologies et des modes d'intervention en santé (AETMIS) to evaluate the efficacy of photodynamic therapy using porfimer sodium for its approved oncological indications. (bvsalud.org)
  • Additionally, diabetic patients got more oxygen therapy (32 hours, p 0.05), injectable antiviral drugs (161, p 0.05), and low molecular weight heparin (105, p 0.05) than non-diabetics. (medrech.com)
  • In particular, if the development of drug resistance is associated with changes in DNA methylation, then demethylation might reverse the resistance phenotype. (ncku.edu.tw)
  • The drug-resistance cells were treated with demethylation agent to see if the resistance phenotype were reversed. (ncku.edu.tw)
  • He also provides lectures for sessions on Molecular Diagnostics, Immunology, Haematology, Haematological Neoplasms, and Autoimmune Diseases for the Northern Ontario School of Medicine. (laurentian.ca)
  • The drug binds to its receptors in the cytoplasm by passing through the cell membrane, and the drug-receptor complex enters the cell nucleus. (firedrug.com)
  • Tumours may be intrinsically drug-resistant or develop resistance to chemotherapy during treatment. (qub.ac.uk)
  • This will facilitate the future development of rational combined chemotherapy regimens, in which the newer targeted therapies are used in combination with cytotoxic drugs to enhance chemotherapy activity. (qub.ac.uk)
  • Inhibition of p-glycoprotein by anti-angiogenic TKI might contribute to the beneficial effect of these small molecules, when combined with chemotherapy, in counteracting acquired drug resistance. (springernature.com)
  • Conclusions Modulation of resistance in conjunction with regional chemotherapy allows for improved tumor responses with minimal toxicity. (utmb.edu)
  • Interestingly, high III beta tubulin expression was associated with chemotherapy resistance and fewer responses [5/20 (25%)] compared to lower III β-tubulin expression [15/23 (65.2%)] ( p = 0.008). (biomedcentral.com)
  • ERCC1 N118 N and MDR1 G2677 T polymorphism also proved of prognostic significance for disease progression, while overexpression of III β-tubulin was positively correlated with chemotherapy resistance. (biomedcentral.com)
  • Resistance to chemotherapy is widely recognized as one of the major factors that limit therapeutic efficacy and influence patient outcomes. (biomedcentral.com)
  • Drug Resistance Updates : Reviews and Commentaries in Antimicrobial and Anticancer Chemotherapy [electronic resource]. (who.int)
  • My scientific focus is leukemia, specifically myeloproliferative neoplasms (MPN) including CML, chronic myelomonocytic leukemia (CMML) and myelofibrosis (MF). (utah.edu)
  • Lim KH, Matsuura S, Xu B. Editorial: Novel Treatment Strategies for Myeloproliferative Neoplasms. (bu.edu)
  • Current work in my lab is focused on understanding the role of the bone marrow microenvironment in leukemia drug resistance, discovering novel therapeutic targets and developing more specific signal transduction inhibitors. (utah.edu)
  • Dana-Farber scientists had a perfectly reasonable theory of why acute myeloid leukemia (AML) and blastic plasmacytoid dendritic cell neoplasm (BPDCN) sometimes become resistant to the targeted drug tagraxofusp. (statnews.com)
  • To this end, we analyzed whole-exome sequencing data of eight chronic lymphocytic leukemia (CLL) patients that developed resistance upon BCL2-inhibition by venetoclax. (researchgate.net)
  • Ponatinib or asciminib are treatment options for patients with T315I mutation and for those with resistance to or intolerance of several TKIs. (medscape.com)
  • Impact of cytidine deaminase activity on intrinsic resistance to cytarabine in carcinoma cells. (illumina.com)
  • Based on the integrative network, we extracted "substructures" (network clusters) representing the drug resistant states (tamoxifen- or fulvestrant-resistance cells) compared to drug sensitive state (parental MCF7 cells). (biomedcentral.com)
  • Recent studies have demonstrated that increased serum GGT level predicted the advanced histological hepatic injury, insulin resistance and other chronic disease [ 6 , 7 ]. (aging-us.com)
  • Study on Uric Acid as Biomarker for Insulin Resistance in Type 2 Diabetic Mellitus. (aimdrjournal.com)
  • ESR1 mutational mediated resistance may be overcome by selective ER degraders (SERD). (cam.ac.uk)
  • Only a small percentage of cases have none of the identified risk factors (male homosexuality, intravenous drug abuse, Haitian origin, and perhaps hemophilia A). To avoid a reporting bias, physicians should report cases regardless of the absence of these factors. (cdc.gov)
  • From medical records and antiepileptic drug (AED) use, Mbizvo looked for risk factors that may have contributed to these epilepsy-related deaths. (medscape.com)
  • Preventive measures include control of risk factors, drugs to make blood less likely to clot, and sometimes surgery or angioplasty to open blocked arteries. (msdmanuals.com)
  • Drug resistance can occur at many levels, including increased drug efflux, drug inactivation, alterations in drug target, processing of drug-induced damage, and evasion of apoptosis. (qub.ac.uk)
  • The exposure of ovarian adenocarcinoma TEC to the TKIs sunitinib or sorafenib was found to abrogate resistance (proliferation and motility) to doxorubicin and paclitaxel in vitro, increasing intracellular drug accumulation. (springernature.com)
  • Additionally, doxorubicin (DOX) as a model drug was loaded on the surface of Q-Graphene via p-p stacking. (cdc.gov)
  • No beneficial effect was observed in combination with cytotoxic drugs that are not p-glycoprotein substrates. (springernature.com)
  • As luck would have it, a drug capable of blocking such methylation, named azacytidine, already exists. (statnews.com)
  • KCNQ1OT1 polymorphism rs35622507 and methylation status of KCNQ1OT1 promoter influence the drug resistance to L-OHP. (cdc.gov)
  • The reversion of the drug-resistance might then be feasible if the association between abnormal DNA methylation and the development of drug-resistance could be identified. (ncku.edu.tw)
  • Targeted methylation of one of the identified locus in normal cell is expected to recapitulate the development of resistance and a two-component reporter system is adopted to monitor the increase of DNA methylation in live cells. (ncku.edu.tw)
  • Finally, we found that methylation of the target gene Casp8AP2 is sufficient to increase drug resistance in different cells. (ncku.edu.tw)
  • Integrating multiple biomarkers in prospective trials may improve outcome prediction and ET resistance mechanisms' identification over a single biomarker. (cam.ac.uk)
  • Acquired resistance is a particular problem, as tumours not only become resistant to the drugs originally used to treat them, but may also become cross-resistant to other drugs with different mechanisms of action. (qub.ac.uk)
  • Exploiting different mechanisms of action, a novel triple drug delivery system of 5-fluorouracil, curcumin, and piperine co-loaded human serum albumin nanoparticles (5FU-CUR-PIP-HSA-NPs) was developed via the self-assembly method for suppressing breast tumor. (bvsalud.org)
  • The current paper reviews the mechanisms of TEC chemoresistance and shows the role of p-glycoprotein in mediating such resistance. (springernature.com)
  • understand the mechanisms that lead to treatment resistance. (researchgate.net)
  • This can manifest through mutations in target proteins that selectively exclude drug binding whilst retaining aberrant function. (oncotarget.com)
  • New medicines for these conditions are needed, and we envisage that a drug designed to mimic the SOCS1 protein to switch off JAK proteins might be a more effective treatment," Dr Kershaw said. (edu.au)
  • Despite great advances in immunology, microbiology, and drug development, TB remains a significant public health challenge. (medscape.com)
  • We made experimental models of cells resistant to the drug and found that they, too, didn't lose CD123," says the study's senior author Andrew Lane, M.D., Ph.D., director of the BPDCN Center at Dana-Farber. (statnews.com)
  • There is evidence that TEC are more resistant to chemotherapeutic drugs, substrates of ATP-binding cassette (ABC) transporters. (springernature.com)
  • Despite advances in available therapies, children with drug-resistant and relapsed neuroblastoma have a dismal outlook with. (hrb.ie)
  • Here, we address the important question of potential resistance to stapled peptide inhibitors. (oncotarget.com)