A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.
An antineoplastic agent. It has significant activity against melanomas. (from Martindale, The Extra Pharmacopoeia, 31st ed, p564)
A class of drugs that differs from other alkylating agents used clinically in that they are monofunctional and thus unable to cross-link cellular macromolecules. Among their common properties are a requirement for metabolic activation to intermediates with antitumor efficacy and the presence in their chemical structures of N-methyl groups, that after metabolism, can covalently modify cellular DNA. The precise mechanisms by which each of these drugs acts to kill tumor cells are not completely understood. (From AMA, Drug Evaluations Annual, 1994, p2026)
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
Neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors. Fibrillary astrocytomas are the most common type and may be classified in order of increasing malignancy (grades I through IV). In the first two decades of life, astrocytomas tend to originate in the cerebellar hemispheres; in adults, they most frequently arise in the cerebrum and frequently undergo malignant transformation. (From Devita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2013-7; Holland et al., Cancer Medicine, 3d ed, p1082)
Highly reactive chemicals that introduce alkyl radicals into biologically active molecules and thereby prevent their proper functioning. Many are used as antineoplastic agents, but most are very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. They have also been used as components in poison gases.
The ability of some cells or tissues to survive lethal doses of IONIZING RADIATION. Tolerance depends on the species, cell type, and physical and chemical variables, including RADIATION-PROTECTIVE AGENTS and RADIATION-SENSITIZING AGENTS.
A systemic, large-cell, non-Hodgkin, malignant lymphoma characterized by cells with pleomorphic appearance and expressing the CD30 ANTIGEN. These so-called "hallmark" cells have lobulated and indented nuclei. This lymphoma is often mistaken for metastatic carcinoma and MALIGNANT HISTIOCYTOSIS.
A member of the tumor necrosis factor receptor superfamily that may play a role in the regulation of NF-KAPPA B and APOPTOSIS. They are found on activated T-LYMPHOCYTES; B-LYMPHOCYTES; NEUTROPHILS; EOSINOPHILS; MAST CELLS and NK CELLS. Overexpression of CD30 antigen in hematopoietic malignancies make the antigen clinically useful as a biological tumor marker. Signaling of the receptor occurs through its association with TNF RECEPTOR-ASSOCIATED FACTORS.
Malignant lymphoma composed of large B lymphoid cells whose nuclear size can exceed normal macrophage nuclei, or more than twice the size of a normal lymphocyte. The pattern is predominantly diffuse. Most of these lymphomas represent the malignant counterpart of B-lymphocytes at midstage in the process of differentiation.
A class of cellular receptors that have an intrinsic PROTEIN-TYROSINE KINASE activity.
Clinically benign, histologically malignant, recurrent cutaneous T-cell lymphoproliferative disorder characterized by an infiltration of large atypical cells surrounded by inflammatory cells. The atypical cells resemble REED-STERNBERG CELLS of HODGKIN DISEASE or the malignant cells of CUTANEOUS T-CELL LYMPHOMA. In some cases, lymphomatoid papulosis progresses to lymphomatous conditions including MYCOSIS FUNGOIDES; HODGKIN DISEASE; CUTANEOUS T-CELL LYMPHOMA; or ANAPLASTIC LARGE-CELL LYMPHOMA.
A group of heterogeneous lymphoid tumors representing malignant transformations of T-lymphocytes.
A type of chromosome aberration characterized by CHROMOSOME BREAKAGE and transfer of the broken-off portion to another location, often to a different chromosome.
Tumors or cancer of the human BREAST.
Primary or secondary neoplasm in the ARACHNOID or SUBARACHNOID SPACE. It appears as a diffuse fibrotic thickening of the MENINGES associated with variable degrees of inflammation.
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.
Inflammation of the coverings of the brain and/or spinal cord, which consist of the PIA MATER; ARACHNOID; and DURA MATER. Infections (viral, bacterial, and fungal) are the most common causes of this condition, but subarachnoid hemorrhage (HEMORRHAGES, SUBARACHNOID), chemical irritation (chemical MENINGITIS), granulomatous conditions, neoplastic conditions (CARCINOMATOUS MENINGITIS), and other inflammatory conditions may produce this syndrome. (From Joynt, Clinical Neurology, 1994, Ch24, p6)
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.
The use of two or more chemicals simultaneously or sequentially in the drug therapy of neoplasms. The drugs need not be in the same dosage form.
Benign and malignant neoplastic processes that arise from or secondarily involve the meningeal coverings of the brain and spinal cord.
Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).
A lesion with cytological characteristics associated with invasive carcinoma but the tumor cells are confined to the epithelium of origin, without invasion of the basement membrane.
Surgical removal of the pancreas. (Dorland, 28th ed)
Carcinoma that arises from the PANCREATIC DUCTS. It accounts for the majority of cancers derived from the PANCREAS.
A cell line derived from cultured tumor cells.
Phenotypic changes of EPITHELIAL CELLS to MESENCHYME type, which increase cell mobility critical in many developmental processes such as NEURAL TUBE development. NEOPLASM METASTASIS and DISEASE PROGRESSION may also induce this transition.
The marking of biological material with a dye or other reagent for the purpose of identifying and quantitating components of tissues, cells or their extracts.
The epithelial lining of the URINARY TRACT.
The determination of the pattern of genes expressed at the level of GENETIC TRANSCRIPTION, under specific circumstances or in a specific cell.
Tumors or cancer of the URINARY BLADDER.
Tumors or cancer of the URINARY TRACT in either the male or the female.
Hybridization of a nucleic acid sample to a very large set of OLIGONUCLEOTIDE PROBES, which have been attached individually in columns and rows to a solid support, to determine a BASE SEQUENCE, or to detect variations in a gene sequence, GENE EXPRESSION, or for GENE MAPPING.
A musculomembranous sac along the URINARY TRACT. URINE flows from the KIDNEYS into the bladder via the ureters (URETER), and is held there until URINATION.
A malignant neoplasm derived from TRANSITIONAL EPITHELIAL CELLS, occurring chiefly in the URINARY BLADDER; URETERS; or RENAL PELVIS.
Tumors or cancer of the MAMMARY GLAND in animals (MAMMARY GLANDS, ANIMAL).
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.
Experimentally induced mammary neoplasms in animals to provide a model for studying human BREAST NEOPLASMS.
Financial support of research activities.
Critical and exhaustive investigation or experimentation, having for its aim the discovery of new facts and their correct interpretation, the revision of accepted conclusions, theories, or laws in the light of newly discovered facts, or the practical application of such new or revised conclusions, theories, or laws. (Webster, 3d ed)
All organized methods of funding.
Research that involves the application of the natural sciences, especially biology and physiology, to medicine.

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 - ...
PubMed comprises more than 30 million citations for biomedical literature from MEDLINE, life science journals, and online books. Citations may include links to full-text content from PubMed Central and publisher web sites.
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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We have recently received and uploaded many new electronic-books into our catalog. Access these titles through our Full Text Finder, or by clicking on the links below. Have questions? Contact us at x68497 or [email protected] Basic Science and Oncology Bacterial Therapy of Cancer: Methods and Protocols. Breast Cancer: Methods and Protocols. Cancer Drug Resistance: Overviews…
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.
The Badr lab is focused on studying the genetic drivers of malignancy and treatment resistance as well as developing targeted and experimental therapeutics for brain tumors.
lonchophylloid A: reverses resistance to doxorubicin in cancer cells; isolated from Ephemerantha lonchophylla; structure in first source
... 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 ...
"Trials to overcome drug resistance to EGFR and ALK targeted therapies-past, present, and future". Frontiers in Oncology. 4 (233 ... Horn, L; Lovly, CM; Johnson, DH (2015). "Chapter 107: Neoplasms of the lung". In Kasper, DL; Hauser, SL; Jameson, JL; Fauci, AS ... Clinical trials are underway to evaluate how well these drugs kill lung cancer cells in humans.[184] Several drugs that target ... Targeting these tags with drugs can kill cancer cells. Early-stage research in NSCLC using drugs aimed at epigenetic ...
"Drug hope for advanced melanoma". BBC News. 2009-06-02. Retrieved 2009-06-07. Harmon, Amy (2010-02-21). "A Roller Coaster Chase ... Three mechanisms of resistance to vemurafenib (covering 40% of cases) have been discovered: Cancer cells begin to overexpress ... a rare type of histiocytic neoplasm. Vemurafenib causes programmed cell death in melanoma cell lines. Vemurafenib interrupts ... Bollag G, Tsai J, Zhang J, Zhang C, Ibrahim P, Nolop K, Hirth P (November 2012). "Vemurafenib: the first drug approved for BRAF ...
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 Res. 44 (5): 1735-42. PMID 6713376. Curt GA, ...
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, ...
... 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- ...
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 ... Neoplasms and Hemosuccus pancreaticus. Pancreatitis is inflammation of the pancreas. There are two forms of pancreatitis, which ...
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). Thus, epigenetic downregulation or ... The disequilibrium caused by these changes often causes withdrawal when the long-term use of a drug is discontinued. However, ...
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 requires ,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. ...
... can occur which prevent the drugs from binding to the protein, leading to resistance to these types of drugs.[117] Drugs used ... Secondary neoplasm[edit]. Development of secondary neoplasia after successful chemotherapy or radiotherapy treatment can occur ... Resistance[edit]. Resistance is a major cause of treatment failure in chemotherapeutic drugs. There are a few possible causes ... Antibody-drug conjugates[edit]. Antibody-drug conjugates (ADCs) comprise an antibody, drug and a linker between them. The ...
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 ...
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 ...
... in P-450 metabolism should be considered when patients exhibit unusual sensitivity or resistance to drug effects at normal ... Oral contraceptives Neoplasms have been described with prolonged exposure to some medications or toxins. Hepatocellular ... Drug metabolism is usually divided into two phases: phase 1 and phase 2. Phase 1 reaction is thought to prepare a drug for ... Drugs interact with the enzyme family in several ways. Drugs that modify cytochrome P-450 enzyme are referred to as either ...
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/ ...
"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 ...
... 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 ...
"Zurampic". Drugs.com. 1 January 2018. Retrieved 14 October 2018. "Drug Trial Snapshot: Zurampic". US Food and Drug ... This may be partly due to its association with insulin resistance and obesity, but some of the increased risk appears to be ... Gouty tophi, in particular when not located in a joint, can be mistaken for basal cell carcinoma or other neoplasms. Light ... "Drug Safety and Availability - FDA adds Boxed Warning for increased risk of death with gout medicine Uloric (febuxostat)". FDA ...
"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 ...
KIT-D816V point mutations in c-KIT exon 17 are responsible for resistance to targeted therapy drugs like imatinib mesylate, a ... Gastrointestinal stromal tumors (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract. GISTs arise in ... Imatinib (Glivec/Gleevec), an orally administered drug initially marketed for chronic myelogenous leukemia based on bcr-abl ...
They may have a role in reducing the duration and severity of cholera, although drug-resistance is mounting and their effect on ... diabetes and various types of neoplasms. It has been shown that tetracyclines are not only active against broad spectrum of ... "Drug Trial Snapshot: Xerava". FDA. Retrieved 2 October 2018. "Drug Trial Snapshot: Seysara". FDA. Retrieved 8 February 2019. " ... "Drug Trial Snapshot: Nuzyra". FDA. Retrieved 8 February 2019. "Drug Trial Snapshot: Nuzyra". FDA. Retrieved 8 February 2019. ...
... drug resistance - drug-drug interaction - DSMB - Duffy antigen system - dysplasia - dyspnea ... New Drug Application - nebulized - Nef - neoplasm - nephrotoxic - neuralgia - neurological complications of AIDS - neuropathy ... antiretroviral drugs - antisense drugs - antitoxins - Antiviral drug - aphasia - aphthous ulcer - apoptosis - approved drugs - ... multi-drug rescue therapy - multiple drug-resistant tuberculosis (MDR-TB) - mutation - myalgia - mycobacterium - mycobacterium ...
Neoplasms 60% increase in death rate 60% increased death rate from neoplasms. In 1999-2003, neoplasms accounted for 17% of all ... 2007 National Drug Strategy Household Survey: detailed findings. Drug statistics series no. 22. Cat. no. PHE 107. Canberra: ... "Resistance". Australian Institute of Aboriginal and Torres Strait Islander studies.. *. Reyes-Centeno, Hugo; Ghirotto, Silvia; ... The 2007 National Drug Strategy Household Survey[233] reported that Indigenous peoples were "more likely than other Australians ...
Examples of radiosensitizing drugs include: Cisplatin, Nimorazole, and Cetuximab. The effect of radiotherapy on control of ... 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 ... In 2002, the United States Food and Drug Administration (FDA) approved ibritumomab tiuxetan (Zevalin), which is an anti-CD20 ...
Seruga B, Ocana A, Tannock IF (January 2011). "Drug resistance in metastatic castration-resistant prostate cancer". Nature ... "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 ... "U.S. Food and Drug Administration. 2011-04-28. Archived from the original on 2013-09-22.. ...
... mediates the resistance of hematopoietic cells to an infection with HIV[35] by complexing with the HIV integrase and ... response to drug. • negative regulation of cell proliferation. • protein stabilization. • positive regulation of cyclin- ... Neoplasm: Tumor suppressor genes/proteins and Oncogenes/Proto-oncogenes. Ligand. Growth factors. ...
Chen HY, Shao CJ, Chen FR, Kwan AL, Chen ZP (2010). "Role of ERCC1 promoter hypermethylation in drug resistance to cisplatin in ... see malignant neoplasms). Thus, CpG island hyper/hypo-methylation in the promoters of DNA repair genes are likely central to ...
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- ... "NCI Drug Dictionary". National Cancer Institute. Archived from the original on 25 April 2015. Retrieved 20 December 2016.. ...
en:Drug resistance (25) → 약물저항 *en:Drugs for acid-related disorders (2) ... en:Neoplasm (40) → 신생물 *en:Nephrotic syndrome (38) → 신증후군 *en:Nervous system disease (4) ...
Lühikokkuvõte., Drug Metab Dispos., juuni 2004;32(6):675-9., 2004. *Tetsuo Nonaka, Yoshio Tamaki, Keiko Higuchi, Hiroyuki Katoh ... Tseng-Tong Kuo, Classification of thymic epithelial neoplasms: a controversial issue coming to an end?, J.Cell.Mol.Med. 5. ... The Jackson Laboratory, Thymus Mediates Cancer Cell Chemo-resistance, 15. november 2010, (vaadatud 30.11.2014) ... The Jackson Laboratory, Thymus Mediates Cancer Cell Chemo-resistance, 15. november 2010 ...
Trials to Overcome Drug Resistance to EGFR and ALK Targeted Therapies - Past, Present, and Future. Frontiers in Oncology. ... Chapter 107: Neoplasms of the lung. (编) Kasper DL, Hauser SL, Jameson JL, Fauci AS, Longo DL, Loscalzo J. Harrison's Principles ... Anti-Cancer Drugs. March 2007, 18 (3): 255-61. PMID 17264756. doi:10.1097/CAD.0b013e328011a547.. ... De-novo and acquired resistance to immune checkpoint targeting. The Lancet. Oncology. December 2017, 18 (12): e731-e741. PMID ...
Alternately obesity may in fact lead the human body to develop resistance to the actions of FABP1 leading to the compensatory ... Wolfrum C, Borrmann CM, Borchers T, Spener F (February 2001). "Fatty acids and hypolipidemic drugs regulate peroxisome ... a marker for studying cellular differentiation in gut epithelial neoplasms". Gastroenterology. 99 (6): 1727-35. PMID 1699834. ... Increased BMI and insulin resistance in subjects demonstrated higher serum FABP1 with a particular correlation in subjects with ...
"U.S. Food and Drug Administration.. *^ "Palliative or Supportive Care". American Cancer Society. Archived from the original on ... Syn NL, Teng MW, Mok TS, Soo RA (December 2017). "De-novo and acquired resistance to immune checkpoint targeting". The Lancet. ... Srikumar Chakravarthi; Baba Krishnan; Malathy Madhavan (1999). "Apoptosis and expression of p53 in colorectal neoplasms". ... "Expert Opinion on Drug Discovery. 10 (11): 1217-29. doi:10.1517/17460441.2015.1079618. PMC 4872297. PMID 26295972.. ...
While topical treatments for superficial venous thrombosis are widely used, the evidence is strongest for the heparin-like drug ... Myeloproliferative neoplasms including essential thrombocytosis and polycythemia vera[8]. *Chemotherapy[7][19] ... Activated protein C resistance[18]. *High factor VIII levels[22]. *Hyperhomocysteinemia[6] ... that heparin or a related drug is used if potential benefits are thought to outweigh potential harms; and that graduated ...
Drug Discovery. 3 (2): 115-124. doi:10.1038/nrd1304. PMID 15040576.. *^ Gao, X.; Cui, Y.; Levenson, R.; Chung, L.; Nie, S. ( ... Water resistance: The skin acts as a water-resistant barrier so essential nutrients are not washed out of the body. ... Diseases of the skin include skin infections and skin neoplasms (including skin cancer). ... Transdermal patches have been limited to administer a small number of drugs, such as nicotine, because of the limitations in ...
The surgeon asks about the ailments' symptoms and their duration, past surgical interventions, allergies, drugs use and drugs ... of the medial brow also lends resistance to the forces of wound contracture. Furthermore, the medial canthal region is ... Neoplasms - malignant and benign tumors. *Septal hematoma - a mass of (usually) clotted blood in the septum ... by intranasal drug use, and by excessive nasal aerosol use. The saddle nose deformity resulting from lost dorsum support is ...
Baselt, Randall Clint (2008). Disposition of Toxic Drugs and Chemicals in Man (8th ed.). Biomedical Publications. pp. 823-6. ... neoplasms of the central nervous system, emotional and behavior disorders, and intellectual disability.[23] ... and corrosion resistance were among the metal's attractions.[142] ... Poisoning and Drug Overdose (5th ed.). McGraw-Hill Professional ... "Current Drug Safety. 3 (1): 54-9. doi:10.2174/157488608783333907. PMC 2538609. PMID 18690981.. ...
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 ... New inhibitors include dasatinib and nilotinib, which are significantly more potent than imatinib and may overcome resistance. ... Tyrosine kinase inhibitors specific to such domains as CC, Y177, and Rho (such as imatinib and sunitinib) are important drugs ...
... found no consistent evidence of excess risks of neoplasms that could have some link to DU, and that "[t]he overall incidence of ... with less aerodynamic drag and deeper penetration due to a higher pressure at point of impact. DU projectile ordnance is often ... and so have less resistance than a normal keel. It was later replaced by a standard lead keel.[72] ...
... although drug-resistance is mounting[11] and their effect on overall mortality is questioned.[12] ... diabetes and various types of neoplasms.[24][25][26] It has been shown that tetracyclines are not only active against broad ... "Drug Trial Snapshot: Xerava". FDA. Retrieved 2 October 2018.. *^ "Drug Trial Snapshot: Seysara". FDA. Retrieved 8 February 2019 ... "Drug Trial Snapshot: Nuzyra". FDA. Retrieved 8 February 2019.. *^ "Drug Trial Snapshot: Nuzyra". FDA. Retrieved 8 February 2019 ...
Pierigè F, Serafini S, Rossi L, Magnani M (2008). "Cell-based drug delivery". Advanced Drug Delivery Reviews. 60 (2): 286-95. ... Rodi PM, Trucco VM, Gennaro AM (2008). "Factors determining detergent resistance of erythrocyte membranes". Biophysical ...
High-risk patients receive higher drug doses of these drugs, plus additional drugs. ... Reiter A, Gotlib J (2017). "Myeloid neoplasms with eosinophilia". Blood. 129 (6): 704-714. doi:10.1182/blood-2016-10-695973. ... Such combination chemotherapy usually offers the benefits of early remission and a lower risk of disease resistance. ... For adults, standard induction plans include prednisone, vincristine, and an anthracycline drug; other drug plans may include L ...
Malignant neoplasms, other cutaneous neoplasms with significant vascular component, and disorders erroneously considered as ... Low-level laser therapy (LLLT) was cleared by the US Food and Drug Administration (FDA) for the treatment of lymphedema in ... In those with lymphedema or at risk of developing lymphedema, following breast cancer treatment, resistance training did not ... resistance training and other forms of exercise were not associated with an increased risk of developing lymphedema in people ...
This evolution is why cancer recurrences will have cells that have acquired cancer-drug resistance (or in some cases, ... Thus, a clone with a mutation in a tumor suppressor gene or oncogene will expand only in a neoplasm if that mutation gives the ... Some of the small polyps in the field defect shown in the photo of the opened colon segment may be relatively benign neoplasms ... resistance to radiation from radiotherapy). Biological properties of cancer cells[edit]. In a 2000 article by Hanahan and ...
Robert L. LaFemina (2009). Antiviral research : strategies in antiviral drug discovery. Washington, DC: ASM Press. p. 1. ISBN ... Standardization of Susceptibility Test Procedure and Relative Resistance of Herpes Simplex Type 2 Strains". Antimicrob. Agents ... Salivary gland neoplasms *Benign: Basal cell adenoma. *Canalicular adenoma. *Ductal papilloma. *Monomorphic adenoma ... Several antiviral drugs are effective for treating herpes, including aciclovir (acyclovir), valaciclovir, famciclovir, and ...
Neoplasms and cancer. *Other. *Symptoms and signs. *Blood tests. Treatment. *Procedures. *Drugs *glycosides ...
Drugs *beta blockers. *channel blockers. *diuretics. *nonsympatholytic vasodilatory antihypertensives. *peripheral vasodilators ...
"Drug Resistance, Neoplasm" by people in this website by year, and whether "Drug Resistance, Neoplasm" was a major or minor ... "Drug Resistance, Neoplasm" is a descriptor in the National Library of Medicines controlled vocabulary thesaurus, MeSH (Medical ... Below are the most recent publications written about "Drug Resistance, Neoplasm" by people in Profiles. ... Below are MeSH descriptors whose meaning is more general than "Drug Resistance, Neoplasm". ...
Drug Design * Drug Resistance, Neoplasm * Glioblastoma / pathology * Glioblastoma / therapy* * Humans * Molecular Targeted ... metastatic competence as well as to therapy resistance. The PI3K-Akt pathway is therefore an attractive therapeutic target in ... GBM, because it serves as a convergence point for malignant processes and intervention might overcome resistance to ...
Drug Resistance, Neoplasm* * Flow Cytometry * Gene Expression Profiling * High-Throughput Nucleotide Sequencing ...
Breast Neoplasms. Neoplasms by Site. Neoplasms. Breast Diseases. Skin Diseases. Paclitaxel. Albumin-Bound Paclitaxel. ... and low drug resistance to paclitaxel using the Extreme Drug Resistance (EDR) Assay in patients with previously treated ... then tested by the Extreme Drug Resistance (EDR) Assay to determine probability of drug resistance to paclitaxel. After ... Evaluation of Drug Resistance in Patients With Metastatic Breast Cancer. The recruitment status of this study is unknown. The ...
Epithelial to mesenchymal transition contributes to drug resistance in pancreatic cancer. Cancer Res. 2009;69(14):5820-5828. ... thus attenuating drug resistance in PDAC. In addition, CAFs are thought to be crucial for the development of pancreatic cancer ... pancreatic intraepithelial neoplasm (PanIN) (5, 6) and intraductal papillary mucinous neoplasm (IPMN) (7, 8). These ... Intraductal papillary mucinous neoplasm: a clinicopathologic review. Surg Clin North Am. 2010;90(2):377-398.. View this article ...
Pages that link to "Drug resistance neoplasm". ← Drug resistance neoplasm. What links here. Page:. Namespace:. all. (Main). ... The following pages link to Drug resistance neoplasm: View (previous 50 , next 50) (20 , 50 , 100 , 250 , 500)*Drug ‎ (← links) ...
Drug Resistance. *Humanized. *Humanized: therapeutic use. *Humans. *Kidney Neoplasms. *Kidney Neoplasms: drug therapy ...
Kinome rewiring during acquired drug resistance in neuroendocrine neoplasms. in Endocrine-Related Cancer ... Cells were chronically exposed to the drugs and assessed for acquired resistance by viability assay. We used microarray-based ... Kawasaki K, Fujii M & Sato T 2018 Gastroenteropancreatic neuroendocrine neoplasms: genes, therapies and models. Disease Models ... allows identifying potential candidates involved in drug resistance in NENs and may be used to broadly investigate markers of ...
Keywords: Pooled shRNA screen; MYC; JAK2; PIM; drug combination; myeloproliferative neoplasms. Received: March 27, 2014 ... Therefore, effective drug combinations are urgently needed to combat such resistance. We set out to generate JAK2 inhibitor- ... Effective drug combination is one way to enhance therapeutic efficacy and combat resistance against JAK2 inhibitors. To ... JAK2 inhibitor-resistant clones are sensitive to JAK2/PIM drug combination. Rapidly emerging resistance to targeted kinase ...
BACKGROUND: As an important stress-response mechanism, autophagy plays crucial role in the tumor formation and drug resistance ... Pharmacogenomics of genes involved in antifolate drug response and toxicity in osteosarcoma.. Expert Opin Drug Metab Toxicol. ... drug resistance and tumor recurrence. However, the relationship between autophagy and OS CSCs still remains unclear.. METHODS: ... The antifolate drug most commonly used for treating human tumors is methotrexate (MTX), which is utilized widely in first-line ...
Induction of multidrug resistance by doxorubicin (DOX), together with non-specific toxicities, has restricted DOX-based ... Drug Delivery Systems. Drug Resistance, Multiple. Drug Resistance, Neoplasm. Endocytosis. Humans. Mice. Mice, Nude. Neoplasm ... Colonic Neoplasms / drug therapy, metabolism, pathology. Doxorubicin / chemistry, pharmacology*. ... Here we investigated whether DOX-EBP is able to overcome drug resistance and the underlying molecular mechanisms.. EXPERIMENTAL ...
Neoplasm Metastasis. *Drug Resistance. *Neoplasm/genetics. *Bladder Neoplasms. *Gene Expression Profiling. *Predictive Value of ... Prediction of combination drug efficacy was obtained based on the final single-drug prediction models, directly using ... We used the single-drug criteria dose and exposed cells to both drugs simultaneously. The growth of cell lines exposed to the ... Prediction Models for Combination Drug Sensitivity. Given the ability to predict single-drug efficacy in vitro, we next asked ...
Drug resistance in the treatment of cancer still remains a major clinical concern. Resistance to tamoxifen is seen in half of ... and myeloproliferative neoplasms (MPNs), and currently available drugs are largely ineffective. Although Stat5 has been ... PAK1-mediated phosphorylation of serine 305 (S305) of ERα leads to resistance to tamoxifen. In our study, PAK1-induced ... suggestive tamoxifen resistance was designed. According to our hypothesis, phosphorylation of ERα-S305 by PAK1 may be reversed ...
Distinct Receptor Tyrosine Kinase Subsets Mediate Anti-HER2 Drug Resistance in Breast Cancer.  Alexander, Peter; Chen, Rui; ...
Survivin expression and cancer cell drug resistance. Fengzhi Li; Fiscal Year: 2008 ... neoplasm metastasis*lung neoplasms*inbred c3h mice*anticarcinogenic agents*pathologic neovascularization*inbred f344 rats* ... experimental mammary neoplasms. Summary. Summary: Experimentally induced mammary neoplasms in animals to provide a model for ... neoplasm transplantation*breast neoplasms*methylnitrosourea*carcinogens*adenocarcinoma*nude mice*transgenic mice*antineoplastic ...
Cell Growth Processes / drug effects. Dose-Response Relationship, Drug. Drug Resistance, Neoplasm. Humans. K562 Cells. Leukemia ... Myelogenous, Chronic, BCR-ABL Positive / drug therapy*, pathology. Membrane Potential, Mitochondrial / drug effects. ... as well as in patients with primary and/or acquired resistance to imatinib.. ...
Microbial resistance to drugs. Neoplasms. Proteins. Resumo em inglês. Glioblastoma multiforme, a highly malignant tumor is ... Analysis of the effect of cyclooxygenase on the expression and activity of Multiple Drug Resistance Proteins (MDRP) in human ... Multidrug resistance proteins can act as efflux pumps allowing. The cells to remove cytotoxic compounds and often leaving the ... A well-established cause of multidrug resistance (MDR) involves the increased expression of members of the ATP binding cassette ...
Kidney Neoplasms. *Neoplasm Metastasis. *Cytochrome P 450. *Multi-Drug Resistance. *P-Glycoprotein ...
Drug Resistance, Neoplasm. 1. 2020. 4909. 0.070. Why? Amino Acid Sequence. 5. 2020. 14946. 0.070. Why? ...
Drug Resistance, Neoplasm. 2. 2014. 4706. 0.070. Why? Instinct. 1. 2001. 6. 0.060. Why? ...
Disialoganglioside-specific human natural killer cells are effective against drug-resistant neuroblastoma. - Diana Seidel, ... Drug Resistance, Neoplasm. *Female. *Gangliosides (genetics, immunology) *Genetic Engineering. *Humans. *Immunotherapy, ... Disialoganglioside-specific human natural killer cells are effective against drug-resistant neuroblastoma.. Abstract. The ... Take advantage of free CureHunter research engine access to explore the best drug and treatment options for any disease. Find ...
Drug Design Drug Resistance, Neoplasm Enhancer of Zeste Homolog 2 Protein Gene Expression Regulation, Neoplastic Humans ... such as drug resistance and the importance of selectivity over EZH1 or somatic EZH2 mutants. ... Areas covered: This review summarizes recent efforts in the drug development of EZH2 inhibitors reported in the patent ...
Discovery of a novel B-Raf fusion protein related to c-Met drug resistance Dillon, Roslyn; Nilsson, Carol L LU ; Shi, Stone D-H ... iframe src="https://lup.lub.lu.se/search/publication?embed=1&q=keywords+exact+%22Drug+Resistance%2C+Neoplasm%22&hide_pagination ... MicroRNA expression profiles associated with development of drug resistance in Ehrlich ascites tumor cells Husted, Susanne; ... Adaptive mitochondrial reprogramming and resistance to PI3K therapy Ghosh, Jagadish C; Siegelin, Markus D; Vaira, Valentina; ...
Drug Resistance, Multiple Gene Expression Regulation Humans Methotrexate Multidrug Resistance-Associated Proteins Neoplasms ... Multidrug resistance protein (MRP)7, MRP8, and MRP9 (gene symbols ABCC10, ABCC11, and ABCC12) are recently identified members ... MRP7 and MRP8 are lipophilic anion pumps that are able to confer resistance to chemotherapeutic agents. MRP7 is competent in ... MRP8 is a cyclic nucleotide efflux pump that is able to confer resistance to nucleoside-based agents, such as PMEA and 5FU. The ...
Chapter 4. Multiple Mechanisms of Drug Resistance in Glioblastoma and Novel Therapeutic Opportunities. (Caleb Yelton and Swapan ... Chapter 5. TNF- α and Its Receptors in Gynecological and Breast Neoplasms. (Rosekeila Simões Nomelini, Cid Almeida de Lima, ... of all tumors recur due to therapy resistance. The most challenging aspect in the treatment of glioblastomas is the invasive ... the immunological mechanisms in these neoplasms, and the role as possible future targets in the treatment. ...
Our previous studies exploring melphalan resistance in the human rhabdomyosarcoma xenograft TE-671 MR revealed elevation of DNA ... Key words Melphalan Drug resistance Antineoplastic agents DNA polymerases Neoplasm transplantation Received: 19 June 1995 / ... Our previous studies exploring melphalan resistance in the human rhabdomyosarcoma xenograft TE-671 MR revealed elevation of DNA ...
Drug Resistance, Neoplasm. en. dc.subject. Embryo, Mammalian. en. dc.subject. Fibroblasts. en. ... the potential mechanisms underlying resistance to this targeted drug in MPM are still unknown. Functional genetic analyses were ... However, MPM tissues from patients who failed to respond to bortezomib and MPM cell lines selected for resistance to bortezomib ... and the observed loss of BAK expression or NOXA transactivation may be relevant mechanisms of resistance in the clinic.. en. ...
Mentions: Hypoxia has been shown to promote resistance to cytotoxic drugs in other human OS cell lines [12]. Thus we asked ... Mentions: Hypoxia has been shown to promote resistance to cytotoxic drugs in other human OS cell lines [12]. Thus we asked ... we show that hypoxia results in resistance of human OS cells to doxorubicin-mediated toxicity (6-13 fold increase, p,0.01). ... we show that hypoxia results in resistance of human OS cells to doxorubicin-mediated toxicity (6-13 fold increase, p,0.01). ...
Drug Resistance, Multiple. *Drug Resistance, Neoplasm. *Gene Expression Regulation, Neoplastic. *HT29 Cells ... Background: The activity of P-glycoprotein (Pgp) and multidrug resistance related protein 1 (MRP1), two membrane transporters ... Background: The activity of P-glycoprotein (Pgp) and multidrug resistance related protein 1 (MRP1), two membrane transporters ... restored the antitumor effects of different chemotherapeutic drugs, restored a proper tumor-immune system recognition in ...
Pancreatic cancer is a malignant neoplasm originating from transformed cells arising in tissues forming the pancreas. The best ... showed several side effects and developed drug resistance over time [3]. In order to bypass these problems, novel strategies ... Pancreatic cancer is a malignant neoplasm originating from transformed cells arising in tissues forming the pancreas, and it is ... showed several side effects and developed drug resistance over time [3]. In order to bypass these problems, novel strategies ...
  • Comprehensive co-detecting observable aneuploid CTCs and CECs by SE-iFISH, along with applicable genomic and/or proteomic single cell molecular profiling, are anticipated to facilitate elucidating how those disparate categories of aneuploid CTCs and CECs cross-talk and functionally interplay with tumor angiogenesis, therapeutic drug resistance, tumor progression, and cancer metastasis. (mdpi.com)
  • Epithelial tumor cells that have undergone epithelial-to-mesenchymal transition (EMT) are typically prone to metastasis and drug resistance and contribute to a poor clinical outcome. (elsevier.com)
  • Resistance or diminished response of a neoplasm to an antineoplastic agent in humans, animals, or cell or tissue cultures. (ouhsc.edu)
  • RATIONALE: Drugs used in chemotherapy use different ways to stop tumor cells from dividing so they stop growing or die. (clinicaltrials.gov)
  • Patients' tumor tissue samples are collected by excisional biopsy, core biopsy, or malignant fluid aspiration, then tested by the Extreme Drug Resistance (EDR) Assay to determine probability of drug resistance to paclitaxel. (clinicaltrials.gov)
  • Glioblastoma multiforme, a highly malignant tumor is difficult to cure because of its resistance to chemotherapy treatment. (usp.br)
  • Furthermore, we demonstrate that NK-92-scFv(ch14.18)-zeta is able to mediate a significant anti- tumor response in vivo in a drug-resistant GD2(+) NB xenograft mouse model. (curehunter.com)
  • Hypoxia is an element intrinsic to most solid-tumor microenvironments, including that of OS, and is associated with resistance to therapy, poor survival, and a malignant phenotype. (nih.gov)
  • Omega 3 PUFAs were incorporated in whole lipids as well as in DRMs of MDR cells, and altered the lipid composition of these compartments.They reduced the amount of Pgp and MRP1 contained in DRMs, decreased the transporters activity, restored the antitumor effects of different chemotherapeutic drugs, restored a proper tumor-immune system recognition in response to chemotherapy in MDR cells. (nih.gov)
  • They reduced the amount of Pgp and MRP1 contained in DRMs, decreased the transporters activity, restored the antitumor effects of different chemotherapeutic drugs, restored a proper tumor-immune system recognition in response to chemotherapy in MDR cells. (nih.gov)
  • Tumor suppressor genes associated with drug resistance in ovarian cancer (review). (semanticscholar.org)
  • This is the first evidence that tumor P450s have the potential to contribute to the development of drug resistance during chemotherapy. (aspetjournals.org)
  • Studies have shown that GST-pi expressed highly in neoplasm and could be regarded as a tumor marker. (sciencecodex.com)
  • Resistance of tumor cells to multiple structurally unrelated cytotoxic drugs, multidrug resistance (MDR), is the major limitation to the successful chemotherapeutic treatment of disseminated neoplasms. (nih.gov)
  • As the results, the tumor uptake of drug-loaded nanoparticles as well as their interstitial penetration within the tumor would be greatly increased for mice pre-treated with erlotinib at the oral feeding dose of 50 mg/kg, leading to remarkably improved chemotherapeutic efficacy of nanomedicine. (bioportfolio.com)
  • Therefore, our work presents a general yet effective strategy using a clinical drug to enhance the efficacies of cancer nanomedicine and immunotherapy by normalizing tumor vasculatures and modulating TME. (bioportfolio.com)
  • Chloroquine in combination with aptamer modified nanocomplexes for tumor vessel normalization and efficient erlotinib/Survivin-shRNA co-delivery to overcome drugresistance in EGFR-mutated NSCLC. (bioportfolio.com)
  • NantHealth has earned Food and Drug Administration (FDA) clearance for the Omics Core, the first whole exome tumor-normal in vitro diagnostic that measures overall tumor mutational burden (TMB). (aacc.org)
  • The test is performed with formalin-fixed paraffin-embedded tumor tissue matched with normal specimens from patients with solid malignant neoplasms. (aacc.org)
  • The modest response of head and neck cancer patients to antiangiogenic therapies suggests the existence of potent interactions between endothelial cells and tumor cells that sustain tumor microvascular networks and contribute to resistance to therapy. (aacrjournals.org)
  • Sharma, N.K. Mutual concessions and compromises between stromal cells and cancer cells: Driving tumor development and drug resistance. (eurekaselect.com)
  • A drug wont to treat chronic myelocytic leukemia seems to be more practical at stopping a sort of medulloblastoma in mouse models than existing treatments for the deadly medicine brain tumor, reports a multi-institutional team semiconductor diode by researchers at Skaggs College of Pharmacy and Pharmaceutical Sciences at University of California point of entry. (dailybayonet.com)
  • In the study, Abagyan and the team discovered that mice bearing human medulloblastoma neoplasms saw tumor growth reduced and no drug resistance occurring. (dailybayonet.com)
  • The PI3K-Akt pathway is therefore an attractive therapeutic target in GBM, because it serves as a convergence point for malignant processes and intervention might overcome resistance to chemotherapy and radiation. (nih.gov)
  • Despite showing differentiated features, NENs exhibit therapeutic resistance to most common treatments, similar to other cancers in many instances. (bioscientifica.com)
  • We aimed at identifying signalling partners responsible of acquired resistance to treatments in order to develop novel therapeutic strategies. (bioscientifica.com)
  • Thus, this sensitive approach, based on the study of kinome activity, allows identifying potential candidates involved in drug resistance in NENs and may be used to broadly investigate markers of NENs therapeutic response. (bioscientifica.com)
  • Effective drug combination is one way to enhance therapeutic efficacy and combat resistance against JAK2 inhibitors. (oncotarget.com)
  • Therefore, it has the potential to be a potent therapeutic agent for treating drug-resistant cancers. (biomedsearch.com)
  • Vincristine and vinblastine differ in their therapeutic value for different neoplasms. (aspetjournals.org)
  • In this timely article, we will review current knowledge surrounding the deregulated bone marrow niche in myeloproliferative neoplasms and suggest how this may be targeted, either directly or indirectly, potentially influencing therapeutic choices both now and in the future. (haematologica.org)
  • Taken together, a pooled short-hairpin library screen identified several potential pathways and drugs that can be therapeutic targets for gefitinib resistant NSCLC. (nus.edu.sg)
  • However, its therapeutic value is substantially limited in pancreatic cancer patients due to occurrence of resistance towards gemcitabine. (springer.com)
  • A strategy of combined chemo-regimens is widely employed in clinical settings in attempt to reduce the chance of developing therapeutic resistance. (springer.com)
  • The present article provides an overview of our current knowledge about the critical role of AKT and STAT5 in the pathophysiology of chronic myeloid leukemia and systemic mastocytosis and on their potential value as therapeutic targets in these neoplasms. (haematologica.org)
  • In this review, we focus on the diagnostic, prognostic, and/or therapeutic utility of molecular biomarkers in mature B-cell neoplasms. (cdc.gov)
  • Detection of the KIT D816V mutation is included as a minor diagnostic criteria for systemic mastocytosis in the World Health Organization (WHO) classification of hematopoietic neoplasms, and it is also of therapeutic relevance as it confers resistance to imatinib, a drug commonly used to treat MPN. (genoptix.com)
  • Nilotinib is already a U.S. Food and Drug Administration-approved treatment for chronic leukemia with a security profile, making it Associate in Nursing honest therapeutic candidate alone or alongside surgery, medical aid, and therapy wrote the authors. (dailybayonet.com)
  • Researched pathways related to Solitary Osseous Plasmacytoma include Cell Proliferation, Drug Resistance, Mitosis, Cell Differentiation, Plasma Cell Differentiation. (novusbio.com)
  • Some patients may develop a resistance to chemotherapy drugs. (clinicaltrials.gov)
  • BACKGROUND AND PURPOSE: Induction of multidrug resistance by doxorubicin (DOX), together with non-specific toxicities, has restricted DOX-based chemotherapy. (biomedsearch.com)
  • Together, our results suggest that chemosensitivity to drug combinations can be predicted based on molecular models and provide the framework for evaluation of such models in patients undergoing combination chemotherapy for cancer. (aacrjournals.org)
  • Thus we asked whether a more broad panel of OS cell lines, and particularly a patient-derived cell line isolate, show resistance under hypoxia to doxorubicin treatment, which is part of the mainstay chemotherapy regimen for OS patients [28]. (nih.gov)
  • The main limitation to a successful treatment for ovarian cancer is the development of drug resistance to combined chemotherapy. (semanticscholar.org)
  • Neuroblastomas can acquire a sustained high-level drug resistance during chemotherapy and especially myeloablative chemoradiotherapy. (aacrjournals.org)
  • These data obtained with neuroblastoma cell lines suggest that the high-level drug resistance observed in some recurrent neuroblastomas is attributable to p53 mutations and/or a loss of p53 function acquired during chemotherapy. (aacrjournals.org)
  • Furthermore, the extracellular matrix was associated with chemotherapy resistance in ovarian cancer as well as endocrine resistance in breast cancer. (eur.nl)
  • Multidrug resistance (MDR), which is mainly caused by the overexpression of ATP-binding cassette (ABC) transporters, limits the effectiveness of clinical chemotherapy. (usda.gov)
  • However, this treatment modality is fraught with difficulties associated with toxicity and also the emergence of chemotherapy resistance is a considerable problem. (surrey.ac.uk)
  • Multiple myeloma (MM), a B-cell neoplasm characterized by clonal expansion of plasma cells in the bone marrow, remains a fatal hematologic malignancy due to the development of intrinsic and acquired drug resistance, despite the introduction of conventional high-dosage chemotherapy. (aacrjournals.org)
  • The disease is treated with a chemotherapy drug, lenalidomide. (wikipedia.org)
  • A well-established cause of multidrug resistance (MDR) involves the increased expression of members of the ATP binding cassette (ABC) transporter superfamily, many of which transport chemotherapeutic compounds from cells. (usp.br)
  • Multidrug resistance proteins can act as efflux pumps allowing. (usp.br)
  • The activity of P-glycoprotein (Pgp) and multidrug resistance related protein 1 (MRP1), two membrane transporters involved in multidrug resistance of colon cancer, is increased by high amounts of cholesterol in plasma membrane and detergent resistant membranes (DRMs). (nih.gov)
  • Similarly, treatment of the human colon adenocarcinoma cell line LS174T with vinblastine selected for a cell population with higher levels of endogenous CYP3A4 as revealed by immunohistochemistry without simultaneous increase of multidrug resistance protein 1 (MDR1). (aspetjournals.org)
  • MDR1/P-glycoprotein (ABCB1) as target for RNA interference-mediated reversal of multidrug resistance. (nih.gov)
  • Risk stratification and treatment of ICU-acquired pneumonia caused by multidrug- resistant/extensively drug-resistant/pandrug-resistant bacteria. (bioportfolio.com)
  • p53 mutations are rare in primary neuroblastomas, but a loss of p53 function could play a role in multidrug resistance. (aacrjournals.org)
  • Although multidrug resistance-associated protein 1 (MRP1) is an important ABC transporter, the relationship between MRP1 expression and drug-resistance has rarely been studied. (usda.gov)
  • Overcoming multidrug resistance in cancer: clinical studies of p-glycoprotein inhibitors. (surrey.ac.uk)
  • The greatest focus has been on the reversal of the multidrug resistance (MDR) phenotype by inhibition of the ATP-binding cassette (ABC) drug transporters. (surrey.ac.uk)
  • Effects on the microenvironment, effects on specific genes and proteins that led to resistance to lenalidomide or Revlimid that in fact ruxolitinib or Jakafi could overcome. (patientpower.info)
  • The Sentosa SQ assay is performed with plasma or serum samples, and detects 342 drug resistance mutations, including Group M subtypes A through K as well as drug resistance mutations in the virus's integrase, protease, and reverse transcriptase genes. (aacc.org)
  • The CE mark has been given to T2 Biosystems for the T2Resistance panel, which identifies 13 of the most serious antibiotic-resistance genes on the 2013 Centers for Disease Control and Prevention Urgent Threat list. (aacc.org)
  • These genes include the gram-negative markers KPC, OXA-48, NDM/VIM/IMP, CTX-M 14/15, and AmpC (CMY/DHA) and the gram-positive markers vanA/B and mecA/C, which indicate resistance to common empiric antibiotic therapies such as carbapenems, vancomycin, and penicillin. (aacc.org)
  • Our explorative pathway analysis on seven published gene-sets associated with platinum resistance in ovarian cancer reveals TP53 and transforming growth factor beta as key genes. (eur.nl)
  • Other genetic abnormalities in PDGFRB lead to various forms of potentially malignant bone marrow disorders: small deletions in and chromosome translocations causing fusions between PDGFRB and any one of at least 30 genes can cause Myeloproliferative neoplasms that commonly involve eosinophilia, eosinophil-induced organ injury, and possible progression to aggressive leukemia (see blow). (wikipedia.org)
  • Human chromosome translocations between the PDGFRB gene and at least any one of 30 genes on other chromosomes lead to myeloid and/or lymphoid neoplasms that are many ways similar to the neoplasm caused by the fusion of the PDGFRA (i.e. platelet derived growth factor receptor A or alpha-type-platelet derived growth factor receptor) gene with the FIP1L1 gene (see FIP1L1-PDGFRA fusion gene. (wikipedia.org)
  • In 2005, V617F point mutations in JAK2 were identified in a subset of myeloproliferative neoplasm (MPN) patients. (oncotarget.com)
  • Niche functionality is likely affected not only by the genomic background of the myeloproliferative neoplasm-associated mutated hematopoietic stem cells, but also by disease-associated 'chronic inflammation', and subsequent adaptive and innate immune responses. (haematologica.org)
  • Essential thrombocythemia is a myeloproliferative neoplasm marked by hyperproliferation of platelets by megakaryocytes in bone marrow. (medscape.com)
  • Mastocytosis is a myeloproliferative neoplasm (MPN) due to a clonal neoplastic proliferation of mast cells that accumulate in one or more organ systems. (genoptix.com)
  • Although there is evidence of a significant rise of neuroendocrine neoplasms (NENs) incidence, current treatments are largely insufficient due to somewhat poor knowledge of these tumours. (bioscientifica.com)
  • 2929 Type III Gastric Neuroendocrine Neoplasms: Is Local Excision Sufficient in Selected Cases? (enets.org)
  • As per ENETS Guidelines, patients with type III gastric neuroendocrine neoplasms (t-III g-NEN), need to undergo partial or total gastrectomy. (enets.org)
  • Pancreatic neuroendocrine neoplasms(NENs) are classified into neuroendocrine tumors (NET) G1, G2, G3, and neuroendocrine carcinoma (NEC), which are different pathogenesis. (enets.org)
  • We found high grade neuroendocrine neoplasms(NENG3) with a diameter of 0.1 cm in a patient with a pancreatic NETG2 (1.7 cm in diameter). (enets.org)
  • Pancreatic neuroendocrine neoplasms (pNENs) and gastrointestinal stromal tumours (GISTs) are both rare neoplasms, and they have an estimated incidence of about 1/100,000 per year and about 1-1.5/100,000 per year, respectively. (enets.org)
  • Previous research on the correlation between different pathological features and the development of gastroenteropancreatic neuroendocrine neoplasms (GEP-NENs) is rare in China. (enets.org)
  • Subjects with catecholamine-dependent hypertension due to a neuroendocrine neoplasm need to undergo preoperative α-adrenergic blockade with phenoxybenzamine or doxazozine. (minervamedica.it)
  • Inhibitors of JAK2 kinase are emerging as an important treatment modality for myeloproliferative neoplasms (MPN). (oncotarget.com)
  • However, similar to other kinase inhibitors, resistance to JAK2 inhibitors may eventually emerge through a variety of mechanisms. (oncotarget.com)
  • Research in our laboratory has focused on defining the mechanisms of drug resistance to inhibitors of mammalian DNA topoisomerase I, II alpha, and II beta. (moffitt.org)
  • Inhibitors of ABC transporters--termed MDR modulators--have in the past been numerous and have occupied industry and academia in drug discovery programs. (surrey.ac.uk)
  • However, most drugs, including new KIT D816V-blocking agents, have failed to achieve long-lasting remissions in advanced systemic mastocytosis, and there is a similar problem in chronic myeloid leukemia, where imatinib-resistant patients sometimes fail to achieve remission, even with second- or third-line BCR-ABL1 specific tyrosine kinase inhibitors. (haematologica.org)
  • However, most drugs, including new KIT D816V-blocking agents, such as midostaurin (PKC412),1 and various BCR-ABL1 inhibitors known to block KIT-activity, such as imatinib or dasatinib,2 have failed to achieve long-lasting remissions in aggressive systemic mastocytosis (ASM). (haematologica.org)
  • Analysis of the effect of cyclooxygenase on the expression and activity of Multiple Drug Resistance Proteins (MDRP) in human glioma. (usp.br)
  • Using a Topo I-deficient murine B lymphoma-derived subclone (P388-45/C) selected for its resistance to high dosage of the antitumor drug camptothecin, we show that Topo I depletion results in the hypophosphorylation of SR proteins and impairs exonic splicing enhancer (ESE)-dependent but not constitutive splicing. (cnrs.fr)
  • The contents of this volume include reviews on dendrimers for anti-cancer drug delivery, treatment methods for advanced cutaneous squamous cell carcinoma, targeting heat shock proteins for cancer treatment, Bayesian systems for optimizing treatment protocols in oncology and much more. (eurekaselect.com)
  • In head and neck squamous cell carcinoma (HNSCC), the incidence of RAS mutation, which is the major cause of cetuximab resistance, is relatively rare compared with the other types of cancers, and the mechanism mediating acquired resistance is unclear compared with the driver gene mutation-mediated de novo resistance. (zfin.org)
  • Sharma, N.K. Macrophage flipping from foe to friend: A matter of interest in breast carcinoma heterogeneity driving drug resistance. (eurekaselect.com)
  • Here, we investigated the driver gene mutation-independent mechanism for cetuximab resistance in HNSCC. (zfin.org)
  • Finally, we assessed drug-resistant cells sensitivity to pharmacological inhibition of 'hit' kinases or their signalling partners. (bioscientifica.com)
  • Inhibition of the drug extrusion activity of MDR1/P-gp by low-molecular weight pharmacologically active compounds as a method to reverse MDR in patients suffering on malignant diseases has been studied capaciously, but the clinical results have generally been disappointing. (nih.gov)
  • We have evaluated the relevance of this metabolism for the chemotherapeutic and the toxicological properties of these drugs. (aspetjournals.org)
  • However, the relevance of this metabolism for the toxicity and the chemotherapeutic value of these anticancer drugs remains unfortunately unknown. (aspetjournals.org)
  • This collection goes on to demonstrate the importance of TNF-alpha and its receptors in malignant gynecological and breast neoplasms, the immunological mechanisms in these neoplasms, and the role as possible future targets in the treatment. (novapublishers.com)
  • Chronic myeloid leukemia and systemic mastocytosis are myeloid neoplasms sharing a number of pathogenetic and clinical features. (haematologica.org)
  • The incidence of HER2 receptor expression, evaluated by IHC in different neoplasms is reported in Table 1 . (jcancer.org)
  • This progress is reflected in the 2016 update of the World Health Organization classification of lymphoid neoplasms, which lists as many as 41 mature B-cell neoplasms (including provisional categories). (cdc.gov)
  • antibiotic resistance (AR) cassettes, which we found associated with mobile genetic elements such as Tn3, Tn7, and Tn10. (bioportfolio.com)
  • Similar efforts by other pharmaceutical companies, such as Yakult Honscha, resulted in the discovery and clinical development of irinotecan (CPT-11 [Camptosar]), which received regulatory approval in the United States for use in patients with drug refractory or recurrent advanced colorectal cancer. (cancernetwork.com)
  • In fact, the low level of this resistance led many investigators to evaluate whether protracted 21-day IV infusions every 4 weeks and/or high doses of topotecan, 3.5 mg/m 2 /d for 5 days plus granulocyte colony-stimulating factor (G-CSF [Neupogen]) every 3 weeks, might, in fact, overcome drug resistance in patients with colorectal cancer and other neoplasms derived from tissues constitutively overexpressing MDR. (cancernetwork.com)
  • Vinca alkaloids such as vincristine and vinblastine are clinically important chemotherapeutic drugs, and are used for the treatment of a variety of tumors ( Rowinsky and Donehower, 1996 ). (aspetjournals.org)
  • Moreover, canine CSCs are relatively resistant to the cytotoxic effects of common chemotherapeutic drugs and ionizing radiation, indicating that failure of clinical therapy to eradicate canine mammary cancer may be due to the survival of CSCs. (mdpi.com)
  • Targeted delivery of doxorubicin through conjugation with EGF receptor-binding peptide overcomes drug resistance in human colon cancer cells. (biomedsearch.com)
  • Experts are successfully repurposing drugs approved for myelofibrosis, chronic lymphocytic leukemia and other diseases to improve outcomes in multiple myeloma. (patientpower.info)
  • Among these, the AKT and STAT5 pathways appear most critical and may result in drug-resistant chronic myeloid leukemia and systemic mastocytosis. (haematologica.org)
  • Chronic lymphocytic leukemia/small lymphocytic lymphoma, diffuse large B-cell lymphoma, follicular lymphoma, mantle cell lymphoma, Burkitt lymphoma, Waldenström macroglobulinemia, hairy cell leukemia, and marginal zone lymphomas of splenic, nodal, and extranodal types represent examples of B-cell neoplasms in which novel molecular biomarkers have been discovered in recent years. (cdc.gov)
  • Valproic acid (VPA) has been reported as a promising anticancer drug in various clinical trials and studies. (springer.com)
  • As the cannabis industry has inherently conflicting economies of scale because of state and federal regulatory variances, the Company has initiated its action plan to comprehensively identify all conflicting operations and barriers to the Company's complete focus on fostering formal clinical trials for its cancer and HIV drug development program. (bio-medicine.org)
  • The eBook series is essential to all scientists involved in clinical drug research who wish to keep abreast of rapid and important developments in the field. (eurekaselect.com)
  • Whether the mechanism is on target or off, the results of the clinical studies published here spark new possibilities for the treatment of myeloproliferative neoplasms. (medscape.com)
  • Weinberg, R.A. EMT, CSCs, and drug resistance: The mechanistic link and clinical implications. (eurekaselect.com)
  • Consequently, molecular genetic studies are increasingly being applied for the clinical workup of many of these neoplasms. (cdc.gov)
  • Furthermore, due to recent advances in pharmaceutical chemistry and the availability of many novel formulations and drug delivery vehicles, the administration of even more potent, water-insoluble camptothecin derivatives, which might portend vastly different spectra of antitumor activity, toxicity, and clinical applicability, is undoubtedly feasible at this time. (cancernetwork.com)
  • This everyone is before proposed to ensure that the can doxycycline cure syphilis clinical note of time on rechallenged design or drug is away underestimated. (transonicaviation.com)
  • In human samples, the expression of TFF1 was specifically observed in pancreatic intraepithelial neoplasm (PanIN), but was frequently lost in the invasive component of pancreatic ductal adenocarcinoma (PDAC). (jci.org)
  • In summary, the block of mitochondrial apoptosis is a limiting factor for achieving efficacy of bortezomib in MPM, and the observed loss of BAK expression or NOXA transactivation may be relevant mechanisms of resistance in the clinic. (le.ac.uk)
  • Activation of the PI3K-Akt pathway results in disturbance of control of cell growth and cell survival, which contributes to a competitive growth advantage, metastatic competence as well as to therapy resistance. (nih.gov)
  • Additionally, the bone marrow microenvironment, where MM cells preferentially home and grow, plays a crucial role in MM cell growth and survival and in developing resistance to conventional and novel therapies for MM. It has been shown that angiogenic factors, including vascular endothelial growth factor (VEGF) and basic fibroblast growth factor, are expressed and secreted by MM cells and contribute to myeloma-bone marrow neovascularization ( 8 ). (aacrjournals.org)
  • Osteosarcoma (OS) is an aggressive malignant neoplasm that still suffers from poor prognosis in the case of distal metastases or occurrence of multi-drug resistance. (medworm.com)
  • Molecular mechanisms responsible for this resistance phenomenon are badly understood. (bioscientifica.com)
  • Here we investigated whether DOX-EBP is able to overcome drug resistance and the underlying molecular mechanisms. (biomedsearch.com)
  • However, the potential mechanisms underlying resistance to this targeted drug in MPM are still unknown. (le.ac.uk)
  • And that led to a slurry of different preclinical studies we did to figure out mechanisms that uncovered immunomodulatory effects unknown with this drug. (patientpower.info)
  • What are the mechanisms of resistance to osimertinib prescribed in first-line? (clinicaltrials.gov)
  • In order to respond to all these questions, this phase II trial will be the first to systemically analyze the mechanisms of resistance to Osimertinib based on the analysis of biopsy, and collection of plasma from all patients during the course of treatment. (clinicaltrials.gov)
  • In this case, nilotinib specifically targets cancer cells that have associate degree abnormal activation of a cellular communication system, referred to as the Hedgehog pathway, via 2 totally different mechanisms, creating it more practical and less toxic than combining drugs. (dailybayonet.com)
  • The recent expansion of quantitative models addresses many questions regarding tumour initiation, progression and metastases as well as intra-tumour heterogeneity, treatment responses and resistance. (nature.com)
  • Cross-talk' between mutated hematopoietic stem cells and multiple niche components may contribute to propagating disease progression and mediating drug resistance. (haematologica.org)
  • Cancer-associated fibroblasts (CAF) are major players in the progression and drug resistance of pancreatic ductal adenocarcinoma (PDAC). (elsevier.com)
  • Drug Resistance, Neoplasm" is a descriptor in the National Library of Medicine's controlled vocabulary thesaurus, MeSH (Medical Subject Headings) . (ouhsc.edu)
  • We've repurposed this drug, and I think it will really lead to a lot of new treatments for myeloma that are not only effective, but really well-tolerated," says Dr. James Berenson, explaining how experts are using ruxolitinib (Jakafi) and other drugs to overcome resistance in multiple myeloma. (patientpower.info)
  • PURPOSE: Phase II trial to determine the reliability of a test for measuring drug resistance to paclitaxel in patients with metastatic breast cancer. (clinicaltrials.gov)
  • OBJECTIVES: I. Evaluate the proportion of patients with extreme, intermediate, and low drug resistance to paclitaxel using the Extreme Drug Resistance (EDR) Assay in patients with previously treated metastatic breast cancer. (clinicaltrials.gov)
  • Distinct Receptor Tyrosine Kinase Subsets Mediate Anti-HER2 Drug Resistance in Breast Cancer. (duke.edu)
  • Experimentally induced mammary neoplasms in animals to provide a model for studying human BREAST NEOPLASMS. (labome.org)
  • Thioguanine is an anticancer (antineoplastic) agent belonging to the class of drugs called antimetabolites. (encyclopedia.com)
  • Cancer scientists and oncologists have worked together for some time to find ways of understanding anticancer drug resistance and also to develop pharmacological strategies to overcome that resistance. (surrey.ac.uk)
  • The results from a number of these trials are eagerly awaited and there are many in the cancer research community who remain committed to this area of anticancer drug discovery. (surrey.ac.uk)
  • Hypoxia has been shown to promote resistance to cytotoxic drugs in other human OS cell lines [12]. (nih.gov)
  • A drug that prevents the growth of a neoplasm by interfering with the maturation or proliferation of the cells of the neoplasm. (encyclopedia.com)
  • Philadelphia chromosome negative' myeloproliferative neoplasms (MPN) are a group of relatively rare hematologic diseases characterized by a clonal proliferation of blood cells, most commonly secondary to acquired hematopoietic stem cell (HSC) mutations that directly or indirectly induce upregulation of the JAK-STAT pathway. (haematologica.org)
  • However, the predictive utility of these molecular correlates of chemosensitivity has not yet been validated for other cellular histologies or for drug combinations. (aacrjournals.org)
  • Specific molecular forms of GST are known to be expressed in preneoplastic cells, and have been known to participate in their resistance to drugs. (sciencecodex.com)
  • Although novel molecular targeted drugs have been recognized as an effective therapy for non-small lung cancer (NSCLC) harboring epidermal growth factor receptor (EGFR) activating mutations, their eff. (bioportfolio.com)
  • Various studies show that only 3‒5% of glioblastoma patients survive longer than 3 years and nearly 100% of all tumors recur due to therapy resistance. (novapublishers.com)
  • Mammary tumors are the most common neoplasms that affect female dogs ( Canis familiaris ), constituting half of all tumors in female dogs and from these approximately half are considered malignant [ 1 - 3 ]. (mdpi.com)
  • The magnitude of topotecan resistance conferred by MDR in vitro is much lower than that noted with classic MDR substrates, such as doxorubicin or vinblastine. (cancernetwork.com)
  • We used microarray-based kinomics to obtain highthroughput kinase activity profiles from drug sensitive vs resistant cells and identified 'hit' kinases hyperactivated in drug-resistant cells, including kinases from FGFR family, cyclin-dependant kinases and PKCs in oxaliplatin-resistant (R-Ox) QGP-1 cells. (bioscientifica.com)
  • Methylation of death-associated protein kinase is associated with cetuximab and erlotinib resistance. (semanticscholar.org)
  • Somatic mutations of the epidermal growth factor receptor often cause resistance to therapy with tyrosine kinase inhibitor in non-small cell lung cancer (NSCLC). (nus.edu.sg)
  • Combination of an EGFR tyrosine kinase inhibitor and a NF-κB inhibitor effectively suppressed cetuximab-resistant HNSCC and interfering with the EGFR-LTβ interaction reverses resistance. (zfin.org)
  • Osimertinib is an epidermal growth factor receptor tyrosine kinase inhibitor (EGFR-TKI) that is selective for both EGFR-TKI sensitizing and T790M resistance mutations in patients with non-small-cell lung cancer. (clinicaltrials.gov)
  • Autophagy and mitophagy are key homeostatic machineries linked to cancer development and drug resistance. (enets.org)
  • However, MPM tissues from patients who failed to respond to bortezomib and MPM cell lines selected for resistance to bortezomib conserved BAK expression. (le.ac.uk)
  • Pancreatic cancer is a malignant neoplasm originating from transformed cells arising in tissues forming the pancreas. (hindawi.com)
  • Pancreatic cancer is a malignant neoplasm originating from transformed cells arising in tissues forming the pancreas, and it is now the fourth most common cause of cancer-related deaths in the United States and the eighth worldwide [ 1 ]. (hindawi.com)
  • This drug suppresses the immune system and interferes with the normal functioning of certain organs and tissues. (encyclopedia.com)
  • The Food and Drug Administration (FDA) has granted de novo authorization to Vela Diagnostics USA for its Sentosa SQ HIV Genotyping assay, making this the first FDA-authorized test that detects HIV type-1 drug resistance mutations using next-generation sequencing (NGS). (aacc.org)
  • By identifying mutations in the HIV-1 virus that impact the efficacy of certain drugs, the Sentosa SQ assay is designed to provide additional information beyond viral load that could help healthcare providers better tailor drug treatment for patients who have developed resistance to HIV drugs, as well as for patients who are just beginning antiviral therapy. (aacc.org)
  • Our findings elucidate the mechanism of driver gene mutations-independent mechanism of acquired resistance to cetuximab in HNSCC and also provide potential strategies for combating cetuximab resistance. (zfin.org)
  • On the basis of these observations we sought to determine whether drug resistance in neuroblastoma cell lines was associated with a lack of p53 function and/or p53 mutations. (aacrjournals.org)

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