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Your search keyword '"Ralph de Vere White"' showing total 2 results
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2 results on '"Ralph de Vere White"'

1. Methionine Adenosyltransferase 1a (MAT1A) Enhances Cell Survival During Chemotherapy Treatment and is Associated with Drug Resistance in Bladder Cancer PDX Mice

Author

Kelly A. Martin, Nicholas R. Hum, Aimy Sebastian, Wei He, Salma Siddiqui, Paramita M. Ghosh, Chong-xian Pan, Ralph de Vere White, and Gabriela G. Loots

Subjects
bladder cancer, drug resistance, methyltransferase, gemcitabine, Biology (General), QH301-705.5, Chemistry, QD1-999
Abstract

Bladder cancer is among the top ten most common cancers, with about ~380,000 new cases and ~150,000 deaths per year worldwide. Tumor relapse following chemotherapy treatment has long been a significant challenge towards completely curing cancer. We have utilized a patient-derived bladder cancer xenograft (PDX) platform to characterize molecular mechanisms that contribute to relapse following drug treatment in advanced bladder cancer. Transcriptomic profiling of bladder cancer xenograft tumors by RNA-sequencing analysis, before and after relapse, following a 21-day cisplatin/gemcitabine drug treatment regimen identified methionine adenosyltransferase 1a (MAT1A) as one of the significantly upregulated genes following drug treatment. Survey of patient tumor sections confirmed elevated levels of MAT1A in individuals who received chemotherapy. Overexpression of MAT1A in 5637 bladder cancer cells increased tolerance to gemcitabine and stalled cell proliferation rates, suggesting MAT1A upregulation as a potential mechanism by which bladder cancer cells persist in a quiescent state to evade chemotherapy.

Published
2019
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2. Methionine Adenosyltransferase 1a (MAT1A) Enhances Cell Survival During Chemotherapy Treatment and is Associated with Drug Resistance in Bladder Cancer PDX Mice

Author

Wei He, Aimy Sebastian, Nicholas R. Hum, Ralph de Vere White, Gabriela G. Loots, Chong-Xian Pan, Paramita M. Ghosh, Kelly A. Martin, and Salma Siddiqui

Subjects
Methyltransferase, medicine.medical_treatment, Drug Resistance, Drug resistance, lcsh:Chemistry, Mice, 0302 clinical medicine, 2.1 Biological and endogenous factors, Medicine, Aetiology, Lung, lcsh:QH301-705.5, Spectroscopy, Cancer, 0303 health sciences, Tumor, Lung Cancer, gemcitabine, General Medicine, 3. Good health, Computer Science Applications, Gene Expression Regulation, Neoplastic, 5.1 Pharmaceuticals, 6.1 Pharmaceuticals, 030220 oncology & carcinogenesis, bladder cancer, Development of treatments and therapeutic interventions, medicine.drug, Urologic Diseases, Cell Survival, Antineoplastic Agents, Article, Catalysis, Cell Line, Inorganic Chemistry, 03 medical and health sciences, Cell Line, Tumor, Genetics, Animals, Humans, Physical and Theoretical Chemistry, Molecular Biology, Cell Proliferation, 030304 developmental biology, Cisplatin, Neoplastic, Chemotherapy, Chemical Physics, drug resistance, Bladder cancer, Animal, Cell growth, business.industry, Gene Expression Profiling, Organic Chemistry, Evaluation of treatments and therapeutic interventions, Methionine Adenosyltransferase, medicine.disease, Xenograft Model Antitumor Assays, Gemcitabine, Disease Models, Animal, Regimen, Good Health and Well Being, lcsh:Biology (General), lcsh:QD1-999, Gene Expression Regulation, Urinary Bladder Neoplasms, Drug Resistance, Neoplasm, Disease Models, Cancer research, Neoplasm, methyltransferase, Other Biological Sciences, Other Chemical Sciences, Transcriptome, business
Abstract

Bladder cancer is among the top ten most common cancers, with about ~380,000 new cases and ~150,000 deaths per year worldwide. Tumor relapse following chemotherapy treatment has long been a significant challenge towards completely curing cancer. We have utilized a patient-derived bladder cancer xenograft (PDX) platform to characterize molecular mechanisms that contribute to relapse following drug treatment in advanced bladder cancer. Transcriptomic profiling of bladder cancer xenograft tumors by RNA-sequencing analysis, before and after relapse, following a 21-day cisplatin/gemcitabine drug treatment regimen identified methionine adenosyltransferase 1a (MAT1A) as one of the significantly upregulated genes following drug treatment. Survey of patient tumor sections confirmed elevated levels of MAT1A in individuals who received chemotherapy. Overexpression of MAT1A in 5637 bladder cancer cells increased tolerance to gemcitabine and stalled cell proliferation rates, suggesting MAT1A upregulation as a potential mechanism by which bladder cancer cells persist in a quiescent state to evade chemotherapy.

Published
2019

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