نتایج جستجو برای: 4 dihydropyrimidine

تعداد نتایج: 1304168  

Journal: :Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 2016

2004
Hany Ezzeldin Robert Diasio

Submitted: Apr 9, 2004; Revised: Jul 19, 2004; Accepted: Jul 19, 2004 Address for correspondence: Robert Diasio, MD, University of Alabama at Birmingham, Department of Pharmacology and Toxicology and UAB Comprehensive Cancer Center, 1824 6th Ave S, Wallace Tumor Institute, Room 620, University of Alabama at Birmingham, Birmingham, AL 35294-3300 Fax: 205-975-5650; e-mail: [email protected]...

Journal: :Cancer research 2005
Kei Ukon Keiji Tanimoto Tatsushi Shimokuni Takuya Noguchi Keiko Hiyama Hiroaki Tsujimoto Masakazu Fukushima Tetsuya Toge Masahiko Nishiyama

Dihydropyrimidine dehydrogenase is the most extensively investigated predictive marker for individual response to 5-fluorouracil. Clinical responses to the anticancer agent, along with various reports, have clearly shown that dihydropyrimidine dehydrogenase activity is closely correlated to its mRNA levels, but the regulatory mechanisms of its expression have remained unclear. We attempted to c...

Journal: :Annals of Oncology 2023

5-fluorouracil (5-FU) and its prodrug capecitabine are Fluoropyrimidines, widely used in colorectal cancer. The prevention of adverse effects related to severe toxicity Fluoropyrimidines essentially involves pre-therapeutic screening for dihydropyrimidine dehydrogenase (DPD) deficiency, which must be carried out systematically before starting treatment with fluorouracil or since the joint HAS/I...

Journal: :Molecular cancer therapeutics 2014
Steven M Offer Gabriel L Butterfield Calvin R Jerde Croix C Fossum Natalie J Wegner Robert B Diasio

Dihydropyrimidine dehydrogenase (DPD, encoded by DPYD) is the rate-limiting enzyme in the uracil catabolic pathway and has a pivotal role in the pharmacokinetics of the commonly prescribed anticancer drug 5-fluorouracil (5-FU). Deficiency of DPD, whether due to inadequate expression or deleterious variants in DPYD, has been linked to severe toxic responses to 5-FU. Little is known about the mec...

Journal: :Molecular cancer therapeutics 2011
Deliang Cao Amy Ziemba James McCabe Ruilan Yan Laxiang Wan Bradford Kim Michael Gach Stuart Flynn Giuseppe Pizzorno

Abrogation of uridine phosphorylase (UPase) leads to abnormalities in pyrimidine metabolism and host protection against 5-fluorouracil (5-FU) toxicity. We elucidated the effects on the metabolism and antitumor efficacy of 5-FU and capecitabine (N(4)-pentyloxycarbonyl-5'-deoxy-5-fluorocytidine) in our UPase knockout (UPase(-/-)) model. Treatment with 5-FU (85 mg/kg) or capecitabine (1,000 mg/kg)...

Journal: :Journal of virology 2006
Christina R Bourne M G Finn Adam Zlotnick

Hepatitis B virus (HBV) is a leading cause of liver disease and hepatocellular carcinoma; over 400 million people are chronically infected with HBV. Specific anti-HBV treatments, like most antivirals, target enzymes that are similar to host proteins. Virus capsid protein has no human homolog, making its assembly a promising but undeveloped therapeutic target. HAP1 [methyl 4-(2-chloro-4-fluoroph...

Journal: :Cell 2014
Yoav D. Shaul Elizaveta Freinkman William C. Comb Jason R. Cantor Wai Leong Tam Prathapan Thiru Dohoon Kim Naama Kanarek Michael E. Pacold Walter W. Chen Brian Bierie Richard Possemato Ferenc Reinhardt Robert A. Weinberg Michael B. Yaffe David M. Sabatini

It is increasingly appreciated that oncogenic transformation alters cellular metabolism to facilitate cell proliferation, but less is known about the metabolic changes that promote cancer cell aggressiveness. Here, we analyzed metabolic gene expression in cancer cell lines and found that a set of high-grade carcinoma lines expressing mesenchymal markers share a unique 44 gene signature, designa...

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