2011
DOI: 10.1007/s00534-011-0376-7
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Gene expression analysis for predicting gemcitabine resistance in human cholangiocarcinoma

Abstract: Increased expression of p53R2 may predict gemcitabine resistance, and upregulated RNR activity may influence gemcitabine resistance in cholangiocarcinoma cells. Glutathione pathway-related genes were induced by continuous exposure to gemcitabine and may contribute to gemcitabine resistance.

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Cited by 34 publications
(36 citation statements)
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“…Under the direct control of Tp53, upregulation of ribonucleo tide reductase p53R2 increases the supply of nucleotides for repairing DNA damage. p53R2 expression is suggested as a predictive marker for resistance to gemcitabine in CCA 304 . Serine/threonine-protein kinase tousled-like kinase 1 is highly expressed in CCA, regulating chromatin assembly and the repair of cisplatin-induced DNA damage 305 .…”
Section: Mechanisms Of Chemoresistancementioning
confidence: 99%
“…Under the direct control of Tp53, upregulation of ribonucleo tide reductase p53R2 increases the supply of nucleotides for repairing DNA damage. p53R2 expression is suggested as a predictive marker for resistance to gemcitabine in CCA 304 . Serine/threonine-protein kinase tousled-like kinase 1 is highly expressed in CCA, regulating chromatin assembly and the repair of cisplatin-induced DNA damage 305 .…”
Section: Mechanisms Of Chemoresistancementioning
confidence: 99%
“…DNA damage induces expression of RRM1 and RRM2b. Overexpression of RNR subunits RRM1 and RRM2a is associated with GEM resistance (11)(12)(13).…”
Section: Gc After the Failure Of Gem For Btcmentioning
confidence: 99%
“…In cholangiocarcinoma, upregulated RNR activity was proposed to influence GEM resistance (13). RNR contains a large subunit [ribonucleotide reductase M1 subunit (RRM1)] and a small subunit [ribonucleotide reductase M2a subunit (RRM2a) and M2b subunit (RRM2b)].…”
Section: Gc After the Failure Of Gem For Btcmentioning
confidence: 99%
“…Gemcitabine is a deoxycytidine analog and is metabolized in tumor cells by deoxycytidine kinase (dCK) to yield active gemcitabine diphosphate (dFdCDP) and gemcitabine triphosphate (dFdCTP). These gemcitabine nucleosides inhibit DNA synthesis in tumor cells 43 . In recent years, gemcitabine and its combination with other anticancer drugs have become popular regimens for the treatment of cholangiocarcinoma 44 .…”
Section: Discussionmentioning
confidence: 99%