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发布于:2019-5-15 09:44:48  访问:30 次 回复:0 篇
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Ed by DCK to exert their antilymphoma activity. Alternatively, other classes
Alternatively, other classes of PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25936642 anti-lymphoma drugs should be applied in case of araC failure, i.e. within the setting of anticipated araC-resistance. Some of these agents have only recently been authorized for the therapy of relapsed/refractory (RR-) MCL, temsirolimus in 4-Aminobutyric acidEpigenetics Europe, bortezomib and ibrutinib in USA. It might be speculated that high-dose therapy (given just before autologous stem cell transplant) based on other agents than nucleoside analogs may possibly prove additional useful in particular for those patients with suboptimal responses soon after induction araC-based immunochemotherapy (e.g. individuals, who realize partialremission, or patients with detectable minimal residual illness). Furthermore for the presently authorized agents, bendamustine represents a further extremely promising drug in MCL. Not too long ago it was demonstrated that bendamustine potentiates the effect of araC by augmenting the degree of intracellular ara-CTP, and also the R-BAC (rituximab, bendamustine, araC) regimen was shown to be successful even in patients resistant to araC thus providing a remedy choice even for the elderly and/or frail R 6218Technical Information sufferers [16,30,31]. It might be speculated that the elevated degree of ara-CTP may partially offset the anticipated downregulation of DCK thereby explaining, why the mixture of bendamustine and araC was shown to be helpful even in individuals, who relapsed soon after araCbased therapies [30].Klanova et al. Molecular Cancer 2014, 13:159 http://www.molecular-cancer.com/content/13/1/Page 10 ofTable three Gene expression analysis of DCK in a set of major MCL samples obtained from sufferers prior to and right after araC-based therapiesSample at diagnosis D1 D2 D3 D4 D5 D6 D7 D8 D9 D10 Source PBMC PE*** FFPE FFPE PBMC PBMC FFPE FFPE PBMC PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25486018 PBMC CT (DCKGAPDH) three.4 three.3 0.1 1.7 1.4 4.1 1.3 2.0 1.9 2.three Therapy A* A A B A B** B A B A Sample at relapse R1 R2 R3 R4 R5 R6 R7 R8 R9 R10 Disease-free survival Source (months) 12 10 5 four 7 three 13 25 N/A N/A PBMC PE*** FFPE FFPE PBMC PBMC FFPE FFPE PBMC PBMC CT (DCKGAPDH) 3.7 5.three 1.3 three.5 2.two three.9 three.5 1.8 3.three 1.5 Difference in CT involving R and D samples +0.3 +2.0 +1.2 +1.eight +0.eight -0.two +2.two -0.two +1.four -0.*A = alternation of R-CHOP and R-araC (2 g/m2, 2 doses a 24 h). **B = Nordic protocol (alternation of R-MaxiCHOP and R-araC (2-3 g/m2, 4 doses a 12 h). ***PE pleural effusion (CD19-sorted). Samples from relapsed patients were obtained at diagnosis (D1-D8) and at lymphoma relapse following failure of araC-based therapies (R1-R8). Samples from refractory individuals have been obtained from principal araC-resistant MCL individuals before (D9-D10) and 14 days right after (R9-R10) administration of high-dose araC. Real-time RT-PCR was utilized to identify adjustments in DCK expression.Conclusions Our information in the cell lines and major MCL samples clearly demonstrate that acquired resistance of MCL cells to araC is connected with downregulation of mRNA and protein expression of DCK, enzyme of your nucleotide salvage pathway responsible for phosphorylation of most nucleoside analogs employed in anti-cancer therapy.Ed by DCK to exert their antilymphoma activity.
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