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发布于:2019-5-22 00:57:16  访问:17 次 回复:0 篇
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Ed by DCK to exert their antilymphoma activity. Alternatively, other classes
***PE pleural Elled clusters sporadic po PEX19 stronger than PEX3 PEX19 stronger than effusion (CD19-sorted). in 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 Europe, bortezomib and ibrutinib in USA. It could be speculated that high-dose therapy (provided ahead of autologous stem cell transplant) primarily based on other agents than nucleoside analogs may well prove a lot more useful especially for those individuals with suboptimal responses immediately after induction araC-based immunochemotherapy (e.g. sufferers, who reach partialremission, or sufferers with detectable minimal residual disease). Furthermore towards the currently authorized agents, bendamustine represents a different extremely promising drug in MCL. Not too long ago it was demonstrated that bendamustine potentiates the impact of araC by augmenting the level of intracellular ara-CTP, plus the R-BAC (rituximab, bendamustine, araC) regimen was shown to become helpful even in individuals resistant to araC therefore giving a treatment choice even for the elderly and/or frail sufferers [16,30,31]. It might be speculated that the enhanced level of ara-CTP may possibly partially offset the anticipated downregulation of DCK thereby explaining, why the combination of bendamustine and araC was shown to become helpful even in sufferers, who relapsed after araCbased therapies [30].Klanova et al. Molecular Cancer 2014, 13:159 http://www.molecular-cancer.com/content/13/1/Page ten ofTable 3 Gene expression evaluation of DCK in a set of main MCL samples obtained from patients prior to and immediately after araC-based therapiesSample at diagnosis D1 D2 D3 D4 D5 D6 D7 D8 D9 D10 Supply PBMC PE*** FFPE FFPE PBMC PBMC FFPE FFPE PBMC PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/25486018 PBMC CT (DCKGAPDH) 3.4 3.three 0.1 1.7 1.four 4.1 1.3 two.0 1.9 2.3 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 Supply (months) 12 10 five four 7 three 13 25 N/A N/A PBMC PE*** FFPE FFPE PBMC PBMC FFPE FFPE PBMC PBMC CT (DCKGAPDH) three.7 five.three 1.three three.5 two.two 3.9 three.five 1.eight 3.three 1.5 Difference in CT involving R and D samples +0.three +2.0 +1.2 +1.eight +0.eight -0.2 +2.2 -0.two +1.four -0.*A = alternation of R-CHOP and R-araC (two g/m2, two 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 individuals had been obtained at diagnosis (D1-D8) and at lymphoma relapse after failure of araC-based therapies (R1-R8). Samples from refractory individuals were obtained from principal araC-resistant MCL sufferers before (D9-D10) and 14 days just after (R9-R10) administration of high-dose araC. Real-time RT-PCR was made use of to ascertain changes in DCK expression.Conclusions Our data in the cell lines and main MCL samples clearly demonstrate that acquired resistance of MCL cells to araC is related with downregulation of mRNA and protein expression of DCK, enzyme on the nucleotide salvage pathway responsible for phosphorylation of most nucleoside analogs applied in anti-cancer therapy.
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