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Ed by DCK to exert their antilymphoma activity. Rather, other classes
Molecular Cancer 2014, 13:159 http://www.molecular-cancer.com/content/13/1/Page 10 ofTable 3 Gene Donaxineprice expression analysis of DCK inside a set of principal MCL samples obtained from individuals before and just 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) three.4 three.three 0.1 1.7 1.four 4.1 1.three two.0 1.9 two.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 ten 5 four 7 3 13 25 N/A N/A PBMC PE*** FFPE FFPE PBMC PBMC FFPE FFPE PBMC PBMC CT (DCKGAPDH) 3.7 5.three 1.3 3.five 2.2 3.9 3.five 1.eight 3.3 1.five Difference in CT amongst R and D samples +0.three +2.0 +1.two +1.eight +0.8 -0.2 +2.2 -0.two +1.4 -0.*A = alternation of R-CHOP and R-araC (2 g/m2, two doses a 24 h). Molecular Cancer 2014, 13:159 http://www.molecular-cancer.com/content/13/1/Page ten ofTable three Gene expression evaluation of DCK within a set of primary MCL samples obtained from individuals just before and soon 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 three.three 0.1 1.7 1.4 4.1 1.three two.0 1.9 two.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 Source (months) 12 10 5 4 7 3 13 25 N/A N/A PBMC PE*** FFPE FFPE PBMC PBMC FFPE FFPE PBMC PBMC CT (DCKGAPDH) 3.7 5.three 1.3 3.5 2.2 3.9 three.5 1.eight three.3 1.5 Distinction in CT in between R and D samples +0.3 +2.0 +1.2 +1.eight +0.8 -0.2 +2.2 -0.2 +1.four -0.*A = alternation of R-CHOP and R-araC (two g/m2, 2 doses a 24 h). **B = Nordic protocol (alternation of R-MaxiCHOP and R-araC (2-3 g/m2, four doses a 12 h). ***PE pleural effusion (CD19-sorted). Samples from relapsed sufferers had been obtained at diagnosis (D1-D8) and at lymphoma relapse after failure of araC-based therapies (R1-R8). Samples from refractory individuals had been obtained from main araC-resistant MCL patients before (D9-D10) and 14 days soon after (R9-R10) administration of high-dose araC. Real-time RT-PCR was employed to identify adjustments in DCK expression.Conclusions Our information in the cell lines and key MCL samples clearly demonstrate that acquired resistance of MCL cells to araC is associated with downregulation of mRNA and protein expression of DCK, enzyme in the nucleotide salvage pathway responsible for phosphorylation of most nucleoside analogs made use of in anti-cancer therapy. In translation, the outcomes suggest that 1.
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