N108 f leader plus инструкция



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Subsequently, significant genes with at least one clinical category (p < 0.05) were extracted. A matrix between the genes and the clinical categories were created based on log odds ratio for the extracted genes. Slides were stained for four mismatch repair (MMR) proteins, MLH1 (clone G168-15), MSH2 (clone FE11) MSH2 (clone BC/44), and PMS2 (clone A16-4), and were scored by two pathologists. For BRAF and KRAS, data were further segregated by hypermutation status (hypermutated versus non-hypermutated). Mutation data from non-hypermutated J-CRC patients (n = 184 tumors) were extracted and clustered by gene mutation patterns. Inhibition of poly(ADP-ribose) polymerase in tumors from BRCA mutation carriers. N Engl J Med. 2009;361:123–34.View ArticlePubMedGoogle ScholarGaron EB, Rizvi NA, Hui R, Leighl N, Balmanoukian AS, Eder JP, et al. Hypermutated and non-hypermutated cancers separated by the dashed line.

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