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F. Thorald, M.B. B.A.O., M.B.B.Ch., Ph.D.
Co-Director, Wayne State University School of Medicine
Since many of these alterations might never have been observed before and might not necessarily reside in coding regions of the genome treating gastritis naturally protonix 20 mg for sale, whole-genome sequencing is increasingly seen as the only rigorous approach that can find all the variants in a cancer genome gastritis diet почта protonix 40mg discount. Among all these alterations are a select few that drive the progression of the disease chronic gastritis rheumatoid arthritis purchase protonix 40 mg without prescription. Real progress in cancer research will come through the measurement and integrated analysis of all these interdependent processes gastritis oatmeal generic protonix 40 mg without prescription. Nat Rev Genet 13: 795-806 4 Cancer Biology Tumor Heterogeneity Every individual carries a unique set of inherited germline mutations. As cancer progresses, additional somatic mutations and genomic rearrangements accumulate. These samples are commonly used to understand the causes of relapse5 and drug resistance. The tumor itself may contain several different clonal types, each with a different response to therapy and potential for recurrence. Tumor samples typically include normal cells, such as stromal cells, blood vessels, and immune cells. Based on conventional pathology estimates, most studies focus on tumors with >60% tumor nuclei present. During cancer progression new mutations may occur in individual cells and these newly mutated cells can go on to proliferate and form clones. As a result latestage cancers often consist of polyclonal tumors, where each clone has a unique set of mutations, unique pathology, and unique drug responses. The progressive accumulation of somatic mutations results in a heterogeneous polyclonal tumor in which different clones may respond differently to treatment. In some genes mutations frequently occur in the same location, which may indicate a specific mechanism at work. However, in the majority of genes mutations can appear apparently randomly throughout the gene, which may reflect the failure of replication and repair mechanisms. The dark boxes indicate exomes and the red bars indicate locations where mutations occur. Panel A: Recurrent mutations in a specific location may indicate the involvement of a biological mechanism to generate the mutations. Panel B: Scattered mutations occurring throughout the gene, such as P53, may be due to the failure of the replication and repair mechanisms. The authors found two general mechanisms: (1) the founding clone in the primary tumor gained mutations and evolved into the relapse clone; or (2) a subclone of the founding clone survived initial therapy, gained additional mutations, and expanded at relapse. This study underscores the importance of detecting and eradicating small cellular populations after diagnosis and also after the initial treatment. The ability of next-generation sequencing to detect de novo mutations in very small cell populations makes it uniquely suited to this type of application. N Engl J Med 366: 883892 the authors used whole-exome sequencing to investigate multiple samples from spatially separated regions of primary renal carcinomas and associated metastatic sites in two patients. Gene-expression signatures of good and poor prognosis were also detected in different regions of the same tumor. This underscores the importance of early diagnosis before the mutations accumulate, as well as the need for multiple biopsy sites in larger tumors. The use of multiple samples from the same patient allows the authors to reconstruct the progression of the disease. This is a remarkably powerful approach that detected not only the trigger events, but also genes that display parallel evolution. Parallel evolution is usually an indication of genes under evolutionary pressure and it implies that those genes could be effective therapeutic targets. This implies that myelodysplastic syndrome samples contain prognostically important mutations. Sci Transl Med 4: 154ra135 7 Metastasis Metastasis is a complex process in which cancer cells break away from the primary tumor and circulate through the bloodstream or lymphatic system to other sites in the body.
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