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oai:recercat.cat:2445/1535582025-12-05T09:21:26Zcom_2072_1057col_2072_478799col_2072_478917
RECERCAT author Yamamoto, Hidemi S. author Gil Santano, Juan author Schwartz Navarro, Simó author Perucho, Manuel 2020-03-24T10:00:20Z2020-03-24T10:00:20Z2000-02-012020-03-24T10:00:20Z Dear Editor, in a letter to the editor in a recent issue of Cell Death and Differentiation, Abdel-Rahman et al1. reported the absence of mutations in the death pathways gene Fas (Apo-1/CD95) in colorectal carcinomas. From the absence of mutations in 24 colon cancers, 12 of which were classified as replication error positive (RER+), Abdel-Rahman et al1. concluded that such mutations confer no substantial growth advantage in colorectal carcinogenesis. In agreement with this report, we identified Fas mutations in only 10% of colon and gastric cancers of the microsatellite mutator phenotype (MMP), also denominated as RER or microsatellite instability (MSI). Mutations were also found in Apaf-1 and Bcl-10, two other genes involved in the cell death pathways. The mutations were detected in mononucleotide tracts within these three genes (Figure 1). The frequency of these frameshift mutations was low (Table 1) and they appeared to be heterozygous (Figure 2). However, considering the peculiar features of these tumors, we suggest that these frameshift mutations contribute to cancer progression by providing survival advantage. (c) Yamamoto, Hidemi S. et al., 2000 info:eu-repo/semantics/openAccess Proteïnes Transducció de senyal cel·lular Càncer gastrointestinal Genètica Proteins Cellular signal transduction Gastrointestinal cancer Genetics Frameshift mutations in Fas, Apaf-1, and Bcl-10 in gastro-intestinal cancer of the microsatellite mutator phenotype info:eu-repo/semantics/article info:eu-repo/semantics/acceptedVersion