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- W2085653208 abstract "Colorectal cancer (CRC) is one of the most common malignancies with high prevalence and low 5-year survival. CRC is a heterogeneous disease with a complex, genetic and biochemical background. It is now generally accepted that a few important intracellular signaling pathways, including Wnt/β-catenin signaling, Ras signaling, and p53 signaling are frequently dysregulated in CRC. Patients with mutant p53 gene are often resistant to current therapies, conferring poor prognosis. Tumor suppressor p53 protein is a transcription factor inducing cell cycle arrest, senescence, and apoptosis under cellular stress. Emerging evidence from laboratories and clinical trials shows that some small molecule inhibitors exert anti-cancer effect via reactivation and restoration of p53 function. In this review, we summarize the p53 function and characterize its mutations in CRC. The involvement of p53 mutations in pathogenesis of CRC and their clinical impacts will be highlighted. Moreover, we also describe the current achievements of using p53 modulators to reactivate this pathway in CRC, which may have great potential as novel anti-cancer therapy." @default.
- W2085653208 created "2016-06-24" @default.
- W2085653208 creator A5035638353 @default.
- W2085653208 creator A5045967361 @default.
- W2085653208 creator A5075282975 @default.
- W2085653208 creator A5086827787 @default.
- W2085653208 date "2015-01-01" @default.
- W2085653208 modified "2023-10-14" @default.
- W2085653208 title "<i>p53</i>mutations in colorectal cancer- molecular pathogenesis and pharmacological reactivation" @default.
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- W2085653208 doi "https://doi.org/10.3748/wjg.v21.i1.84" @default.
- W2085653208 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/4284363" @default.
- W2085653208 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/25574081" @default.
- W2085653208 hasPublicationYear "2015" @default.