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10.28092/j.issn.2095-3941.2015.0103 http://scihub22266oqcxt.onion/10.28092/j.issn.2095-3941.2015.0103 C4850121!4850121!27144067     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cancer+Biol+Med 2016 ; 13 (1): 120-35 Nephropedia Template TP {{tp|p=27144067|t=2016. Colorectal cancer carcinogenesis: a review of mechanisms |pdf=|usr=}}{{27144067}} gab.com Text Colorectal cancer carcinogenesis: a review of mechanisms JO: Cancer Biol Med http://www.kidney.de/pget.php?&tw=1&pmid=27144067 #FOAvip Colorectal cancer (CRC) is the second most common cancer in women and the third most common in men globally. CRC arises from one or a combination of chromosomal instability, CpG island methylator phenotype, and microsatellite instability. Genetic instability is usually caused by aneuploidy and loss of heterozygosity. Mutations in the tumor suppressor or cell cycle genes may also lead to cellular transformation. Similarly, epigenetic and/or genetic alterations resulting in impaired cellular pathways, such as DNA repair mechanism, may lead to microsatellite instability and mutator phenotype. Non-coding RNAs, more importantly microRNAs and long non-coding RNAs have also been implicated at various CRC stages. Understanding the specific mechanisms of tumorigenesis and the underlying genetic and epigenetic traits is critical in comprehending the disease phenotype. This paper reviews these mechanisms along with the roles of various non-coding RNAs in CRCs. Twit Text FOAVip Colorectal cancer carcinogenesis: a review of mechanisms ????Cancer Biol Med http://www.kidney.de/pget.php?&tw=1&pmid=27144067 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27144067 #FOAvip English Wikipedia <ref>{{Cite pmid|27144067}}</ref> Colorectal cancer carcinogenesis: a review of mechanisms #MMPMID27144067 Tariq K; Ghias K Cancer Biol Med 2016[Mar]; 13 (1): 120-35 PMID27144067show ga Colorectal cancer (CRC) is the second most common cancer in women and the third most common in men globally. CRC arises from one or a combination of chromosomal instability, CpG island methylator phenotype, and microsatellite instability. Genetic instability is usually caused by aneuploidy and loss of heterozygosity. Mutations in the tumor suppressor or cell cycle genes may also lead to cellular transformation. Similarly, epigenetic and/or genetic alterations resulting in impaired cellular pathways, such as DNA repair mechanism, may lead to microsatellite instability and mutator phenotype. Non-coding RNAs, more importantly microRNAs and long non-coding RNAs have also been implicated at various CRC stages. Understanding the specific mechanisms of tumorigenesis and the underlying genetic and epigenetic traits is critical in comprehending the disease phenotype. This paper reviews these mechanisms along with the roles of various non-coding RNAs in CRCs. äColorectal cancer carcinogenesis: a review of mechanisms (epmc).pdf DeepDyve Pubget Overpricing