By Jim Cassidy, Patrick Johnston, Eric Van Cutsem
Written via global specialists at the topic, this reference comprehensively covers each element of colorectal melanoma. Addressing the molecular mechanisms, genetics, identity, and remedy of affliction, this consultant covers new pharmaceutical advancements, present screening protocols, and smooth tools of illness administration via experts at popular associations comparable to the Royal Marsden health center, the Memorial Sloan Kettering melanoma middle, and the Vanderbilt-Ingram melanoma middle.
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Extra resources for Colorectal Cancer (2006)
The problem with such a situation is that there is only one risk haplotype and so ﬁne mapping of the region is problematical. However, once the causative mutation is identiﬁed, other smaller families and unselected cancer cases can be tested as a candidate colorectal cancer susceptibility gene, other than the family that has resulted in the linkage signal at the colorectal adenomata and carcinoma (CRAC) locus. Notwithstanding that some high-penetrance alleles have yet to be identiﬁed, it is likely that the majority of the unexplained genetic contribution to colorectal cancer is due to multiple low-risk alleles contributing to colorectal cancer etiology (146).
The C677T variant inﬂuences enzyme activity, while the A1298C variant may be in LD with C677T, or both may be in LD with a separate pathogenic variant (146) Thus, there is a considerable rationale for studies investigating variation in MTHFR. However, despite the substantial background rationale, the evidence to date remains inconclusive that genetic variants in MTHFR are involved in 28 Barnetson and Dunlop colorectal cancer susceptibility (155). At best, the evidence is only suggestive of a moderately reduced colorectal cancer risk associated with the 677TT genotype, especially when folate intake is high.
Further clinical studies are required to assess whether mutations in this gene predispose to other extracolonic manifestations. Clinical Management of MAP Since the identiﬁcation of MAP is so recent and there are only limited data available, it is unwise to make ﬁrm recommendations about clinical management. However, some broad conclusions can be made on the basis of ﬁndings of available studies. It is clear that the risk of colorectal cancer is very high for carriers of biallelic MYH mutations and so surveillance seems appropriate, based on experience with cancer risk reduction in FAP.