Carcinogenesis in IBD: potential targets for the prevention of colorectal cancer
被引:242
作者:
Feagins, Linda A.
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机构:
Dallas Vet Affairs Med Ctr, Div Gastroenterol 111B1, Dallas, TX 75216 USA
Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USADallas Vet Affairs Med Ctr, Div Gastroenterol 111B1, Dallas, TX 75216 USA
Feagins, Linda A.
[1
,2
]
Souza, Rhonda F.
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机构:
Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USADallas Vet Affairs Med Ctr, Div Gastroenterol 111B1, Dallas, TX 75216 USA
Souza, Rhonda F.
[2
]
Spechler, Stuart J.
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机构:
Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USADallas Vet Affairs Med Ctr, Div Gastroenterol 111B1, Dallas, TX 75216 USA
Spechler, Stuart J.
[2
]
机构:
[1] Dallas Vet Affairs Med Ctr, Div Gastroenterol 111B1, Dallas, TX 75216 USA
[2] Univ Texas SW Med Ctr Dallas, Dallas, TX 75390 USA
In patients with IBD, chronic colonic inflammation increases the risk of colorectal cancer, perhaps because inflammation predisposes these tissues to genomic instability. Carcinogenesis in the inflamed colon seems to follow a different sequence of genetic alterations than that observed in sporadic cancers in the uninflamed colon. in this review, we focus on the genetic alterations in colitis-associated colorectal cancer that contribute to the acquisition of the essential hallmarks of cancer, and on how those alterations differ from sporadic colorectal cancers. Our intent is to provide a conceptual basis for categorizing carcinogenetic molecular abnormalities in IBD, and for understanding how cancer-preventive therapies might target reversal of acquired abnormalities in specific biochemical pathways.