APC mutations are sufficient for the growth of early colorectal adenomas.

APC mutations are sufficient for the growth of early colorectal adenomas.

It is not clear whether APC mutations are sufficient for early colorectal adenomas to grow or whether additional mutations at other loci are required. We previously have screened 210 early colorectal adenomas from familial adenomatous polyposis patients for mutations and allelic loss at APC. Here, w...

وصف كامل

التفاصيل البيبلوغرافية
المؤلفون الرئيسيون:	Lamlum, H, Papadopoulou, A, Ilyas, M, Rowan, A, Gillet, C, Hanby, A, Talbot, I, Bodmer, W, Tomlinson, I
التنسيق:	Journal article
اللغة:	English
منشور في:	2000

مواد مشابهة

APC mutations in sporadic colorectal tumors: A mutational "hotspot" and interdependence of the "two hits".
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Analysis of chromosomal instability in human colorectal adenomas with two mutational hits at APC.
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Germline APC variants in patients with multiple colorectal adenomas, with evidence for the particular importance of E1317Q.
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Investigation of pathogenic mechanisms in multiple colorectal adenoma patients without germline APC or MYH/MUTYH mutations.
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Whole-gene APC deletions cause classical familial adenomatous polyposis, but not attenuated polyposis or "multiple" colorectal adenomas
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Whole-gene APC deletions cause classical familial adenomatous polyposis, but not attenuated polyposis or "multiple" colorectal adenomas.
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APC mutation spectrum in ileoanal pouch polyps resembles that of colorectal polyps.
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Loss of heterozygosity at APC and beta-catenin expression in sporadic colorectal carcinogenesis
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Association between cigarette smoking, <it>APC </it>mutations and the risk of developing sporadic colorectal adenomas and carcinomas
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Reduced expression of molecules of the cadherin/catenin complex in the transition from colorectal adenoma to carcinoma.
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The APC variants I1307K and E1317Q are associated with colorectal tumors, but not always with a family history.
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Colorectal tumors from APC*I1307K carriers principally harbor somatic APC mutations outside the A8 tract
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Promoter hypermethylation leads to decreased APC mRNA expression in familial polyposis and sporadic colorectal tumours, but does not substitute for truncating mutations.
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Germline epimutations of APC are not associated with inherited colorectal polyposis.
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Bottom-up histogenesis of colorectal adenomas: origin in the monocryptal adenoma and initial expansion by crypt fission.
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