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...

Bibliografski detalji
Glavni autori:	Lamlum, H, Papadopoulou, A, Ilyas, M, Rowan, A, Gillet, C, Hanby, A, Talbot, I, Bodmer, W, Tomlinson, I
Format:	Journal article
Jezik:	English
Izdano:	2000

Slični predmeti

APC mutations in sporadic colorectal tumors: A mutational "hotspot" and interdependence of the "two hits".
od: Rowan, A, i dr.
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Defects in mismatch repair occur after APC mutations in the pathogenesis of sporadic colorectal tumours.
od: Homfray, T, i dr.
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Analysis of chromosomal instability in human colorectal adenomas with two mutational hits at APC.
od: Sieber, O, i dr.
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Germline APC variants in patients with multiple colorectal adenomas, with evidence for the particular importance of E1317Q.
od: Lamlum, H, i dr.
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Investigation of pathogenic mechanisms in multiple colorectal adenoma patients without germline APC or MYH/MUTYH mutations.
od: Thirlwell, C, i dr.
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Whole-gene APC deletions cause classical familial adenomatous polyposis, but not attenuated polyposis or "multiple" colorectal adenomas
od: Sieber, O, i dr.
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Whole-gene APC deletions cause classical familial adenomatous polyposis, but not attenuated polyposis or "multiple" colorectal adenomas.
od: Sieber, O, i dr.
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Allele loss, replication errors and loss of expression of E-cadherin in colorectal cancers.
od: Ilyas, M, i dr.
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The type of somatic mutation at APC in familial adenomatous polyposis is determined by the site of the germline mutation: a new facet to Knudson's 'two-hit' hypothesis.
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Bcl-2 expression in colorectal tumors: evidence of different pathways in sporadic and ulcerative-colitis-associated carcinomas.
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Location in the large bowel influences the APC mutations observed in FAP adenomas.
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Frequency of germline hereditary non-polyposis colorectal cancer gene mutations in patients with multiple or early onset colorectal adenomas.
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Clinico-pathological features and p53 expression in left-sided sporadic colorectal cancers with and without microsatellite instability.
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APC protein immunoexpression in colorectal adenoma and adenocarcinoma
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Genetic basis of variation in adenoma multiplicity in ApcMin/+ Mom1S mice.
od: Haines, J, i dr.
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The spectrum of p53 mutations in colorectal adenomas differs from that in colorectal carcinomas.
od: Hao, X, i dr.
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Beta-catenin mutations in cell lines established from human colorectal cancers.
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The low frequency of beta-catenin mutations in cell lines established from human colorectal cancers
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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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Molecular characteristics of serrated adenomas of the colorectum.
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Beta-catenin expression and allelic loss at APC in sporadic colorectal carcinogenesis.
od: Hao, X, i dr.
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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.
od: Frayling, I, i dr.
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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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od: Lewis, A, i dr.
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The C-terminus of Apc does not influence intestinal adenoma development or progression.
od: Lewis, A, i dr.
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Five quantitative trait loci control radiation-induced adenoma multiplicity in Mom1R Apc Min/+ mice.
od: Elahi, E, i dr.
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Five quantitative trait loci control radiation-induced adenoma multiplicity in Mom 1R ApcMin/+ mice
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Putative direct and indirect Wnt targets identified through consistent gene expression changes in APC-mutant intestinal adenomas from humans and mice.
od: Segditsas, S, i dr.
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The interactions of APC, E-cadherin and beta-catenin in tumour development and progression.
od: Ilyas, M, i dr.
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O(6)-methylguanine methyltransferase in colorectal cancers: detection of mutations, loss of expression, and weak association with G:C>A:T transitions.
od: Halford, S, i dr.
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Germline epimutations of APC are not associated with inherited colorectal polyposis.
od: Hitchins, M, i dr.
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Bottom-up histogenesis of colorectal adenomas: origin in the monocryptal adenoma and initial expansion by crypt fission.
od: Preston, S, i dr.
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Using somatic APC mutations as clonal markers in colonic polyps
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Statin Treatment as a Targeted Therapy for APC-Mutated Colorectal Cancer
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Heterozygous APC germline mutations impart predisposition to colorectal cancer
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