Colorectal cancer and genetic alterations in the Wnt pathway

[1]  M. Fraga,et al.  Epigenetic inactivation of the Wnt antagonist DICKKOPF-1 (DKK-1) gene in human colorectal cancer , 2006, Oncogene.

[2]  J. Behrens,et al.  Truncated APC is required for cell proliferation and DNA replication , 2006, International journal of cancer.

[3]  N. Reguart,et al.  Wnt inhibitory factor-1, a Wnt antagonist, is silenced by promoter hypermethylation in malignant pleural mesothelioma. , 2006, Biochemical and biophysical research communications.

[4]  O. Sieber,et al.  Disease severity and genetic pathways in attenuated familial adenomatous polyposis vary greatly but depend on the site of the germline mutation , 2006, Gut.

[5]  W. Foulkes,et al.  Familial Adenomatous Polyposis , 2006, The American Journal of Gastroenterology.

[6]  Andrew J. Wilson,et al.  Mechanisms of inactivation of the receptor tyrosine kinase EPHB2 in colorectal tumors. , 2005, Cancer research.

[7]  D. Chung,et al.  Oncogenic K-ras stimulates Wnt signaling in colon cancer through inhibition of GSK-3beta. , 2005, Gastroenterology.

[8]  J Martin,et al.  Exon 3 β-catenin mutations are specifically associated with colorectal carcinomas in hereditary non-polyposis colorectal cancer syndrome , 2005, Gut.

[9]  I. Tomlinson,et al.  Evidence for genetic predisposition to desmoid tumours in familial adenomatous polyposis independent of the germline APC mutation , 2004, Gut.

[10]  Bruce Winney,et al.  Multiple rare variants in different genes account for multifactorial inherited susceptibility to colorectal adenomas. , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[11]  I. Thesleff,et al.  Mutations in AXIN2 cause familial tooth agenesis and predispose to colorectal cancer. , 2004, American journal of human genetics.

[12]  Wei Dong Chen,et al.  Epigenetic inactivation of SFRP genes allows constitutive WNT signaling in colorectal cancer , 2004, Nature Genetics.

[13]  Yvonne Wallis,et al.  The Wnt Antagonist sFRP1 in Colorectal Tumorigenesis , 2004, Cancer Research.

[14]  L. Lipton,et al.  Refining the relation between ‘first hits’ and ‘second hits’ at the APC locus: the ‘loose fit’ model and evidence for differences in somatic mutation spectra among patients , 2003, Oncogene.

[15]  L. Lipton,et al.  Colorectal tumourigenesis in carriers of the APC I1307K variant: lone gunman or conspiracy? , 2003, The Journal of pathology.

[16]  R. Houlston,et al.  Explaining variation in familial adenomatous polyposis: relationship between genotype and phenotype and evidence for modifier genes , 2002, Gut.

[17]  R. Fodde,et al.  The 'just-right' signaling model: APC somatic mutations are selected based on a specific level of activation of the beta-catenin signaling cascade. , 2002, Human molecular genetics.

[18]  I. Tomlinson,et al.  Mutation cluster region, association between germline and somatic mutations and genotype-phenotype correlation in upper gastrointestinal familial adenomatous polyposis. , 2002, The American journal of pathology.

[19]  L. Lipton,et al.  Whole-gene APC deletions cause classical familial adenomatous polyposis, but not attenuated polyposis or “multiple” colorectal adenomas , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[20]  Alison L. Livingston,et al.  Inherited variants of MYH associated with somatic G:C→T:A mutations in colorectal tumors , 2002, Nature Genetics.

[21]  T. Asahara,et al.  Frequent alterations in the Wnt signaling pathway in colorectal cancer with microsatellite instability , 2002, Genes, chromosomes & cancer.

[22]  I. Tomlinson,et al.  Variability in the severity of colonic disease in familial adenomatous polyposis results from differences in tumour initiation rather than progression and depends relatively little on patient age , 2001, Gut.

[23]  W F Bodmer,et al.  The ABC of APC. , 2001, Human molecular genetics.

[24]  M. Leppert,et al.  A molecular variant of the APC gene at codon 1822: its association with diet, lifestyle, and risk of colon cancer. , 2001, Cancer research.

[25]  C. J. Barnes,et al.  Inactivation of germline mutant APC alleles by attenuated somatic mutations: a molecular genetic mechanism for attenuated familial adenomatous polyposis. , 2000, American journal of human genetics.

[26]  J. Herman,et al.  Analysis of adenomatous polyposis coli promoter hypermethylation in human cancer. , 2000, Cancer research.

[27]  T. Dale,et al.  Sequence variants of the axin gene in breast, colon, and other cancers: An analysis of mutations that interfere with GSK3 binding , 2000, Genes, chromosomes & cancer.

[28]  G. Thomas,et al.  The human T-cell transcription factor-4 gene: structure, extensive characterization of alternative splicings, and mutational analysis in colorectal cancer cell lines. , 2000, Cancer research.

[29]  Ian Tomlinson,et al.  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 , 1999, Nature Medicine.

[30]  R Kucherlapati,et al.  Apc1638T: a mouse model delineating critical domains of the adenomatous polyposis coli protein involved in tumorigenesis and development. , 1999, Genes & development.

[31]  M. von Knebel Doeberitz,et al.  Dominant negative effect of the APC1309 mutation: a possible explanation for genotype-phenotype correlations in familial adenomatous polyposis. , 1999, Cancer research.

[32]  S. Gallinger,et al.  Inherited colorectal polyposis and cancer risk of the APC I1307K polymorphism. , 1999, American journal of human genetics.

[33]  M. Leppert,et al.  Alleles of APC modulate the frequency and classes of mutations that lead to colon polyps , 1998, Nature Genetics.

[34]  W F Bodmer,et al.  The APC variants I1307K and E1317Q are associated with colorectal tumors, but not always with a family history. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[35]  P. Polakis,et al.  Loss of beta-catenin regulation by the APC tumor suppressor protein correlates with loss of structure due to common somatic mutations of the gene. , 1997, Cancer research.

[36]  H. Ostrer,et al.  Familial colorectal cancer in Ashkenazim due to a hypermutable tract in APC , 1997, Nature Genetics.

[37]  W F Bodmer,et al.  Beta-catenin mutations in cell lines established from human colorectal cancers. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[38]  Hans Clevers,et al.  Activation of β-Catenin-Tcf Signaling in Colon Cancer by Mutations in β-Catenin or APC , 1997, Science.

[39]  W. Bodmer,et al.  Phenotypic expression in familial adenomatous polyposis: partial prediction by mutation analysis. , 1994, Gut.

[40]  G. Thomas,et al.  Alleles of the APC gene: An attenuated form of familial polyposis , 1993, Cell.

[41]  S Ichii,et al.  Somatic mutations of the APC gene in colorectal tumors: mutation cluster region in the APC gene. , 1992, Human molecular genetics.

[42]  S. Bülow,et al.  Attenuated familial adenomatous polyposis (AFAP): a review of the literature , 2004, Familial Cancer.

[43]  David I. Smith,et al.  Mutations in AXIN2 cause colorectal cancer with defective mismatch repair by activating beta-catenin/TCF signalling (vol 26, pg 146, 2000) , 2000 .

[44]  Thierry Soussi,et al.  APC gene: database of germline and somatic mutations in human tumors and cell lines , 1996, Nucleic Acids Res..