Somatic Apc mutations are selected upon their capacity to inactivate the β-catenin downregulating activity

Genes Chromosomes and Cancer

Volumn 29, Issue 3, 2000, Pages 229-239

  Smits, Ron ^a   Hofland, Nandy ^a   Edelmann, Winfried ^b   Geugien, Marjan ^a   Jagmohan Changur, Shantie ^a   Albuquerque, Cristina ^c   Breukel, Cor ^a   Kucherlapati, Raju ^b   Kielman, Menno F ^a   Fodde, Riccardo ^a  

^a LEIDEN UNIVERSITY MEDICAL CENTER   (Netherlands)

^b ALBERT EINSTEIN COLLEGE OF MEDICINE   (United States)

^c INSTITUTO PORTUGUÊS DE ONCOLOGIA DE LISBOA FRANCISCO GENTIL   (Portugal)

Author keywords

[No Author keywords available]

Indexed keywords

BETA CATENIN; DINUCLEOTIDE; DNA; POLYPEPTIDE; PROTEIN;

ADENOMATOUS POLYP; ALLELE; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CARCINOGENESIS; CODON; DOWN REGULATION; FAMILIAL POLYPOSIS; GENE; GENE MUTATION; HETEROZYGOSITY LOSS; MOUSE; NONHUMAN; PRIORITY JOURNAL; SOMATIC MUTATION;

ADENOMATOUS POLYPOSIS COLI; ANIMAL; COMPARATIVE STUDY; CYTOSKELETAL PROTEINS; DISEASE MODELS, ANIMAL; DOWN-REGULATION; FEMALE; GENES, APC; MALE; MICE; MICE, INBRED C57BL; MICE, KNOCKOUT; MUTATION; PROTO-ONCOGENE PROTEINS; SUPPORT, NON-U.S. GOV'T; SUPPORT, U.S. GOV'T, P.H.S.;

ANIMALIA; PYRONIA TITHONUS;

EID: 0033804719     PISSN: 10452257     EISSN: None     Source Type: Journal    
DOI: 10.1002/1098-2264(2000)9999:9999<::AID-GCC1033>3.0.CO;2-R     Document Type: Article

References (43)

1. Functional interaction of an axin homolog, conductin, with β-catenin, APC, and GSK3β
2. Inactivation of the mouse Msh2 gene results in mismatch repair deficiency, methylation tolerance, hyperrecombination, and predisposition to cancer
3. Mouse models for hereditary nonpolyposis colorectal cancer
4. Dominant negative effect of the APC1309 mutation: A possible explanation for genotype-phenotype correlations in familial adenomatous polyposis
5. Hereditary desmoid disease due to a frameshift mutation at codon 1924 of the APC gene
6. A targeted chain-termination mutation in the mouse Apc gene results in multiple intestinal tumors
7. Chain-terminating mutations in the APC gent lead to alterations in APC RNA and protein concentration
8. Identification and characterization of the familial adenomatous polyposis coli gene
9. Downregulation of beta-catenin by human Axin and its association with the APC tumor suppressor, beta-catenin and GSK3 beta
10. Detailed analysis of genetic alterations in colorectal tumors from patients with and without familial adenomatous polyposis (FAP)
11. Constitutive transcriptional activation by a beta-catenin-Tcf complex in APC(-/-) colon carcinoma
12. 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
13. Genetic instabilities in human cancers
14. Inactivation of both APC alleles in human and mouse tumors
15. + in intestinal adenomas from Min mice
16. Apc gene mutation is associated with a dominant-negative effect upon intestinal cell migration
17. Genotype-phenotype correlation in routine Apc mutation: Differences in enterocyte migration and response to sulindac
18. Characteristics of somatic mutation of the adenomatous polyposis coli gene in colorectal tumors
19. Somatic mutations of the APC gene in colorectal tumors: Mutation cluster region in the APC gene
20. Activation of beta-catenin-Tcf signaling in colon cancer by mutations in beta-catenin or APC
21. A dominant mutation that predisposes to multiple intestinal neoplasia in the mouse
22. Regulation of intracellular beta-catenin levels by the adenomatous polyposis coli (APC) tumor-suppressor protein
23. Axin, an inhibitor of the Wnt signaling pathway, interacts with beta-catenin, GSK-3beta and APC and reduces the beta-catenin level
24. Mutations of chromosome 5q21 genes in FAP and colorectal cancer patients
25. Loss of Apc heterozygosity and abnormal tissue building in nascent intestinal polyps in mice carrying a truncated Apc gene
26. The adenomatous polyposis coli (APC) tumor suppressor
27. APC mutations occur early during colorectal tumorigenesis
28. MSH2 deficient mice are viable and susceptible to lymphoid tumors
29. MSH2 deficiency contributes to accelerated APC-mediated intestinal tumorigenesis
30. Spontaneous intestinal carcinomas and skin neoplasms in Msh2-deficient mice
31. Association of the APC gene product with beta-catenin
32. Loss of beta-catenin regulation by the APC tumor suppressor protein correlates with loss of structure due to common somatic mutations of the gene
33. Somatic mutational mechanisms involved in intestinal tumor formation in Min mice
34. The APC gene product in normal and tumor cells
35. Loss of Apc and the entire chromosome 18 but absence of mutations at the Ras and Tp53 genes in intestinal tumors from Apc1638N, a mouse model for Apc-driven carcinogenesis
36. Apc1638N: A mouse model for familial adenomatous polyposis-associated desmoid tumors and cutaneous cysts
37. Apc1638T: A mouse model delineating critical domains of the adenomatous polyposis coli protein involved in tumorigenesis and development
38. Multiple intestinal neoplasia caused by a mutation in the murine homolog of the APC gene
39. Association of the APC tumor suppressor protein with catenins
40. Selection, the mutation rate and cancer: Ensuring that the tail does not wag the dog
41. Protein truncation test for presymptomatic diagnosis of familial adenomatous polyposis
42. Germline mutations in the 3' part of APC exon 15 do not result in truncated proteins and are associated with attenuated adenomatous polyposis coli
43. Beta-catenin: A key mediator of Wnt signaling