Multistep progression of colorectal cancer in the setting of microsatellite instability: New details and novel insights

Gastroenterology

Volumn 121, Issue 6, 2001, Pages 1497-1501

  Goel, Ajay ^a   Arnold, Christian N ^a   Boland, C Richard ^a  

^a UNIVERSITY OF CALIFORNIA   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

MICROSATELLITE DNA;

CARCINOGENESIS; COLORECTAL CANCER; COLORECTAL TUMOR; CPG ISLAND; DNA METHYLATION; DNA REPAIR; DNA SEQUENCE; EDITORIAL; GENE MUTATION; GENE SILENCING; GENETIC MODEL; HETEROZYGOSITY LOSS; MICROSATELLITE INSTABILITY; ONCOGENE K RAS; PHENOTYPE; PRIORITY JOURNAL; PROMOTER REGION; STOMACH POLYP; TRANSACTIVATION; TUMOR SUPPRESSOR GENE; X CHROMOSOME;

EID: 0035214221     PISSN: 00165085     EISSN: None     Source Type: Journal    
DOI: 10.1053/gast.2001.29978     Document Type: Article

References (40)

1. Genetic alterations during colorectal-tumor development
2. Evidence that genetic instability occurs at an early stage of colorectal tumorigenesis
3. Mutator phenotype may be required for multistage carcinogenesis
4. Genetic instabilities in human cancers
5. Extensive methylation of hMLH1 promoter region predominates in proximal colon cancer with microsatellite instability
6. Wnt1 inducible signaling pathway protein 3, WISP-3, a novel target gene in colorectal carcinomas with microsatellite instability
7. A genetic model for colorectal tumorigenesis
8. Genetic mapping of a locus predisposing to human colorectal cancer
9. Ubiquitous somatic mutations in simple repeated sequences reveal a new mechanism for colonic carcinogenesis
10. Microsatellite instability in cancer of the proximal colon
11. Hereditary nonpolyposis colorectal cancer: The syndrome, the genes, and historical perspectives
12. A role for MLH3 in hereditary nonpolyposis colorectal cancer
13. Methylation of the hMLH1 promoter correlates with lack of expression of hMLH1 in sporadic colon tumors and mismatch repair-defective human tumor cell lines
14. Incidence and functional consequences of hMLH1 promoter hypermethylation in colorectal carcinoma
15. Hypermethylation of the hMLH1 promoter in colon cancer with microsatellite instability
16. Steadystate regulation of the human DNA mismatch repair system
17. Microsatellites in the eukaryotic DNA mismatch repair genes as modulators of evolutionary mutation rate
18. Genetic instability occurs in the majority of young patients with colorectal cancer
19. The role of hypermethylation of the hMLH1 promoter region in HNPCC versus MSI+ sporadic colorectal cancers
20. Biallelic inactivation of hMLH1 by epigenetic gene silencing, a novel mechanism causing human MSI cancers
21. CpG island methylator phenotype in colorectal cancer
22. Aberrant methylation of gene promoters in cancer-concepts, misconcepts, and promise
23. Cancer epigenetics comes of age
24. Epigenetic phenotypes distinguish microsatellite-stable and -unstable colorectal cancers
25. Methylation of CpG in a small region of the hMLH1 promoter invariably correlates with the absence of gene expression
26. Detection of aberrantly methylated hMLH1 promoter DNA in the serum of patients with microsatellite unstable colon cancer
27. Methylation pattern of different regions of the MLH1 promoter and silencing of gene expression in hereditary and sporadic colorectal cancer
28. Hypermutability and mismatch repair deficiency in RER+ tumor cells
29. Human chromosome 3 corrects mismatch repair deficiency and microsatellite instability and reduces N-methyl-N′-nitro-N- nitrosoguanidine tolerance in colon tumor cells with homozygous hMLH1 mutation
30. Evidence for a connection between the mismatch repair system and the G2 cell cycle checkpoint
31. Involvement of PTEN mutations in the genetic pathways of colorectal cancerogenesis
32. Inactivation of the type II TGF-beta receptor in colon cancer cells with microsatellite instability
33. Microsatellite instability in the insulin-like growth factor II receptor gene in gastrointestinal tumours
34. Somatic frameshift mutations in the BAX gene in colon cancers of the microsatellite mutator phenotype
35. Frameshift mutations at mononucleotide repeats in caspase-5 and other target genes in endometrial and gastrointestinal cancer of the microsatellite mutator phenotype
36. Frameshift mutator mutations
37. Frequent frameshift mutations of the TCF-4 gene in colorectal cancers with microsatellite instability
38. Instabilotyping: Comprehensive identification of frameshift mutations caused by coding region microsatellite instability
39. WISP-1 is a Wnt-1- and beta-catenin-responsive oncogene
40. WISP genes are members of the connective tissue growth factor family that are up-regulated in wnt-l-transformed cells and aberrantly expressed in human colon tumors