• Publications
  • Influence
Genetic alterations during colorectal-tumor development.
TLDR
It is found that ras-gene mutations occurred in 58 percent of adenomas larger than 1 cm and in 47 percent of carcinomas, which are consistent with a model of colorectal tumorigenesis in which the steps required for the development of cancer often involve the mutational activation of an oncogene coupled with the loss of several genes that normally suppress tumors.
The SLUG zinc-finger protein represses E-cadherin in breast cancer.
TLDR
Analysis of the expression patterns of SLUG, SNAIL, and E-cadherin in breast cancer cell lines demonstrated that expression of SLug was strongly correlated with loss of E- cadheringin transcripts, and the data indicate the E-box elements in the proximal E-Cadher in promoter are critical in transcriptional repression of the E -cadhersin gene.
Molecular genetics of colorectal cancer.
  • E. Fearon
  • Biology
    Annual review of pathology
  • 24 January 2011
TLDR
The gene defects in CRC often target proteins and pathways that exert pleiotropic effects on the cancer cell phenotype, and particular genetic and epigenetic alterations are linked to biologically and clinically distinct subsets of CRC.
Mitogenic Signaling Mediated by Oxidants in Ras-Transformed Fibroblasts
TLDR
H-RasV12-induced transformation can lead to the production of ·O2− through one or more pathways involving a flavoprotein and Rac1, suggesting a possible mechanism for the effects of antioxidants against Ras-induced cellular transformation.
Suppression of human colorectal carcinoma cell growth by wild-type p53.
TLDR
It is shown that the wild-type gene can specifically suppress the growth of human colorectal carcinoma cells in vitro and that an in vivo-derived mutation resulting in a single conservative amino acid substitution in the p53 gene product abrogates this suppressive ability.
Identification of a chromosome 18q gene that is altered in colorectal cancers.
TLDR
A contiguous stretch of DNA comprising 370 kilobase pairs has now been cloned from a region of chromosome 18q suspected to reside near the DCC gene, which may play a role in the pathogenesis of human colorectal neoplasia, perhaps through alteration of the normal cell-cell interactions controlling growth.
Adenoma-linked barrier defects and microbial products drive IL-23/IL-17-mediated tumour growth
TLDR
It is proposed that barrier deterioration induced by colorectal-cancer-initiating genetic lesions results in adenoma invasion by microbial products that trigger tumour-elicited inflammation, which in turn drives tumour growth.
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