p53 Point mutations in dysplastic and cancerous ulcerative colitis lesions

Yin, Jing; Harpaz, Noam; Tong, Yi; Huang, Ying; Laurin, Jacqueline; Greenwald, Bruce D.; Hontanosas, M.; Newkirk, Carnell; Meltzer, Stephen J.

doi:10.1016/0016-5085(93)90639-t

Cited by 217 publications

(114 citation statements)

References 24 publications

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“…Consistently, several studies have reported that genetic aberrations are frequently detected in non-tumorous inflamed epithelial tissues where the risk of cancer development is remarkably high [38][39][40] . For example, TP53 mutations are detected in the inflamed mucosa of the colonic epithelium of patients with inflammatory bowel disease 41,42 . A recent sequencing study on Barrett's esophagus revealed that the mutational profiles of Barrett's esophagus and esophageal adenocarcinoma are remarkably similar, suggesting that genetic alterations in the metaplasia-carcinoma sequence of Barrett's esophagus occur much earlier than the histologic changes of frank dysplasia 40 .…”

Section: Discussionmentioning

confidence: 99%

Accumulation of Somatic Mutations in TP53 in Gastric Epithelium With Helicobacter pylori Infection

et al. 2014

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Section: Discussionmentioning

confidence: 99%

Accumulation of Somatic Mutations in TP53 in Gastric Epithelium With Helicobacter pylori Infection

et al. 2014

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“…Relative allelic loss of 18q is found in dysplastic and non-dysplastic epithelium [24]. Inactivation of p53 by mutation and LOH is a common mechanism of malignant transformation in UC that, unlike SCRC, occurs relatively early, non-invasive stage [28,29]. In UC, single base miss-sense mutations in p53 that lead to amino acid substitutions as well as two 5-base micro-deletions at codon 287-288 lead to a frame shift and premature stop codon downstream [29].…”

Section: Discussionmentioning

confidence: 99%

“…Inactivation of p53 by mutation and LOH is a common mechanism of malignant transformation in UC that, unlike SCRC, occurs relatively early, non-invasive stage [28,29]. In UC, single base miss-sense mutations in p53 that lead to amino acid substitutions as well as two 5-base micro-deletions at codon 287-288 lead to a frame shift and premature stop codon downstream [29]. Other mutations in specific codons such as codon 248 are not only present in cancer/dysplasia but in histologically non-dysplastic/indefinite epithelium as well [26].…”

Section: Discussionmentioning

confidence: 99%

“…Mutations in p53 precede LOH and may be a relatively earlier genetic event in the process of CC that contributes to initial survival advantage, as with SCRC, LOH appears to be a late event in tumorigenesis [28]. P53 mutations are preserved from primary tumor to lymph node metastasis indicating that the mutation maintains malignant phenotype [29]. Unlike non-CC, the role of MSI in CC is not well defined [28].…”

Section: Discussionmentioning

confidence: 99%

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Ulcerative colitis and cancer

Kulaylat

Dayton

2010

Journal of Surgical Oncology

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Patients with ulcerative colitis (UC) are at an increased risk for the development of colorectal cancer (CRC). Unlike sporadic CRC, the cancer in UC patients arises from a focal or multifocal dysplastic mucosa in areas of inflammation. The clinical features of UC-associated cancer are similar to those found in patients with hereditary non-polyposis colorectal cancer. As with other varieties of CRC, UC-associated cancer exhibits a variety of genetic and molecular changes/abnormalities. These abnormalities are however clustered in areas of mucosae with histological abnormalities. The magnitude and timing of these changes are however significantly different. Surveillance and identification of patients at risk for cancer are a challenging problem.

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“…Screening patients for K-ra.v mutations combined with another genetic marker, such as the p53 oncosuppressor gene (10)(11)(12). may cluster patients with UC and Crohn's disease into subpopulations of increased risk for the development of colon cancer.…”

Section: Discussionmentioning

confidence: 99%

Activating Mutations in the K-Ras Gene in Ulcerative-Colitis and Crohns-Disease

et al. 1994

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Abstract. Patients with ulcerative colitis (UC) and Crohn's disease have an increased risk for developing cancer of the colon. Mutations in the K-ras gene are relatively frequent in specimens from patients with sporadic colon cancer, but less frequent in cases of cancer complicating ulcerative colitis. In order to study the problem further we used the polymerase chain reaction (PCR) technique followed by a restriction fragment length polymorphism (RFLP) assay, to detect mutations at codon 12 of K-ras in biopsy specimens from patients with UC or Crohn's disease. Six among 27 patients (22.2%) with UC and 2 of the 19 patients (10.5%) with Crohn's disease examined, carried a mutation at codon 12 of K-ras. Our results indicate that mutations in K-ras may be a genetic marker that would reveal the predisposition to colon cancer among this group of patients.

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p53 Point mutations in dysplastic and cancerous ulcerative colitis lesions

Cited by 217 publications

References 24 publications

Accumulation of Somatic Mutations in TP53 in Gastric Epithelium With Helicobacter pylori Infection

Accumulation of Somatic Mutations in TP53 in Gastric Epithelium With Helicobacter pylori Infection

Ulcerative colitis and cancer

Activating Mutations in the K-Ras Gene in Ulcerative-Colitis and Crohns-Disease

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