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Associations of Ki-ras proto-oncogene mutation and p53 gene overexpression in sporadic colorectal adenomas with demographic and clinicopathologic characteristics.

Associations of Ki-ras proto-oncogene mutation and p53 gene overexpression in sporadic colorectal adenomas with demographic and clinicopathologic characteristics. Research Abstract Details 

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  • Associations of Ki-ras proto-oncogene mutation and p53 gene overexpression in sporadic colorectal adenomas with demographic and clinicopathologic characteristics. Abstract Text:

    janine g einspahrJanine G Einspahr,maria elena martinezMaria Elena Martinez,ruiyun jiangRuiyun Jiang,chiu-hsieh hsuChiu-Hsieh Hsu,asif rashidAsif Rashid,achyut k bhattacharryaAchyut K Bhattacharrya,dennis j ahnenDennis J Ahnen,elizabeth t jacobsElizabeth T Jacobs,p scott houlihanP Scott Houlihan,c renee webbC Renee Webb,david s albertsDavid S Alberts,stanley r hamiltonStanley R Hamilton,

    In colorectal tumorigenesis, Ki-ras proto-oncogene mutation often occurs early in the adenoma-adenocarcinoma sequence, whereas mutation of the p53 gene is associated with late progression to carcinoma. We evaluated the relationship of demographic and clinicopathologic characteristics to Ki-ras mutation and p53 gene product overexpression in 1,093 baseline sporadic colorectal adenomas from 926 individuals enrolled in a phase III recurrence prevention trial. Ki-ras mutation was found in 14.7% of individuals and p53 overexpression was found in 7.0% of those tested. Multivariate analysis found older age, rectal location, and villous histology to be independently associated with Ki-ras mutation. Individuals with an advanced adenoma (>or=1 cm or high-grade dysplasia or villous histology) had a 4-fold higher likelihood of Ki-ras mutation [odds ratios (OR), 3.96; 95% confidence intervals (CI), 2.54-6.18]. Ki-ras mutations in codon 12 and of the G-to-A transition type were more frequent in older individuals, whereas G-to-T transversion was more frequent in rectal adenomas than in the colon. Multivariate analysis showed that previous history of a polyp (P = 0.03) was inversely associated with p53 overexpression. Large adenoma size (>or=1 cm), high-grade dysplasia, and villous histology were independently associated with p53 overexpression, with the strongest association for advanced adenomas (OR, 7.20; 95% CI, 3.01-17.22). Individuals with a Ki-ras mutated adenoma were more likely to overexpress p53 (OR, 2.46; 95% CI, 1.36-4.46), and 94.8% of adenomas with both alterations were classified as advanced (P

    Associations of Ki-ras proto-oncogene mutation and p53 gene overexpression in sporadic colorectal adenomas with demographic and clinicopathologic characteristics. Publishing Authors By Initials

    jg einspahrJG Einspahr,me martinezME Martinez,r jiangR Jiang,ch hsuCH Hsu,a rashidA Rashid,ak bhattacharryaAK Bhattacharrya,dj ahnenDJ Ahnen,et jacobsET Jacobs,ps houlihanPS Houlihan,cr webbCR Webb,ds albertsDS Alberts,sr hamiltonSR Hamilton,

    For similar abstracts research abstracts see: abstracts research

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    Associations of Ki-ras proto-oncogene mutation and p53 gene overexpression in sporadic colorectal adenomas with demographic and clinicopathologic characteristics. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: Cancer epidemiology, biomarkers & prevention : a p

    VOLUME: 15

    Page Numbers: 1443-50

    Journal Abbreviation:

    ISSN: 1055-9965

    DAY: 3

    MONTH: Aug

    YEAR: 2006

    Associations of Ki-ras proto-oncogene mutation and p53 gene overexpression in sporadic colorectal adenomas with demographic and clinicopathologic characteristics. Information

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    LANGUAGE: eng

    NlmUniqueID: 9200608

    Associations of Ki-ras proto-oncogene mutation and p53 gene overexpression in sporadic colorectal adenomas with demographic and clinicopathologic characteristics. Keywords Mesh Terms:

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    Grant and Affiliation Information for Associations of Ki-ras proto-oncogene mutation and p53 gene overexpression in sporadic colorectal adenomas with demographic and clinicopathologic characteristics.

    AFFILIATION: Department of Medicine, Arizona Cancer Center, P.O. Box 245024, Tucson, AZ 85724, USA. jeinspahr@azcc.arizona.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Cancer Epidemiol Biomarkers Pr

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