Is the development of adenoma and carcinoma in proximal colon related to apolipoprotein E phenotype?

Kervinen, Kari; Södervik, Hannu; Mäkelä, Jyrki; Lehtola, J; Niemi, Mari; Kairaluoma, Matti I.; Ya, Kesäniemi

doi:10.1053/gast.1996.v110.pm8964404

Cited by 58 publications

(60 citation statements)

References 2 publications

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“…(32) In a case-control study, lower levels of serum total and LDL cholesterol were observed in cases of proximal colon cancer alone than in controls. (33) In that study, individuals with the E4 allele for apolipoprotein E, in whom bile acid synthesis is decreased, (34) had a lower risk of proximal colon cancer and adenomas.…”

Section: Discussionmentioning

confidence: 87%

Genetic polymorphism of cholesterol 7α‐hydroxylase (CYP7A1) and colorectal adenomas: Self Defense Forces Health Study

et al. 2006

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Bile acids have long been implicated in colorectal carcinogenesis, but epidemiological evidence is limited. Cholesterol 7α α α α-hydroxylase (CYP7A1) is the rate-limiting enzyme producing bile acids from cholesterol. A recent case-control study showed a decreased risk of proximal colon cancer associated with the CC genotype of the CYP7A1 A-203C polymorphism. The present study examined the relationship between the CYP7A1 A-203C polymorphism and colorectal adenoma, which is a well-established precursor lesion of colorectal cancer. The study subjects comprised 446 cases of colorectal adenomas and 914 controls of normal total colonoscopy among men receiving a preretirement health examination at two hospitals of the Self Defense Forces (SDF). The CYP7A1 genotype was determined by the polymerase chain reaction-restriction fragment length polymorphism method. Statistical adjustment was made for age, hospital, rank in the SDF, smoking, alcohol use, body mass index, physical activity and parental history of colorectal cancer. The CYP7A1 polymorphism was not measurably related to the overall risk of colorectal adenomas. However, the CC genotype was associated with a decreased risk of proximal colon adenomas, but not of distal colon and rectal adenomas.

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Section: Discussionmentioning

confidence: 87%

Genetic polymorphism of cholesterol 7α‐hydroxylase (CYP7A1) and colorectal adenomas: Self Defense Forces Health Study

et al. 2006

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“…Although this inverse association is generally ascribed to the effect of preclinical cancer existing at the baseline (30), an increased risk of proximal colon cancer associated with low levels of serum total cholesterol persisted 10 to 20 years later in a prospective study in Hawaii (31). Furthermore, a case-control study observed lower levels of total and low-density lipoprotein cholesterol in cases of proximal colon cancer, but not of distal colon cancer, than in controls (32). These findings are congruent with decreased risk of proximal colon cancer associated with the CYP7A1 CC genotype.…”

Section: Discussionmentioning

confidence: 93%

Genetic Polymorphism in Cytochrome P450 7A1 and Risk of Colorectal Cancer: The Fukuoka Colorectal Cancer Study

et al. 2005

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Bile acids have long been implicated in the etiology of colorectal cancer, but epidemiologic evidence remains elusive. Cholesterol 7A-hydroxylase (CYP7A1) is the rate-limiting enzyme in the synthesis of bile acids from cholesterol in the liver, and thus may be an important determinant of bile acid production. We examined the association between the CYP7A1 A-203C polymorphism and colorectal cancer. The CYP7A1 A-203C polymorphism was determined by the PCR-RFLP method in 685 incident cases of colorectal cancer and 778 controls randomly selected from a community in the Fukuoka area, Japan. The CC genotype was slightly less frequent in the case group, and the adjusted odds ratio for the CC versus AA genotype was 0.88 (95% confidence interval, 0.65-1.20). In the analysis by subsite of the colorectum, a decreased risk associated with the CYP7A1 CC genotype was observed for proximal colon cancer, but not for either distal colon or rectal cancer. The adjusted odds ratios (95% confidence intervals) of proximal colon cancer for the CC genotype were 0.63 (0.36-1.10) compared with the AA genotype, and 0.59 (0.37-0.96) compared with the AA and AC genotypes combined. A decreased risk of proximal colon cancer in relation to the CC genotype of CYP7A1 A-203C, which probably renders less activity of the enzyme converting cholesterol to bile acids, is new evidence for the role of bile acids in colorectal carcinogenesis. (Cancer Res 2005; 65(7): 2979-82)

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“…29,30) Furthermore, the genetic backgrounds of individuals are now widely accepted to have a substantial impact on the development of colon cancers. 6,7,31) In the present gene expression analysis, we used normal portions of colon epithelial tissues from PhIP-treated animals at experimental week 60 in order to see differences in the environment of colon cancers, in the expectation that differences in gene expression at later stages of carcinogenesis could also have a substantial impact on the formation of cancers in the colon. Seventy-four genes were differentially expressed by 3-fold or greater in normal regions of colon epithelium between the susceptible F344 and resistant ACI strains.…”

Section: Discussionmentioning

confidence: 99%

Differential gene expression profiles in colon epithelium of two rat strains with distinct susceptibility to colon carcinogenesis after exposure to PhIP in combination with dietary high fat

et al. 2003

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Colon cancers develop through accumulation of multiple genetic and epigenetic alterations in colon epithelial cells, and the environment of the genetically altered epithelial cells may also have a substantial impact on their further development to cancer. In the present study, groups of 6-week-old F344 and ACI male rats, the former strain being susceptible to colon carcinogenesis induced by 2-amino-1-methyl-6-phenylimidazo[4,5-b]pyridine (PhIP) and the latter being relatively resistant, were subjected to a longterm carcinogenesis experiment using our intermittent feeding protocol of PhIP in combination with a high-fat diet, which serves as a relevant risk factor that promotes the development of colon cancers. Animals were sacrificed at 60 weeks, and global gene expression analyses of normal parts of colon epithelial tissues were conducted using a high-density oligonucleotide microarray to elucidate the differential gene expression profile ( umerous studies have indicated that multiple genetic and epigenetic events are involved in the development of colon cancers. Dysregulation of the adenomatous polyposis coli (Apc), β-catenin, p53 and K-ras genes by either genetic alteration or promoter inactivation by CpG methylation plays a key role in colon carcinogenesis.

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Is the development of adenoma and carcinoma in proximal colon related to apolipoprotein E phenotype?

Cited by 58 publications

References 2 publications

Genetic polymorphism of cholesterol 7α‐hydroxylase (CYP7A1) and colorectal adenomas: Self Defense Forces Health Study

Genetic polymorphism of cholesterol 7α‐hydroxylase (CYP7A1) and colorectal adenomas: Self Defense Forces Health Study

Genetic Polymorphism in Cytochrome P450 7A1 and Risk of Colorectal Cancer: The Fukuoka Colorectal Cancer Study

Differential gene expression profiles in colon epithelium of two rat strains with distinct susceptibility to colon carcinogenesis after exposure to PhIP in combination with dietary high fat

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