Effect of alcohol on gastrointestinal cell regeneration as a possible mechanism in alcohol-associated carcinogenesis

Simanowski, Ulrich A.; Stickel, Felix; Maier, H.; Gärtner, Ulrich; Seitz, Helmut K.

doi:10.1016/0741-8329(94)00091-3

Cited by 59 publications

(33 citation statements)

References 29 publications

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“…Elevated body fatness is a well-established risk factor for colorectal neoplasms, and consistent with these observations, we found a lower APC/b-catenin score among people with a larger WHR and body mass index. In line with reports that smoking and alcohol consumption are associated with increased proliferation (30,31), we found that people who formerly or currently consumed alcohol or smoked had higher b-catenin expression. Higher intakes of total fat and processed meats, both of which are hypothesized to increase risk for colorectal neoplasms (2,32), were associated with lower APC/b-catenin scores.…”

Section: Discussionsupporting

confidence: 79%

Markers of the APC/β-Catenin Signaling Pathway as Potential Treatable, Preneoplastic Biomarkers of Risk for Colorectal Neoplasms

Ahearn

Shaukat

Flanders

et al. 2012

Cancer Epidemiology, Biomarkers &Amp; Prevention

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Background: Malfunctioning of the adenomatous polyposis coli (APC)/b-catenin signaling pathway is both an early and common event in sporadic colorectal cancer. To assess the potential of APC/b-catenin signaling pathway markers as treatable, preneoplastic biomarkers of risk for colorectal neoplasms, we conducted a pilot colonoscopy-based case-control study (51 cases and 154 controls) of incident, sporadic colorectal adenoma.Methods: We evaluated APC, b-catenin, and E-cadherin expression in normal mucosa from the rectum and ascending and sigmoid colon using automated immunohistochemical and quantitative image analysis. Diet, lifestyle, and medical history were assessed with validated questionnaires.Results: In the normal rectal mucosa, the ratio of the proportion of APC expression in the upper 40% of crypts with total b-catenin expression (APC/b-catenin score) was 14.3% greater in controls than in cases [P ¼ 0.02; OR, 0.40; 95% confidence interval (CI), 0.14-1.14]. Compared with controls, in cases, APC expression was 3.2% lower, b-catenin expression was 3.0% higher, and E-cadherin expression was 0.7% lower; however, none of these differences were statistically significant. The APC/b-catenin score statistically significantly differed according to categories of plausible risk factors for colorectal cancer [e.g., it was 17.7% higher among those with 25(OH) vitamin D 3 concentrations ! 27 ng/mL].Conclusions: These preliminary data suggest that the combined expression of APC and b-catenin in the normal rectal mucosa may be associated with risk for incident, sporadic colorectal neoplasms, as well as with modifiable risk factors for colorectal neoplasms.Impact: Our results may help advance the development of treatable, preneoplastic biomarkers of risk for colorectal neoplasms. Cancer Epidemiol Biomarkers Prev; 21(6); 969-79. Ó2012 AACR.

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Section: Discussionsupporting

confidence: 79%

Markers of the APC/β-Catenin Signaling Pathway as Potential Treatable, Preneoplastic Biomarkers of Risk for Colorectal Neoplasms

Ahearn

Shaukat

Flanders

et al. 2012

Cancer Epidemiology, Biomarkers &Amp; Prevention

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“…Ethanol consumption is described as a risk factor for colorectal cancer, a hypothesis supported by both clinical (5-8) and experimental trials in rats (16,17).…”

Section: Discussionmentioning

confidence: 97%

“…Nevertheless, they report some contradictory results, supporting cancer promotion (13) or adenoma promotion only (14). On other hand, experimental studies have shown an increased risk of CRC due to the effect of alcohol both in vitro (15) and in rodent models (16,17).…”

Section: Introductionmentioning

confidence: 99%

Effect of ethanol consumption on colon cancer in an experimental model

Pérez-Holanda¹,

Rodrigo

Salas

et al. 2005

Rev. esp. enferm. dig.

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Pérez-Holanda S, Rodrigo L, Viñas-Salas J, Piñol-Felis C. Effect of ethanol consumption on colon cancer in an experimen tal model. Rev Esp Enferm Dig 2003; 95: 87-96. ABSTRACTAims: the present study was designed to examine the effect of an ethanol supplement on experimental colon carcinogenesis.Material and methods: one hundred and ten 10-week-old Sprague-Dawley rats were divided into five groups: group A (20 rats) received no treatment. Group B (20 rats) received a supplement of ethanol at 1.23 g/kg of body weight per day added to their drinking water for 24 weeks. Group C (30 rats) received 18 weekly doses of dimethylhydrazine (DMH) at 21 mg/kg of body weight from the beginning of the study. Group D (20 rats) received ethylen-diamin-tetracetic acid (EDTA) solution only for 18 weeks. Group E (20 rats) received ethanol at the same dose as group B plus DMH injections at the same dose as the rats in group C from the beginning of the study. All experimental animals were sacrified after 25-27 weeks.Results: no significant differences in the number of rats that developed tumors, number of tumor-free animals, and number of tumors per rat, as well as in macro-microscopic tumoral findings were observed for animals in group C compared to animals in group E.Conclusions: we concluded that the addition of an ethanol supplement does not modify colorectal carcinogenesis using a dynamic model of tumor induction with DMH.

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“…Cancers of the colon and rectum: Authoritative reviews of studies of alcohol and colorectal cancer have found evidence of a weak but fairly consistent positive association, particularly for rectal cancer (Doll et al, 1993;Longnecker, 1992;Longnecker et al, 1990;Seitz and Poschl, 1997;Seitz et al, 1998a;Seitz et al, 1998b;Simanowski et al, 1995). These reviews tend to agree in their conclusion that a positive dose-response association exists between alcohol intake and colorectal cancer risk, but that there is inadequate evidence of a direct causal role.…”

Section: 23mentioning

confidence: 99%

Evidence Regarding the Level of Alcohol Consumption Considered to be Low-Risk for Men and Women

Single¹,

Ashley²,

Bondy³

et al. 2000

PsycEXTRA Dataset

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The strategic intent of the NHMRC is to work with others for the health of all Australians, by promoting informed debate on ethics and policy, providing knowledge based advice, fostering a high quality and internationally recognised research base, and applying research rigour to health issues. NHMRC documents are prepared by panels of experts drawn from appropriate Australian academic, professional, community and government organisations. NHMRC is grateful to these people for the excellent work they do on its behalf. This work is usually performed on an honorary basis and in addition to their usual work commitments.

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Effect of alcohol on gastrointestinal cell regeneration as a possible mechanism in alcohol-associated carcinogenesis

Cited by 59 publications

References 29 publications

Markers of the APC/β-Catenin Signaling Pathway as Potential Treatable, Preneoplastic Biomarkers of Risk for Colorectal Neoplasms

Markers of the APC/β-Catenin Signaling Pathway as Potential Treatable, Preneoplastic Biomarkers of Risk for Colorectal Neoplasms

Effect of ethanol consumption on colon cancer in an experimental model

Evidence Regarding the Level of Alcohol Consumption Considered to be Low-Risk for Men and Women

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