Organochlorine Exposure and Colorectal Cancer Risk

Howsam, Michael; Grimalt, Joan O.; Guinó, Elisabet; Navarro, Matilde; Martí-Ragué, Joan; Peinado, Miguel A.; Capellà, Gabriel; Moreno, Vı́ctor

doi:10.1289/ehp.7143

Cited by 73 publications

(44 citation statements)

References 36 publications

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“…26 Part of these differences may be attributed to differences in exposure to compounds associated with the intake of calcium or dairy products, such as vitamin B2 and organochlorines. 44 Indeed, the association with vitamin B2, a cofactor in folate metabolism, 30 tended to be stronger than the association with calcium in our study, and organochlorines, that none of the aforementioned studies assessed, were associated with K-ras mutations in other tumours. 44 Inconsistent findings were also observed regarding other factors, including consumption of red meat, 26,28,29,38,43 and intake of fat 26,29,40,42 and folate.…”

Section: Discussioncontrasting

confidence: 54%

Diet, lifestyle and risk of K‐ras mutation‐positive and ‐negative colorectal adenomas

Wark

Kuil

Ploemacher

et al. 2006

Intl Journal of Cancer

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K‐ras mutation‐positive (K‐ras+) and ‐negative (K‐ras−) colorectal adenomas may differ clinically and pathologically. As environmental compounds may cause mutations in the growth‐related K‐ras oncogene or affect clonal selection depending on mutational status, we evaluated whether the aetiology of K‐ras+ and K‐ras− adenomas differs. K‐ras mutations in codons 12 and 13 were assessed in colorectal adenoma tissue (K‐ras+: n = 81, K‐ras−: n = 453). Dietary and lifestyle data were collected through questionnaires that were also administered to 709 polyp‐free controls. Multiple logistic regression analyses showed that intake of vitamin B2 and monounsaturated fat were differently associated with risk of K‐ras+ and K‐ras− adenomas; vitamin B2 was inversely associated with K‐ras− (highest vs. lowest tertile: odds ratio (OR) = 0.70, 95% confidence interval (CI) = 0.50–0.97, p trend = 0.020), but not with K‐ras+ adenomas, and a positive association with monounsaturated fat was confined to K‐ras− adenomas (OR = 1.57, 95% CI = 1.06–2.34, p trend = 0.029). Besides, potential, not statistically significant, differences in risk arose because red meat was distinctly positively associated with K‐ras+ adenomas (OR = 1.70, 95% CI = 0.94–3.09, p trend = 0.061); total dietary and polyunsaturated fat tended to be inversely associated with risk of K‐ras+ but not of K‐ras− adenomas; inverse associations with dairy products, calcium, protein and tea were confined to K‐ras− adenomas, and smoking was more markedly positively associated with K‐ras− adenomas. No differences in risk of K‐ras+ and K‐ras− adenomas could be detected for other factors. In conclusion, dietary and lifestyle factors may influence risk of K‐ras+ and K‐ras− adenomas differently. However, epidemiological literature on diet, lifestyle and colorectal K‐ras mutations is inconsistent. © 2006 Wiley‐Liss, Inc.

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Section: Discussioncontrasting

confidence: 54%

Diet, lifestyle and risk of K‐ras mutation‐positive and ‐negative colorectal adenomas

Wark

Kuil

Ploemacher

et al. 2006

Intl Journal of Cancer

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“…Similarly, other investigators have found that different chemicals and insecticides pollute water and sediments [17][18][19].…”

Section: Journal Of Adenocarcinoma Issn 2572-309xmentioning

confidence: 73%

Correlation of Vascular Endothelial Growth Factor Expression and Neovascularization with Colorectal Carcinoma: A Pilot Study

Mohamed¹,

All²,

Kamel³

et al. 2016

J Adenocarcinoma

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Background: In Egypt, there is an increasing incidence of colorectal cancer (CRC), especially among patients under 40 years of age, affecting a very important age group in our community. The basic pathogenic step in the process of tumor growth, invasion and metastasis is tumor induced angiogenesis. The aim of this study was to evaluate the angiogenesis in colorectal carcinoma by detect the expression of VEGF vascular endothelial growth factor and micro vascular density (MVD) determination with IHC (immunohistochemistry) method and to determine if and how angiogenesis correlates with clinicopathologic parameters. Methods and findings:Sixty five archival, paraffin embedded tissue samples of colorectal carcinoma from Pathology Lab of Suez Canal University Teaching Hospital (Egypt) with complete follow-up files in Oncology Unit from. VEGF and micro vessels were identified immunohistochemically, using monoclonal VEGF antibody and CD34 antibody, respectively. VEGF IHC expression was positive in 94.7% of cases and MVD ranged from 9 to 42 mean 24.55 ± 13.79. A significant positive relation was found between VEGF expression; and histological type, tumor grade, lymph node (LN) involvement, UICC TNM classification, perineural and lympho-vascular invasions (p<0.05). A significant positive relation was found between VEGF expression and MVD (p<0.001). There is a significant correlation has been found between MVD and size of the tumor, histological subtype, tumor grade, LN involvement, UICC TNM classification, vascular and perineural invasion and survival (p<0.05). Conclusions:This study has highlighted the prognostic significance of VEGF and MVD to predict survival in CRC patients, as well as some of traditional prognostic factors as tumor histologic type, tumor size, tumor grade, LN involvement, tumor stage and lympho-vascular and perineural invasion to identify patients at high risk for relapse who may benefit from adjuvant treatment including new therapeutic strategies in the future.

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“…The tandem increase in both seric pro-inflammatory cytokines IL-6 and TNFa and increase in tissue levels of P-selectin and b-catenin is consistent with the recent report of Zhang et al (2015) noting increased P-selectin in the plasma and IL-1b in the sub-endothelial layer of the abdominal aorta in rats treated with 5 or 10 mg ENDO/kg/day. Although Howsam et al (2004) correlated exposure to OC pesticides, such as ENDO, with a risk of colon cancer. Bedor et al (2010) also reported on the carcinogenic potential of these compounds.…”

Section: Discussionmentioning

confidence: 99%

Chronic exposure to endosulfan induces inflammation in murine colon via β-catenin expression and IL-6 production

Téllez‐Bañuelos

Haramati

Franco-Topete

et al. 2016

Journal of Immunotoxicology

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Endosulfan (ENDO) is a widely used organochlorine (OC) pesticide and persistent organo-pollutant. Epidemiological studies have shown that high levels of OC exposure were related to colorectal cancer (CRC) incidence. The objectives of the present study were to evaluate histological changes in the colon, as well as in in situ expression of b-catenin and P-selectin, and serum levels of select pro-inflammatory cytokines in mice administered ENDO; there is a relationship between increased serum IL-6 and P-selectin levels in CRC patients and aberrant b-catenin signaling is important in initiation/maintenance of most CRCs. Mice were exposed to ENDO (at dose < LD 50 ) orally once a week for up to 24 weeks, and monitored (inclusive) for a total of 42 weeks. The experiment was comprised of three groups, one that did not receive ENDO (olive oil vehicle), one administered 2 mg ENDO/kg/week and a positive control (for induction of CRC) given a weekly 20 mg 1,2-dimethylhydrazine (DMH)/kg injection. The results indicated that oral administration of ENDO provoked moderate inflammation starting at six weeks, and severe colonic inflammation with an appearance of dysplastic formations (aberrant crypts) in mice treated with ENDO (or DMH) for 12 weeks or longer. Serum IL-6 levels significantly increased starting at six weeks and rose to a peak of 15-fold higher than in controls at 42 weeks; TNFa levels likewise significantly increased, with a later peak (%four-fold higher than controls) at 30-42 weeks. Immunohistochemical analysis of the colon also showed that expression of b-catenin and P-selectin increased with length of exposure to ENDO. Taken together, the results indicate that continued repeated oral exposure to ENDO induces increased expression of b-catenin and P-selectin, inflammation in the colon, and, ultimately, local tissue dysplasia. ARTICLE HISTORY

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Organochlorine Exposure and Colorectal Cancer Risk

Cited by 73 publications

References 36 publications

Diet, lifestyle and risk of K‐ras mutation‐positive and ‐negative colorectal adenomas

Diet, lifestyle and risk of K‐ras mutation‐positive and ‐negative colorectal adenomas

Correlation of Vascular Endothelial Growth Factor Expression and Neovascularization with Colorectal Carcinoma: A Pilot Study

Chronic exposure to endosulfan induces inflammation in murine colon via β-catenin expression and IL-6 production

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