Colorectal adenomas

LIN H J, PROBST-HENSCH N M, LOUIE A D, KAU I H, WITTE J S, INGLES S A, FRANKL H D, LEE E R and HAILE R w (1998) Glutathione transferase null genotype, broccoli and lower prevalence of colorectal adenomas . Cancer Epidemiol Biomarkers Prev, 7 647-52. 

Paganelli, G.M., Biasco, G., Brandi, G., Santucci, R., Gizzi, G., Villani, V., Cianci, M., Miglioli, M. and Barbara, L. (1992). Effect of vitamin A, C and E supplementation on rectal cell proliferation in patients with colorectal adenomas. J. Natl Cancer Inst. 84, 47-51. 

Calcium supplementation appears to be associated with a moderate reduction in risk of recurrent colorectal adenomas, with prospective studies demonstrating a nonstatistical decrease in adenoma recurrence, and the role of calcium as a chemoprevention agent remains under investigation.47... 

It is well recognised that the faecal bile acid content of random stool samples is highly variable with marked daily variation.Therefore, studies testing the association between luminal bile acid exposure and the presence of colorectal neoplasia have usually measured serum bile acid levels, which demonstrate less variability and are believed to reflect the total bile acid pool more accurately. Serum DCA levels have been shown to be higher in individuals with a colorectal adenoma compared with individuals without a neoplasm. Only one study has assessed future risk of CRC in a prospective study of serum bile-acid levels. The study was hampered by the small sample size (46 CRC cases). There were no significant differences in the absolute concentrations of primary and secondary bile acids or DCA/CA ratio between cases and controls although there was a trend towards increased CRC risk for those with a DCA/ CA ratio in the top third of values (relative risk 3.9 [95% confidence interval 0.9-17.0 = 0.1]). It will be important to test the possible utility of the DCA/ CA ratio as a CRC risk biomarker in larger, adequately powered studies. A recent study has demonstrated increased levels of allo-DCA and allo-LCA metabolites in the stool of CRC patients compared with healthy controls. ... 

Additionally, two studies have measured colorectal epithelial cell proliferation and apoptosis in human non-neoplastic mucosa in combination with serum bile acid quantification. Ochsenkuhn et al have reported a positive correlation between serum DCA levels and proliferation measured by flow cytometric cell cycle analysis. However, a more recent study of colorectal adenoma patients failed to detect a correlation between serum DCA and immuno-histochemical Ki-67 antigen labelling. Instead, this latter study revealed a positive correlation between serum DCA and the degree of TUNEL-positive epithelial cell apoptosis. ... 

The mechanistic basis of the anti-neoplastic activity of UDCA and the explanation for the significant difference in bioactivity of UDCA compared with DCA despite marked similarity in chemical structure remain unresolved. UDCA administration in healthy volunteers and colorectal adenoma patients has been demonstrated to decrease the proportion of DCA in aqueous phase stool. Therefore, one possible mechanism of the chemopreventative activity of UDCA is reduction of mucosal secondary bile acid exposure. Consistent with this idea, UDCA administration has been demonstrated to reduce the incidence of K-ras mutations and decrease Cox-2 expression in AOM-induced tumors, which is the opposite of the reported effects of DCA in the same model. However, it is clear that exogenous administration of UDCA has direct anti-neoplastic activity on human CRC cells in vitro, either alone or in combination with DCA, including anti-proliferative and anti-apoptotic effects, as well as induction of cell senescence. " ... 

Anti-neoplastic activity of UDCA was demonstrated first in the context of ulcerative colitis-associated colorectal carcinogenesis. Subsequently, encouraging (but not definitive) results have been obtained in clinical trials of UDCA for prevention of sporadic colorectal adenoma recurrence, which should prompt further evaluation of UDCA for polyp prevention, particularly given its excellent safety profile compared with other candidate chemoprevention agents such as the nonsteroidal anti-inflammatory drugs. 

E. Bayerdorffer, G. A. Marines, T. Ochsenkuhn, P. Dirschedl and G. Paumgartner, Variation of serum bile aeids in patients with colorectal adenomas during a one-year follow-up, Digestion, 1994, 55, 121. 

E. Bayerdorffer, G. A. Mannes, W. O. Richter, Ochsenkuhn, B. Wiebecke, W. Kopcke and G. Paumgartner, Increased serum deoxychloic acid levels in men with colorectal adenomas. Gastroenterology, 1993, 104, 145. 

M. Fracchia, G. Galatola, I. Sarotto, V. Guraldo, M. Perona, A. Pera and M. Risio, Serum bile acids, programmed cell death and cell proliferation in the mucosa of patients with colorectal adenomas. Dig. Liver Dis., 2005, 37, 509. 

W. Wang, S. Xue, S. A. Ingles, Q. Chen, A. T. Diep, H. D. Frankl, A. Stolz and R. W. Haile, An association between genetic polymorphisms in the ileal sodium-dependent bile-acid transporter gene and the risk of colorectal adenomas, Cancer Epidemiol. Biomarkers Prev., 2001, 10, 931. 

L. Serfaty, A. De Leusse, O. Rosmorduc, B. Desaint, J.-F. Flejou, O. Chaouilleres, R. E. Poupon and R. Poupon, Ursodeoxycholic acid therapy and the risk of colorectal adenoma inpatients with primary biliary cirrhosis An observational study, Hepatology, 2003, 38, 203. 

Eberhart CE, Coffey RJ, Radhika A, et al. Up-regulation of cyclooxygenase 2 gene expression in human colorectal adenomas and adenocarcinomas. Gastroenterology 1994 107 1183-1188. 

Carcinogenic activity. Decoction of the seed, administered orally to adults, was inactive. There was no association between colorectal adenomas and consumption of extract . Roasted seed, administered to male rats at a dose of 6% of diet for 2 years, was inactive. Water extract of the roasted seed, administered to female rats at a dose of 6% of diet, was inactive. Regular and decaffeinated instant coffees were studied. Coffees with highest caffeine content showed lower tumor incidence k Hot water extract of the roasted seed, administered orally to 18 rats at a dose of 2% for 120 days... 

Baron, J. A., E. R. Greenberg, R. Haile, J. Mandel, R. S. Sandler, and L. Mott. Coffee and tea and the risk of recurrent colorectal adenomas. Cancer Epidemiol Biomark Prevent 1997 6(1) 7-10. 

Arsenic exposure contributes to cancer risk and has been associated with decreased ERCCl expression in isolated lymphocytes at the mRNA and protein levels (51). Along the same lines, increased expression of defense genes, like ERCCl, has been observed in premalignant lesions, such as colorectal adenomas (52). In early-stage NSCLC, high ERCC 1 expression has been observed in almost half of the patients, indicating both a lower risk of relapse and a lower probability of benefit from adjuvant cisplatin-based chemotherapy. 

Saebo M, Skjelbred CF, Nexo BA et al. Increased mRNA expression levels of ERCCl, OGGI, and RAI in colorectal adenomas and carcinomas. BMC Cancer 2006 6 208. 

E. Giovannucci et al., Folate, Methionine, and Alcohol Intake and Risk of Colorectal Adenoma, J. Natl. Cancer Inst. 85 (1993) 875-84. 

Erhardt, J.G., Meisner, C., Bode, J.C., Bode, C. (2003). Lycopene, beta-carotene and colorectal adenomas. American Journal of Clinical Nutrition, 78, 1219-1224. 

Bresalier RS, Sandler RS, Quan H, et al. Cardiovascular events associated with rofecoxib in a colorectal adenoma chemoprevention trial. N Engl J Med. 2005 352 1092-1102. 

Wahlqvist, M., Wattanapenpaiboon, N., Macrae, F., Lambert, J., MacLennan, R., and Hsu-Hage, B. 1994. Changes in serum carotenoids in subjects with colorectal adenomas after 24 mo of beta-carotene supplementation. Am. J. Clin. Nutr. 60, 936-943. 

BP Kennedy, C Soravia, J Moffat, L Xia, T Hiruki, S Collins, S Gallinger, B Bapat. Overexpression of the nonpancreatic secretory group II PLA2 messenger RNA and protein in colorectal adenomas from familial adenomatous polyposis patients. Cancer Res 58 500-503, 1998. 

In a pooled analysis (88) of three studies (Wheat Bran Fiber Trial Polyp Prevention Trial Polyp Prevention Study) subjects with colorectal adenoma and Se levels in the highest quartile (median 150 ng/ml ) had significant lower odds of developing new adenoma compared with those in the lowest quartile (median I 13 ng/mL),... 

Jacobs ET, Jiang R, Alberts DS, et al, Selenium and colorectal adenoma results of a pooled analysis, J Natl Cancer Inst 2004 96 1669-1675. 

Recently, Mu et al. (2003) have reported that the KCNK9 potassium channel (TASK) gene is amplified and overexpressed in breast cancers, lung and prostate cancers. Moreover, overexpression of KCNK9 was found in 57 (46.0%) of the 124 patients with colorectal carcinomas, but not in the patients with colorectal adenoma (Kim et al. 2004). Interestingly, overexpression of KCNK9 promotes tumor formation and induces resistance to both hypoxia and serum deprivation. 

Fearnhead NS, Wilding JL, Winney B, Tonks S, Bartlett S, et al. 2004. Multiple rare variants in different genes account for multifactorial inherited susceptibility to colorectal adenomas. Proc Natl Acad Sci USA 101 15992-15997. 

Greenberg, R.E., et al. A Clinical Trial of Antioxidant Vitamins to Prevent Colorectal Adenoma. The New England Journal of Medicine 331 (1994) 141-147. 

A study of Colorectal adenomas and cancers in human patients revealed sei eral types of mutations occurring in RAS. The mtwt common mutations affected codon 12, which consists of GGT, and codes for the I2th amino acid of the polypeptide. Most of these mutations resulted in the conversion of GGT, which codes for glycine, to GAT (aspartate), to GTT (valine), and to GCT (alanine) (Zhu ef ai, 1997). The mutations t ccurred at the central base of codon 12 and can be summarized as ... 

A case-control study was designed to explore risk factors for colorectal adenomas. Adenomas are precursors to 80-90% of all colorectal cancers. The study used 236 cases (with adenomas or polyps) and 409 controls (no adenomas) (Tseng ef aF., 1996) (Tabic 11,2). All subjects were patients receiving colonoscopy exams. The subjects were not recruited from the general public, A month or so after the exam, the subjects were asked to fill out a food choice questionnaire. 

Shibata, H Toyama, fC, Shioya, fl Jto, M., Hi rota, M., Hasegawa, S., Matsumoto, H., Takano, H., Akiyama, T., Toyo.shima, K., Kanamuru, R., Kancgae, Y Saito, 1 Nakamura, y., Shiba, K., and Noda, T. (1997). Rapid colorectal adenoma formation initiated by conditional targeting of the ape gene. Science 27S, 120-123,... 

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