The effect of administering marine oil that was rich in omega-3 fatty acids on tumor growth was studied in female inbred F344 rats that received transplants of R3230AC mammary adenocarcinoma. Four groups of rats were maintained on a normal rat chow diet containing 5% fat, and marine oil supplementation was started 1 week prior to transplantation of the tumors. The marine oil provided 17, 33, and 67 mg of 5, 8, 11, 14, 17-eicosapentaenoic acid (EPA) and 16, 32, and 64 mg 4, 7, 10, 13, 16, 19-docosahexaenoic acid (DHA) a day. A significant reduction in weight (g) and volume (cm3) of the rat R3230AC mammary tumor was observed after 4 weeks of treatment. EPA (20:5 omega-3) and DHA (22:6 omega-3) were found in choline phospholipid fractions of mammary tumors from rats given marine oil. Both tumor content and synthesis in vitro of prostaglandins of two series were inhibited in the marine oil-treated groups. These data indicated that the mechanism underlying inhibition of mammary tumorigenesis may be linked, in part, to the inhibitory effect of both EPA and DHA on arachidonic acid metabolism.

A family history of colorectal cancer may increase colorectal cancer risk by influencing adenoma growth or enhancing the formation of new lesions. Data of men from the prospective Health Professionals Follow-Up Study who underwent an endoscopy between 1986 and 2004 were used to evaluate whether a family history of colorectal cancer is associated with adenoma multiplicity or advanced adenoma stage (1 cm, histology with villous component or carcinoma in situ). 21.4% of the 3,881 adenoma patients and 13.9% of the 24,959 adenoma-free men had a first-degree relative with colorectal cancer. Thousand four hundred and ninety-six men were classified as having advanced and 1,507 as having nonadvanced adenomas. Six hundred and twenty-two men had multiple and 1,985 had single adenomas in the distal colon and rectum. A family history of colorectal cancer was similarly associated with advanced and nonadvanced adenomas [multivariable odds ratio (OR) (95% confidence interval): advanced vs. nonadvanced, 0.98 (0.82-1.17), advanced vs. adenoma-free: 1.67 (1.47-1.91), nonadvanced vs. adenoma-free: 1.70 (1.49-1.94)], although potential differences according to adenoma location were seen. A family history of colorectal cancer was more strongly associated with multiple distally located adenomas [odds ratio (95% confidence interval): multiple vs. single, 1.35 (1.09-1.68), multiple vs. no distally located adenomas: 2.02 (1.67-2.44), single vs. no distally located adenomas: 1.49 (1.32-1.68)]. The number of adenomas was also positively associated with a family history of colorectal cancer. Our findings suggest that at the population level, heritable factors may be more important in earlier stages of adenoma formation than at stages of adenoma advancement for at least distally located adenomas. ' 2009 UICC Key words: family history; cohort study; colorectal neoplasm; colorectal adenomas; colorectal cancer First-degree relatives of individuals with colorectal cancer are approximately twice as likely to get diagnosed with colorectal cancer or their precursor lesions adenomatous polyps as people with unaffected relatives.1,2 The risk of colorectal cancer is 4 times higher for people who have more than one such relative compared with those without one.1,2 A study on twins suggested that about 35% of all colorectal cancer cases can be attributed to heritable factors.3 Thus considering that well-understood familial syndromes such as the familial adenomatous polyposis (FAP) or hereditary nonpolyposis colorectal cancer syndrome (HPNCC) account for less than 5% of all colorectal cancers, 4 genetic factors must also be involved in sporadic colorectal carcinogenesis.There are various ways by which a family history of colorectal cancer may affect colorectal cancer risk. A family history of colorectal cancer may convey a genetic susceptibility that enhances the formation of new lesions or affects the transition from adenomas to carcinomas. Shared behavioral risk factors have also been proposed to underlie part of the association between a family histor...

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Higher folate has been associated with a reduced colorectal cancer (CRC) risk, but excessive folate may promote tumor progression. The role of unmetabolized folic acid (UFA) from high folic acid consumption in carcinogenesis is largely unexplored. We evaluated prediagnostic plasma levels of UFA in relation to CRC risk in nested case-control studies (618 CRC case patients and 1207 matched control) with blood samples collected prior to folic acid fortification. UFA was detected in 21.4% of control UFA levels were not associated with CRC risk. Compared with undetectable levels, the multivariable relative risks (RRs) of CRC were 1.03 (95% confidence interval [CI] = 0.73 to 1.46) for less than 0.5 nmol/L and 1.12 (95% CI = 0.81 to 1.55) for 0.5 nmol/L or more (Ptrend = .32). A positive association between UFA levels and CRC risk was observed among men (RR = 1.57, 95% CI = 0.99 to 2.49 for ≥0.5 nmol/L vs undetectable, Pinteraction = .04), and a positive association was also observed among those with the methylene-tetrahydrofolate reductase (MTHFR) CT/TT genotype (RR = 2.20, 95% CI = 1.22 to 3.94 for ≥0.5 nmol/L vs undetectable, Pinteraction=0.02). In conclusion, prediagnostic plasma levels of UFA from the prefortification period were not associated with risk of CRC.