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  • American Association for Cancer Research (AACR)  (4)
  • Trevisan, Maurizio  (4)
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  • American Association for Cancer Research (AACR)  (4)
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  • 1
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 13, No. 9 ( 2004-09-01), p. 1480-1484
    Abstract: Specific fatty acids may have differential effects on breast cancer etiology. Animal studies have suggested that conjugated linoleic acids (CLA), a group of fatty acids found predominantly in dairy products and the meat of ruminants, have potent anticarcinogenic properties. We examined breast cancer risk and dietary CLA intake among 1,122 women with primary, incident, histologically confirmed breast cancer and 2,036 controls frequency matched to cases by age, race, and county of residence. Diet was assessed with a self-administered 104-item food frequency questionnaire and other relevant data were collected by detailed in-person interviews. We examined risk with intake of total CLAs and the 9c,11t-18:2 isomer of CLA (9,11 CLA). Odds ratios and 95% confidence intervals were estimated by unconditional logistic regression, adjusting for age, the residual of fat adjusted for energy, and other breast cancer risk factors. No association was observed between intakes of total CLA or 9,11 CLA and overall risk of premenopausal or postmenopausal breast cancer. We observed little association between CLA intakes and risk of estrogen receptor (ER)–negative or ER-positive tumors, although, compared with premenopausal women in the lowest quartile of 9,11 CLA intake, those in the highest quartile had a marginally significant reduction in risk of having an ER-negative tumor (odds ratio, 0.40; 95% confidence interval, 0.16–1.01). Our findings suggest that, although CLA intake was not related to overall breast cancer risk, there may be associations with tumor biology at least among premenopausal women.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2004
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 2
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 68, No. 9_Supplement ( 2008-05-15), p. 5814-5814
    Abstract: Alcohol consumption has been found to be associated with breast cancer with some consistency. Alcohol dehydrogenase is rate limiting in alcohol metabolism. We investigated the association of haplotype tag SNPs in ADH1B and ADH1C with breast cancer risk and the interaction with alcohol drinking in a population-based case control study (the WEB Study) conducted in western New York between 1996 and 2001. Genomic DNA and SNP genotyping was performed by allelic discrimination real time PCR for 991 cases and 1698 controls. Haplotype tag SNPs were selected from the Caucasian HapMap data. Lifetime alcohol consumption was queried by interview. Logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI). Backwards selection was employed to obtain the most parsimonious model starting with the full model with interactions. Two tag SNPs, rs1042026 in ADH1B and rs1614972 in ADH1C, were associated with risk for postmenopausal women. The ADH1B SNP rs1042026 located in the 3’UTR is in LD with several functional SNPs from ADH6, ADH1A, ADH1B and ADH1C. This SNP was in Hardy Weinberg equilibrium in the postmenopausal control and not in postmenopausal cases, which strengthens the evidence of association. This SNP showed evidence of significant interaction with alcohol consumption. The OR for postmenopausal breast cancer in women with both CC genotype and who consume alcohol versus without the AA genotype and who abstain was 1.94, 95%CI 1.13-3.30. In addition, we found evidence of a trend for dose response depending on the amount of alcohol consumption when alcohol consumption was examined in three categories of abstainers, low and high consumption (p=0.08). The ADH1C SNP rs1614972 located in intron 8 is in LD with other six nonsynonymous exonic SNPs including the functional I350V (rs698). There was an interaction with alcohol consumption with the presence of the CC genotype and risk conferring a protective effect varying inversely proportional with the drinking level (p=0.0092). Moreover, the CC genotype decreased the odds of breast cancer in women who consume alcohol versus those that abstain regardless of the menopausal status (OR=0.56, 95%CI 0.35-0.90). In conclusion, haplotype tag SNPs in ADH1B and ADH1C were associated with breast cancer risk especially in postmenopausal women, and showed evidence of significant interaction with alcohol consumption. Supported by the following grants: DAMD-17-03-1-0446, DAMD-17-00-1-0417 and NCI-RO1CA92040 Marian C. was supported by an AVON-AACR International Scholar in Breast Cancer Research award
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2008
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 3
    Online Resource
    Online Resource
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 21, No. 1 ( 2012-01-01), p. 239-242
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 21, No. 1 ( 2012-01-01), p. 239-242
    Abstract: Background: While there is accumulating evidence that use of nonsteroidal anti-inflammatory drugs (NSAID) decreases breast cancer risk, little is known about the impact of NSAIDs on survival after breast cancer diagnosis. Methods: We assessed whether recent, prediagnostic NSAID use and lifetime cumulative aspirin use before diagnosis were associated with survival among 1,024 women with incident, primary, invasive breast cancer. Results: Recent prediagnostic use of aspirin, ibuprofen, and acetaminophen and lifetime use of aspirin up to diagnosis were not associated with either all-cause mortality or breast cancer–specific mortality. Neither dose nor frequency of use was associated with risk. Associations were not different for pre- and postmenopausal women. Conclusion: In our data, prediagnostic NSAID use and lifetime cumulative aspirin use were not associated with breast cancer survival. Impact: Our findings do not support a role of NSAIDs prior to diagnosis in breast cancer survival. Cancer Epidemiol Biomarkers Prev; 21(1); 239–42. ©2011 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
    Location Call Number Limitation Availability
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  • 4
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 18, No. 9 ( 2009-09-01), p. 2453-2459
    Abstract: It has been hypothesized that effects of alcohol consumption on one-carbon metabolism may explain, in part, the association of alcohol consumption with breast cancer risk. The methylenetetrahydrofolate reductase (MTHFR) and 5-methyltetrahydrofolate-homocysteine methyltransferase (MTR) genes express key enzymes in this pathway. We investigated the association of polymorphisms in MTHFR (rs1801133 and rs1801131) and MTR (rs1805087) with breast cancer risk and their interaction with alcohol consumption in a case-control study—the Western New York Exposures and Breast Cancer study. Cases (n = 1,063) were women with primary, incident breast cancer and controls (n = 1,890) were frequency matched to cases on age and race. Odds ratios (OR) and 95% confidence intervals (95% CI) were estimated by unconditional logistic regression. We found no association of MTHFR or MTR genotype with risk of breast cancer. In the original case-control study, there was a nonsignificant increased odds of breast cancer among women with higher lifetime drinking. In the current study, there was no evidence of an interaction of genotype and alcohol in premenopausal women. However, among postmenopausal women, there was an increase in breast cancer risk for women who were homozygote TT for MTHFR C677T and had high lifetime alcohol intake (≥1,161.84 oz; OR, 1.92; 95% CI, 1.13-3.28) and for those who had a high number of drinks per drinking day ( & gt;1.91 drinks/day; OR, 1.80; 95% CI, 1.03-3.28) compared with nondrinkers who were homozygote CC. Our findings indicate that among postmenopausal women, increased breast cancer risk with alcohol consumption may be as a result of effects on one-carbon metabolism. (Cancer Epidemiol Biomarkers Prev 2009;18(9):2453–9)
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
    Location Call Number Limitation Availability
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