CORK Bibliography: Breast Cancer and Alcohol Use and Nicotine Use

21 citations. January 2009 to present

Prepared: March 2011

Abramowitz MC; Li TY; Morrow M; Anderson PR; Bleicher RJ; Goldstein LJ et al. History of smoking is associated with younger age at diagnosis of breast cancer. Breast Cancer 16(4): 344-349, 2010. (43 refs.)

Smoking tobacco has been associated with incidence, response and outcomes after treatment of some cancers. We hypothesized that tobacco use could result in an observable effect on breast cancer stage and characteristics at diagnosis. There were 6,000 patients with Tis-4, N0-3 breast cancers who presented to a comprehensive cancer center at initial diagnosis between 1970 and 2006. Patients were included who had a known smoking history, and subdivided into any tobacco use 2683 (45%) or never tobacco use 3317 (55%). Analyses were performed to evaluate the association of smoking with clinical, pathologic and treatment-related factors at cancer presentation. Median age at diagnosis for all breast cancers was 55 years, for nonsmokers was 56 years, for any smoking history was 55 years, and the subgroup of current smokers was 52 years. The difference in median age for current smokers versus nonsmokers was statistically significant (p < 0.0001). The probability of age <55 years at breast cancer diagnosis for any smoking history compared to nonsmokers was 1.2 for white patients (p < 0.0003) but 0.81 for black patients (p = 0.25). There was no statistically significant association between smoking and T stage, N stage, ER/PR status, or Her-2/neu status, although smokers were less likely to utilize breast-conserving treatment. Smoking was associated with a younger age at diagnosis and lower utilization of breast conservation, and observed in the subgroup of white patients but not black patients. Further efforts to clarify potential reasons for any racial differences and lower utilization of breast conservation with smoking are warranted.

Bottorff JL; McKeown SB; Carey J; Haines R; Okoli C; Johnson KC et al. Young women's responses to smoking and breast cancer risk information. Health Education Research 25(4): 668-677, 2010. (26 refs.)

Current evidence confirms that young women who smoke or who have regular long-term exposure to secondhand smoke (SHS) have an increased risk of developing premenopausal breast cancer. The aim of this research was to examine the responses of young women to health information about the links between active smoking and SHS exposure and breast cancer and obtain their advice about messaging approaches. Data were collected in focus groups with 46 women, divided in three age cohorts: 15-17, 18-19 and 20-24 and organized according to smoking status (smoking, non-smoking and mixed smoking status groups). The discussion questions were preceded by information about passive and active smoking and its associated breast cancer risk. The study findings show young women's interest in this risk factor for breast cancer. Three themes were drawn from the analysis: making sense of the information on smoking and breast cancer, personal susceptibility and tobacco exposure and suggestions for increasing awareness about tobacco exposure and breast cancer. There was general consensus on framing public awareness messages about this risk factor on 'protecting others' from breast cancer to catch smokers' attention, providing young women with the facts and personal stories of breast cancer to help establish a personal connection with this information and overcome desensitization related to tobacco messages, and targeting all smokers who may place young women at risk. Cautions were also raised about the potential for stigmatization. Implications for raising awareness about this modifiable risk factor for breast cancer are discussed.

Brown LM; Gridley G; Wu AH; Falk RT; Hauptmann M; Kolonel LN et al. Low level alcohol intake, cigarette smoking and risk of breast cancer in Asian-American women. Breast Cancer Research and Treatment 120(1): 203-210, 2010. (40 refs.)

Studies have shown that breast cancer incidence rates among Asian migrants to the United States approach US incidence rates over several generations, implicating potentially modifiable exposures such as moderate alcohol use that has been linked to excess breast cancer risk in other populations. The goal of this study was to investigate the effect of alcohol intake, primarily low levels, on breast cancer risk in Asian-American women and explore whether smoking and alcohol contributed to the breast cancer incidence rates observed among Asian migrants to the United States. Study subjects in this population-based case-control study included 597 incident cases of breast cancer of Chinese, Japanese, and Filipino ethnicity living in San Francisco-Oakland, Los Angeles, and Oahu, Hawaii, and 966 population controls frequency matched on age, ethnicity, and area of residence. The fraction of smokers and drinkers was significantly higher in women born in Western compared with Eastern countries. However, breast cancer risk was not significantly associated with smoking (odds ratio (OR) = 1.2, 95% confidence interval (95% CI) = 0.9-1.6) or alcohol drinking (OR = 0.9, 95% CI = 0.7-1.1) in this population of low consumers of alcohol (median intake among drinkers in grams per day was 0.48 for cases and 0.40 for controls). These data suggest that low alcohol intake is not related to increased breast cancer risk in Asian-American women and that neither alcohol nor cigarette use contributed to the elevated risks in Asian-American women associated with migration patterns and Westernization.

Butler LM; Gold EB; Conroy SM; Crandall CJ; Greendale GA; Oestreicher N et al. Active, but not passive cigarette smoking was inversely associated with mammographic density. Cancer Causes & Control 21(2): 301-311, 2010. (65 refs.)

The opposing carcinogenic and antiestrogenic properties of tobacco smoke may explain why epidemiologic studies have not consistently reported positive associations for active smoking and breast cancer risk. A negative relation between mammographic density, a strong breast cancer risk factor, and active smoking would lend support for an antiestrogenic mechanism. We used multivariable linear regression to assess the associations of active smoking and secondhand smoke (SHS) exposure with mammographic density in 799 pre- and early perimenopausal women in the Study of Women's Health Across the Nation (SWAN). We observed that current active smoking was associated with 7.2% lower mammographic density, compared to never active smoking and no SHS exposure (p = 0.02). Starting to smoke before 18 years of age and having smoked a parts per thousand yen20 cigarettes/day were also associated with statistically significantly lower percent densities. Among nulliparous women having smoked a parts per thousand yen20 cigarettes/day was associated with 23.8% lower density, compared to having smoked a parts per thousand currency sign9 cigarettes/day (p < 0.001). Our findings support the hypothesis that tobacco smoke exerts an antiestrogenic effect on breast tissue, but counters the known increased risk of breast cancer with smoking prior to first full-term birth. Thus, our data suggest that the antiestrogenic but not the carcinogenic effects of smoking may be reflected by breast density.

Croghan IT; Pruthi S; Hays JT; Cha S; Johnson RE; Kosel M et al. The role of smoking in breast cancer development: An analysis of a Mayo Clinic cohort. Breast Journal 15(5): 489-495, 2009. (22 refs.)

The purpose of this study was to assess the predictive value of smoking history on breast cancer diagnosis in a referral clinic population. We conducted a case-control study using clinical data collected on 8,097 female patients (1,225 breast cancer cases and 6,872 controls) seen in the Mayo Clinic Breast Clinic between August 1, 1993 and November 31, 2003. Breast cancer patients and noncancer patients significantly differed with respect to age at time of the index visit (p < 0.001), number of pregnancies (p = 0.006), number of live births (p = 0.002), vital status at last known follow-up (p < 0.001), current menstruation (p < 0.001), age at menopause (p < 0.001), history of hysterectomy (p < 0.001), use of oral contraception (p = 0.05), duration of oral contraception use (p = 0.001), use of other exogenous hormones (p < 0.001), duration of exogenous hormone use (p = 0.05), breast pain at time of index visit (p = 0.002), smoking status (p < 0.001), and use of five or more alcoholic beverages per week (p = 0.002). After adjustment for these baseline characteristics, having a personal history of smoking was found to be predictive of breast cancer diagnosis (odds ratios [OR] = 1.25, p = 0.004). Other positive predictors for breast cancer diagnosis were: age (OR = 1.02, p < 0.001), history of hysterectomy (OR = 0.66, p < 0.001), prior use of oral contraception for more than 11 years (OR = 2.10, p < 0.001), and prior use of other exogenous hormones/estrogen (OR = 1.81, p < 0.001). In this referral practice having a personal history of smoking is predictive of breast cancer diagnosis. Further studies are needed to further explore this relationship.

Johnson KC; Miller AB; Collishaw NE; Palmer JR; Hammond SK; Salmon AG; Cantor KP; Miller MD; Boyd NF; Millar J; Turcotte F. Active smoking and secondhand smoke increase breast cancer risk: the report of the Canadian Expert Panel on Tobacco Smoke and Breast Cancer Risk (2009). Tobacco Control 20(1): e-article 2, 2011. (48 refs.)

Four authoritative reviews of active smoking and breast cancer have been published since 2000, but only one considered data after 2002 and conclusions varied. Three reviews of secondhand smoke (SHS) and breast cancer (2004-2006) each came to different conclusions. With 30 new studies since 2002, further review was deemed desirable. An Expert Panel was convened by four Canadian agencies, the Ontario Tobacco Research Unit, the Public Health Agency of Canada, Physicians for a Smoke-Free Canada and the Canadian Partnership Against Cancer to comprehensively examine the weight of evidence from epidemiological and toxicological studies and understanding of biological mechanisms regarding the relationship between tobacco smoke and breast cancer. This article summarises the panel's full report (http: www. otru. org/pdf/special/expert_panel_ tobacco_breast_cancer. pdf). There are 20 known or suspected mammary carcinogens in tobacco smoke, and recognised biological mechanisms that explain how exposure to these carcinogens could lead to breast cancer. Results from the nine cohort studies reporting exposure metrics more detailed than ever/never and ex /current smoker show that early age of smoking commencement, higher pack-years and longer duration of smoking increase breast cancer risk 15% to 40%. Three meta-analyses report 35% to 50% increases in breast cancer risk for long-term smokers with N-acetyltransferase 2 gene (NAT2) slow acetylation genotypes. The active smoking evidence bolsters support for three meta-analyses that each reported about a 65% increase in premenopausal breast cancer risk among never smokers exposed to SHS. The Panel concluded that: 1) the association between active smoking and breast cancer is consistent with causality and 2) the association between SHS and breast cancer among younger, primarily premenopausal women who have never smoked is consistent with causality.

Kabat GC; Kim M; Kakani C; Tindle H; Wactawski-Wende J; Ockene JK et al. Cigarette smoking in relation to risk of ductal carcinoma in situ of the breast in a cohort of postmenopausal women. American Journal of Epidemiology 172(5): 591-599, 2010. (52 refs.)

In numerous studies, investigators have examined the association of active smoking with risk of invasive breast cancer, but to the authors' knowledge, no cohort study has assessed smoking in relation to the risk of in situ breast cancer, the postulated penultimate stage preceding invasive breast cancer. The authors examined the latter association using data collected at baseline from 63,393 women in the Women's Health Initiative Clinical Trial. A total of 486 cases of ductal carcinoma in situ (DCIS) of the breast were identified during 8 years of follow-up between 1993 and 2005. Cox proportional hazards models were used to estimate hazard ratios and 95% confidence intervals. For the primary analysis, invasive breast cancer was treated as a competing risk. After adjustment for covariates, associations with smoking status, smoking intensity, duration, pack-years, and age at quitting were all close to the null value and showed few meaningful trends. Sensitivity analyses performed to address different possibilities with respect to the natural history of breast cancer also did not provide consistent evidence of an association of smoking with DCIS. The results of this large cohort study provide little support for an association of cigarette smoking with risk of DCIS in postmenopausal women.

Kawase T; Matsuo K; Hiraki A; Suzuki T; Watanabe M; Iwata H et al. Interaction of the effects of alcohol drinking and polymorphisms in alcohol-metabolizing enzymes on the risk of female breast cancer in Japan. Journal of Epidemiology 19(5): 244-250, 2009. (35 refs.)

Background: Epidemiological studies consistently indicate that alcoholic beverages are an independent risk factor for female breast cancer. Although the mechanism underlying this effect remains unknown, the predominant hypothesis implicates mutagenesis via the ethanol metabolite acetaldehyde, whose impact on the carcinogenesis of several types of cancer has been shown in both experimental models and molecular epidemiological studies. Many of the epidemiological Studies have investigated genetic polymorphisms of alcohol dehydrogenase-1B (ADH1B) His48Arg and aldehyde dehydrogenase-2 (ALDH2) Glu504Lys, because of the strong impact these polymorphisms have on exposure to and accumulation of acetaldehyde. With regard to breast cancer, however, evidence is scarce. Methods: To clarify the impact on female breast cancer risk of the interaction of the effects of alcohol consumption and polymorphisms in the alcohol-metabolizing enzymes ADH1B and ALDH2, we conducted a case-control study of 456 newly and histologically diagnosed breast cancer cases and 912 age- and menopausal status-matched noncancer controls. Gene-gene and gene-environment interactions between individual and combined ADH1B and ALDH2 gene polymorphisms and alcohol consumption were evaluated. Results: Despite sufficient statistical power, there was no significant impact of ADH1B and ALDH2 on the risk of breast cancer. Neither was there any significant gene-environment interactions between alcohol drinking and polymorphisms in ADH1B and ALDH2. Conclusions: Our findings do not support the hypothesis that acetaldehyde is the main contributor to the careinogenesis of alcohol-induced breast cancer.

Knight JA; Bernstein L; Largent J; Capanu M; Begg CB; Mellemkjaer L et al. Alcohol intake and cigarette smoking and risk of a contralateral breast cancer. American Journal of Epidemiology 169(8): 962-968, 2009. (25 refs.)

Women with primary breast cancer are at increased risk of developing second primary breast cancer. Few studies have evaluated risk factors for the development of asynchronous contralateral breast cancer in women with breast cancer. In the Women's Environmental Cancer and Radiation Epidemiology Study (1985-2001), the roles of alcohol and smoking were examined in 708 women with asynchronous contralateral breast cancer (cases) compared with 1,399 women with unilateral breast cancer (controls). Cases and controls aged less than 55 years at first breast cancer diagnosis were identified from 5 population-based cancer registries in the United States and Denmark. Controls were matched to cases on birth year, diagnosis year, registry region, and race and countermatched on radiation treatment. Risk factor information was collected by telephone interview. Rate ratios and 95% confidence intervals were estimated by using conditional logistic regression. Ever regular drinking was associated with an increased risk of asynchronous contralateral breast cancer (rate ratio = 1.3, 95% confidence interval: 1.0, 1.6), and the risk increased with increasing duration (P = 0.03). Smoking was not related to asynchronous contralateral breast cancer. In this, the largest study of asynchronous contralateral breast cancer to date, alcohol is a risk factor for the disease, as it is for a first primary breast cancer.

Kwan ML; Kushi LH; Weltzien E; Tam EK; Castillo A; Sweeney C et al. Alcohol consumption and breast cancer recurrence and survival among women with early-stage breast cancer: The Life After Cancer Epidemiology Study. Journal of Clinical Oncology 28(29): 4410-4416, 2010. (55 refs.)

Purpose: To examine the association of alcohol consumption after breast cancer diagnosis with recurrence and mortality among early-stage breast cancer survivors. Patients and Methods: Patients included 1,897 LACE study participants diagnosed with early-stage breast cancer between 1997 and 2000 and recruited on average 2 years postdiagnosis, primarily from the Kaiser Permanente Northern California Cancer Registry. Alcohol consumption (ie, wine, beer, and liquor) was assessed at cohort entry using a food frequency questionnaire. Cox proportional hazards models were used to estimate hazard ratios (HR) and 95% CI with adjustment for known prognostic factors. Results Two hundred ninety-three breast cancer recurrences and 273 overall deaths were ascertained after an average follow-up of 7.4 years. Nine hundred fifty-eight women (51%) were considered drinkers (> 0.5 g/d of alcohol), and the majority drank wine (89%). Drinking >= 6 g/d of alcohol compared with no drinking was associated with an increased risk of breast cancer recurrence (HR, 1.35; 95% CI, 1.00 to 1.83) and death due to breast cancer (HR, 1.51; 95% CI, 1.00 to 2.29). The increased risk of recurrence appeared to be greater among postmenopausal (HR, 1.51; 95% CI, 1.05 to 2.19) and overweight and obese women (HR, 1.60; 95% CI, 1.08 to 2.38). Alcohol intake was not associated with all-cause death and possibly associated with decreased risk of non-breast cancer death. Conclusion: Consuming three to four alcoholic drinks or more per week after a breast cancer diagnosis may increase risk of breast cancer recurrence, particularly among postmenopausal and overweight/obese women, yet the cardioprotective effects of alcohol on non-breast cancer death were suggested.

Lew JQ; Freedman ND; Leitzmann MF; Brinton LA; Hoover RN; Hollenbeck AR et al. Alcohol and risk of breast cancer by histologic type and hormone receptor status in postmenopausal women. American Journal of Epidemiology 170(3): 308-317, 2009. (36 refs.)

Little is known about the association between alcohol and breast cancer by different tumor characteristics. The study consisted of 184,418 postmenopausal women aged 50-71 years in the National Institutes of Health-AARP Diet and Health Study (1995-2003). Alcohol use, diet, and potential risk factors for cancer were assessed with a mailed questionnaire at baseline. The relative risks and 95% confidence intervals were estimated by using Cox proportional hazards regression. Breast cancer cases and estrogen receptor and progesterone receptor status were identified through linkage to state cancer registries. During an average of 7 years of follow-up, 5,461 breast cancer cases were identified. Alcohol was significantly positively associated with total breast cancer: Even a moderate amount of alcohol (> 10 g/day) significantly increased breast cancer risk. In a comparison of > 35 g versus 0 g/day, the multivariate relative risks were 1.35 (95% confidence interval (CI): 1.17, 1.56) for total breast cancer, 1.46 (95% CI: 1.22, 1.75) for ductal tumors, and 1.52 (95% CI: 0.95, 2.44) for lobular tumors. The multivariate relative risks for estrogen receptor-positive/progesterone receptor-positive, estrogen receptor-positive/progesterone receptor-negative, and estrogen receptor-negative/progesterone receptor-negative tumors were 1.46 (95% CI: 1.12, 1.91) for > 35 g versus 0 g/day, 1.13 (95% CI: 0.73, 1.77) for > 20 g versus 0 g/day, and 1.21 (95% CI: 0.79, 1.84) for > 20 g versus 0 g/day, respectively. Moderate consumption of alcohol was associated with breast cancer, specifically hormone receptor-positive tumors.

Li CI; Chlebowski RT; Freiberg M; Johnson KC; Kuller L; Lane D et al. Alcohol consumption and risk of postmenopausal breast cancer by subtype: The Women's Health Initiative Observational Study26. Journal of the National Cancer Institute 102(18): 1422-1431, 2010. (26 refs.)

Background Alcohol consumption is a well-established risk factor for breast cancer. This association is thought to be largely hormonally driven, so alcohol use may be more strongly associated with hormonally sensitive breast cancers. Few studies have evaluated how alcohol-related risk varies by breast cancer subtype. Methods We assessed the relationship between self-reported alcohol consumption and postmenopausal breast cancer risk among 87 724 women in the Women's Health Initiative Observational Study prospective cohort from 1993 through 1998. Multivariable adjusted Cox regression models were used to calculate hazard ratios (HRs) and 95% confidence intervals (CIs). All statistical tests were two-sided. Results A total of 2944 invasive breast cancer patients were diagnosed during follow-up through September 15, 2005. In multivariable adjusted analyses, alcohol consumption was positively related to risk of invasive breast cancer overall, invasive lobular carcinoma, and hormone receptor-positive tumors (all P-trend <= .022). However, alcohol consumption was more strongly related to risk of certain types of invasive breast cancer compared with others. Compared with never drinkers, women who consumed seven or more alcoholic beverages per week had an almost twofold increased risk of hormone receptor-positive invasive lobular carcinoma (HR = 1.82; 95% CI = 1.18 to 2.81) but not a statistically significant increased risk of hormone receptor-positive invasive ductal carcinoma (HR = 1.14; 95% CI = 0.87 to 1.50; difference in HRs per drink per day among current drinkers = 1.15; 95% CI = 1.01 to 1.32, P = .042). The absolute rates of hormone receptor-positive lobular cancer among never drinkers and current drinkers were, 5.2 and 8.5 per 10 000 person-years, respectively, whereas for hormne receptor-positive ductal cancer they were 15.2 and 17.9 per 10 000 person-years, respectively. Conclusions: Alcohol use may be more strongly associated with risk of hormone-sensitive breast cancers than hormone-insensitive subtypes, suggesting distinct etiologic pathways for these two breast cancer subtypes.

Linnoila RI. From nicotine to breast cancer, implications of cholinergic receptor pathway. (editorial). Journal of the National Cancer Institute 102(17): 1298-U11, 2010. (23 refs.)

Lynch HT. Cigarette smoking and breast cancer risk: Limited evidence of genotypic and exogenous carcinogenic factors and their interactions. (editorial). Breast Journal 16(4): 341-343, 2010. (19 refs.)

McCarty KM; Santella RM; Steck SE; Cleveland RJ; Ahn J; Ambrosone CB et al. PAH-DNA adducts, cigarette smoking, GST polymorphisms, and breast cancer risk. Environmental Health Perspectives 117(4): 552-558, 2009. (65 refs.)

BACKGROUND: Polycyclic aromatic hydrocarbons (PAHs) may increase breast cancer risk, and the association may be modified by inherited differences in deactivation of PAH intermediates by glutathione S-transferases (GSTs). Few breast cancer studies have investigated the joint effects of multiple GSTs and a PAH biomarker. OBJECTIVE: We estimated the breast cancer risk associated with multiple polymorphisms in the GST gene (GSTA1, GSTM1, GSTP1, and GSM) and the interaction with PAH-DNA adducts and cigarette smoking. METHODS: We conducted unconditional logistic regression using data from a population-based sample of women (cases/controls, respectively): GST polymorphisms were genotyped using polymerase chain reaction and matrix-assisted laser desorption/ionization time-of-flight assays (n = 926 of 916), PAH-DNA adduct blood levels were measured by competitive enzyme-linked immunosorbent assay (n = 873 of 94 1), and smoking status was assessed by in-person questionnaires (n = 943 of 973). RESULTS: Odds ratios for joint effects on breast cancer risk among women with at least three variant alleles were 1.56 (95% confidence interval (CI), 1.13-2.16] for detectable PAH-DNA adducts and 0.93 (95% CI, 0.56-1.56) for no detectable adducts; corresponding odds ratios for three or more variants were 1.18 (95% CI, 0.82-1.69) for ever smokers and 1.44 (95% CI, 0.97-2.14) for never smokers. Neither interaction was statistically significant (p = 0.43 and 0.62, respectively). CONCLUSION: We found little statistical evidence that PAHs interacted with GSM, GSTM1, GSTP1, and GSTA1 polymorphisms to further increase breast cancer risk.

Public Domain

Pieta B; Samulak D; Opala T; Iwanowicz-Palus G; Wilczak M; Grodecka-Gazdecka S et al. Women's lifestyle and the risk of breast tumors. European Journal of Gynaecological Oncology 30(2): 186-189, 2009. (47 refs.)

The first behavioral aspect of mankind that has been commonly acknowledged as one of the main reasons for neoplasms is lifestyle. The specified lifestyle determines the exposure to the variety of carcinogens, whose crucial role in carcinogenesis is doubtless. The purpose of this study was to analyze women's lifestyle and its influence on the risk of developing breast cancer and benign tumors. The participants of the study were healthy women with no changes in mammary glands and women with diagnosed breast cancer or benign tumor. The total number of participants was 555 females aged 35-70 years. Every patient voluntarily filled in an anonymous questionnaire consisting of questions about socioeconomic conditions, number of cigarettes/daily, alcohol consumption, and physical activity. Proper education concerning a healthy lifestyle can positively contribute to a reduction in breast cancer. A high value of BMI, especially in the postmenopausal period, is a negative predictive factor increasing the risk of breast cancer. Physical activity decreases the risk of breast cancer. No such relation concerning smoking cigarettes has been proven.

Platek ME; Shields PG; Marian C; McCann SE; Bonner MR; Nie J et al. Alcohol consumption and genetic variation in methylenetetrahydrofolate reductase and 5-methyltetrahydrofolate-homocysteine methyltransferase in relation to breast cancer risk. Cancer Epidemiology, Biomarkers & Prevention 18(9): 2453-2459, 2009. (47 refs.)

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 (>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.

Soerjomataram I; de Vries E; Engholm G; Paludan-Muller G; Bronnum-Hansen H; Storm HH et al. Impact of a smoking and alcohol intervention program on lung and breast cancer incidence in Denmark: An example of dynamic modeling with Prevent. European Journal of Cancer 46(14, special issue): 2617-2624, 2010. (28 refs.)

Purpose: Among the known risk factors, smoking is clearly related to the incidence of lung cancer and alcohol consumption to breast cancer. In this manuscript we modeled the potential benefits of reductions in smoking or alcohol prevalence for the burden of these cancers. Method: We used Prevent v.3.01 to assess the changes in incidence as a result of risk factor changes. Incidence of lung and breast cancer until 2050 was predicted under two scenarios: ideal (total elimination of smoking and reduction of alcohol intake to maximum 1 units/d for women) and optimistic (decreasing prevalence of risk factors because of a 10% increase in cigarette and alcohol beverage price, repeated every 5 years). Danish data from the household surveys, cancer registration and Eurostat were used. Results: Up to 49% less new lung cancer cases can be expected in 2050 if smoking were to be completely eliminated. Five-yearly 10% price increases may prevent 521. new lung cancer cases in 2050 (21% less cases). An intervention that immediately reduces population alcohol consumption to the recommended level (below 12 g/d) may lower breast cancer by 7%, preventing 445 out of the 6060 expected new cases in 2050. Five-yearly 10% price increases in alcoholic beverages achieved a reduction of half as expected by the ideal scenario, i.e. 4% (262) preventable cases in 2050. Conclusions: The future burden of lung and breast cancer could be markedly reduced by intervening in their risk factors. Prevent illustrates the benefit of interventions and may serve as guidance in political decision-making.

Thomsen T; Esbensen BA; Samuelsen S; Tonnesen H; Moller AM. Brief preoperative smoking cessation counselling in relation to breast cancer surgery: A qualitative study. European Journal of Oncology Nursing 13(5): 344-349, 2009. (30 refs.)

Aim: To describe how women smokers with newly diagnosed breast cancer experienced brief preoperative smoking cessation intervention in relation to breast cancer surgery. Background: Preoperative smoking cessation intervention is relevant for short- and long-term risk reduction in newly diagnosed cancer patients. Our knowledge of how patients with malignant diagnoses experience preoperative smoking intervention is however scarce. Methods: A qualitative descriptive study that collected data through one-time individual, semi-structured interviews with 11 Danish women. Ricoeur's theory of interpretation was used for the analysis. Results: The women experienced that brief preoperative smoking intervention triggered reflection upon smoking and health. They furthermore experienced the smoking intervention as an opportune aid to escaping the social stigma of being a smoker. Quitting in the context of cancer diagnosis was difficult for some women. They relapsed to smoking as an ingrown response to emotional distress. The smoking intervention heightened the women's awareness of their addiction to smoking; however, they expressed a need for prolonged smoking cessation support. For others, the smoking intervention was supportive of cessation, and these women experienced smoking cessation as an enactment of a duty of responsibility to themselves and those nearest to them. They furthermore experienced a sense of personal achievement, improved well-being and endorsement from family and friends. Conclusion: In newly diagnosed breast cancer patients, brief preoperative smoking intervention motivated smoking cessation. However, prolonged intervention, pre- and postoperatively, may more effectively support cessation in breast cancer patients and should therefore be evaluated in this patient population.

Thomsen T; Tonnesen H; Okholm M; Kroman N; Maibom A; Sauerberg ML et al. Brief smoking cessation intervention in relation to breast cancer surgery: A randomized controlled trial. Nicotine & Tobacco Research 12(11): 1118-1124, 2010. (27 refs.)

Smokers are more prone to develop postoperative complications. Smoking cessation intervention beginning 4-8 weeks prior to surgery improves the postoperative outcome. Cancer patients, however, often undergo surgery less than 4 weeks after diagnosis. The primary objective of this study was therefore to examine if a brief smoking cessation intervention shortly before breast cancer surgery would influence postoperative complications and smoking cessation. A randomized controlled multicentre trial with blinded outcome assessment conducted at 3 hospitals in Denmark. One hundred and thirty patients were randomly assigned to brief smoking intervention (n = 65) or standard care (n = 65). The intervention followed the principles of motivational interviewing and included personalized nicotine replacement therapy aimed at supporting smoking cessation from 2 days before to 10 days after surgery. The overall postoperative complication rate (including seroma requiring aspiration) was 61% in both groups risk ratio (RR) 1.00 (95% CI 0.75-1.33). The wound complication rate was 44% versus 45%. The effect on perioperative smoking cessation was modest, 28% intervention versus 11% control group patients, RR 2.49 (95% CI 1.10-5.60). There was no effect on smoking cessation at 12 months, 13% versus 9%. Brief smoking intervention administered shortly before breast cancer surgery modestly increased self-reported perioperative smoking cessation without having any clinical impact on postoperative complications. The study adds to the body of evidence indicating that brief intervention has no clinical importance for surgical patients in regard to postoperative morbidity. Future studies should be designed to determine the optimal time of smoking cessation before surgery.

Xue F; Willett WC; Rosner BA; Hankinson SE; Michels KB. Cigarette smoking and the incidence of breast cancer. Archives of Internal Medicine 171(2): 125-133, 2011. (57 refs.)

Background: Tobacco smoke contains carcinogens, which may increase the risk of breast cancer (BC). Conversely, cigarette smoking also has antiestrogenic effects, which may reduce the risk of BC. The association between smoking and BC remains controversial. Methods: Prospective cohort study of 111 140 participants of the Nurses' Health Study from 1976 to 2006 for active smoking and 36 017 women from 1982 to 2006 for passive smoking. Results: During 3 005 863 person-years of follow-up, 8772 incident cases of invasive BC were reported. After adjustment for potential confounders, the hazard ratio (HR) of BC was 1.06% (95% confidence interval [CI], 1.01%-1.10%) for ever smokers relative to never smokers. Breast cancer incidence was associated with a higher quantity of current (P for trend=.02) and past (P for trend=.003) smoking, younger age at smoking initiation (P for trend=.01), longer duration of smoking (P for trend=.01), and more pack-years of smoking (P for trend=.005). Premenopausal smoking was associated with a slightly higher incidence of BC (HR, 1.11; 95% CI, 1.07-1.15 for every increase of 20 pack-years), especially smoking before first birth (1.18; 1.10-1.27 for every increase of 20 pack-years). Conversely, the direction of the association between postmenopausal smoking and BC was inverse (0.93; 0.85-1.02 for every increase of 20 pack-years). Passive smoking in childhood or adulthood was not associated with BC risk. Conclusion: Active smoking, especially smoking before the first birth, may be associated with a modest increase in the risk of BC.