Search

Background The ongoing debate of whether use of cellular telephones increases the risk of developing a brain tumor was recently fueled by the launch of the fifth generation of wireless technologies. Here, we update follow-up of a large-scale prospective study on the association between cellular telephone use and brain tumors. Methods During 1996-2001, 1.3 million women born in 1935-1950 were recruited into the study. Questions on cellular telephone use were first asked in median year 2001 and again in median year 2011. All study participants were followed via record linkage to National Health Services databases on deaths and cancer registrations (including nonmalignant brain tumors). Results During 14 years follow-up of 776 156 women who completed the 2001 questionnaire, a total of 3268 incident brain tumors were registered. Adjusted relative risks for ever vs never cellular telephone use were 0.97 (95% confidence interval = 0.90 to 1.04) for all brain tumors, 0.89 (95% confidence interval = 0.80 to 0.99) for glioma, and not statistically significantly different to 1.0 for meningioma, pituitary tumors, and acoustic neuroma. Compared with never-users, no statistically significant associations were found, overall or by tumor subtype, for daily cellular telephone use or for having used cellular telephones for at least 10 years. Taking use in 2011 as baseline, there were no statistically significant associations with talking for at least 20 minutes per week or with at least 10 years use. For gliomas occurring in the temporal and parietal lobes, the parts of the brain most likely to be exposed to radiofrequency electromagnetic fields from cellular telephones, relative risks were slightly below 1.0. Conclusion Our findings support the accumulating evidence that cellular telephone use under usual conditions does not increase brain tumor incidence.

Background: Participation in social activities is thought to prevent heart disease, but evidence is inconclusive. Design: We assessed whether participating in social activities reduces the risk of coronary heart disease (CHD) in a large prospective study of 735,159 middle-aged UK women. Methods: Women reported their participation in eight social activities (religious group, voluntary work, adult education, art/craft/music, dancing, sports club, yoga, bingo) and were followed for first CHD event (hospital admission or death) over the next 8.6 years. Cox regression models were used to estimate relative risks for CHD incidence by participation in each and in any of the social activities. Results: After adjustment for age and region only, every activity except bingo was associated with a reduced risk of CHD (n = 30,756 cases in total). However, after additional adjustment for 11 factors (deprivation, education, smoking, physical activity, body mass index, alcohol, marital status, self-rated health, happiness, hypertension, diabetes), every relative risk estimate moved close to 1.0. For example, for participation in any of the activities compared with none, the relative risk adjusted for age and region only was 0.83 (99% confidence interval 0.81–0.86), but changed to 1.06 (99% confidence interval 1.02–1.09) after additional adjustment. Adjustment for education, self-rated health, smoking and physical activity attenuated the associations most strongly. Residual confounding and other unmeasured factors may well account for any small remaining associations. Conclusions: Associations between participation in various social activities and CHD risk appear to be largely or wholly due to confounding by personal characteristics of the participants.

Background The role of diet in breast cancer aetiology is unclear; recent studies have suggested associations may differ by estrogen receptor status. Methods Baseline diet was assessed in 2000–04 using a validated questionnaire in 691 571 postmenopausal UK women without previous cancer, who had not changed their diet recently. They were followed by record linkage to national cancer and death databases. Cox regression yielded adjusted relative risks for breast cancer for 10 food items and eight macronutrients, subdivided mostly into five categories of baseline intake. Trends in risk across the baseline categories were calculated, assigning re-measured intakes to allow for measurement error and changes in intake over time; P-values allowed for multiple testing. Results Women aged 59.9 (standard deviation (SD 4.9)) years at baseline were followed for 12 (SD 3) years; 29 005 were diagnosed with invasive breast cancer. Alcohol intake had the strongest association with breast cancer incidence: relative risk (RR) 1.08 [99% confidence interval (CI) 1.05–1.11] per 10 g/day higher intake, P = 5.8 × 10−14. There were inverse associations with fruit: RR 0.94 (99% CI 0.92–0.97) per 100 g/day higher intake, P = 1.1 × 10−6, and dietary fibre: RR 0.91 (99% CI 0.87–0.96) per 5 g/day increase, P = 1.1 × 10−4. Fruit and fibre intakes were correlated (ρ = 0.62) and were greater among women who were not overweight, so residual confounding cannot be excluded. There was no heterogeneity for any association by estrogen receptor status. Conclusions By far the strongest association was between alcohol intake and an increased risk of breast cancer. Of the other 17 intakes examined, higher intakes of fruit and fibre were associated with lower risks of breast cancer, but it is unclear whether or not these associations are causal.

Risk of adult lymphoid malignancy is associated with recent adiposity. Some have reported apparent associations with adiposity in childhood or early adulthood, but whether these associations are independent of recent adiposity is unknown. Birth weight, body size at age 10 years, clothes size at age 20 years, and recent body mass index (BMI) were recorded in 745,273 UK women, mean age 60.1 (SD 4.9) at baseline, without prior cancer. They were followed for 11 years, during which time 5,765 lymphoid malignancies occurred. Using Cox regression, a higher risk of lymphoid malignancy was strongly associated with higher recent BMI (RR=1.33, 95%CI 1.17‐1.51, for BMI 35+ vs, What's new? Previous research has found a link between obesity and adult lymphoid malignancy risk. In this paper, the researchers report on the relative importance of body size not only at the time of diagnosis, but also at birth, childhood, and age 20. They collected data from more than 750,000 women followed up for a period of 11 years. They showed that BMI at the time of diagnosis was the strongest determinant of risk. Being overweight at age 20 also conferred a small additional risk of lymphoid malignancy. There was comparably little evidence to support an additional role of body size at birth or childhood.

Ovarian cancer risk is known to be reduced amongst women who have had children, but reported associations with breastfeeding are varied. Few studies have had sufficient power to explore reliably these associations by tumour histotype. In a prospective study of 1.1 million UK women, 8719 developed ovarian cancer during follow-up. Cox regression yielded adjusted relative risks (RRs) overall and by tumour histotype amongst women with different childbearing patterns. Nulliparous women had a 24% greater ovarian cancer risk than women with one child, with significant heterogeneity by histotype (p=0.01). There was no significant increase in serous tumours, a modest increase in mucinous tumours, but a substantial increase in endometrioid (RR=1.49, 95% CI: 1.18-1.89) and clear-cell tumours (RR=1.68, 1.29-2.20). Among parous women, each additional birth was associated with an overall 6% reduction in ovarian cancer risk; this association also varied by histotype (p=0.0006), with the largest reduction in risk for clear-cell tumours (RR per birth=0.75, 0.65-0.85, p In this large prospective study, ovarian cancer risk associated with parity varied substantially by tumour histotype. Nulliparity was associated with a substantially greater overall risk than expected from the effect of a single birth, especially for clear cell and endometrioid tumours, perhaps suggesting that infertility is associated with these histotypes.

Some investigators have reported an excess risk of venous thromboembolism (VTE) associated with depression and with use of antidepressant drugs. We explored these associations in a large prospective study of UK women.The Million Women Study recruited 1.3 million women through the National Health Service Breast Screening Programme in England and Scotland. Three years after recruitment, women were sent a second questionnaire that enquired about depression and regular use of medications in the previous 4 weeks. The present analysis included those who responded and did not have prior VTE, cancer, or recent surgery. Follow-up for VTE was through linkage to routinely collected National Health Service statistics. Cox regression analyses yielded adjusted hazard ratios and 95% CIs. A total of 734 092 women (mean age 59.9 years) were included in the analysis; 6.9% reported use of antidepressants, 2.7% reported use of other psychotropic drugs, and 1.8% reported being treated for depression or anxiety but not use of psychotropic drugs. During follow-up for an average of 7.3 years, 3922 women were hospitalized for and/or died from VTE. Women who reported antidepressant use had a significantly higher risk of VTE than women who reported neither depression nor use of psychotropic drugs (hazard ratio, 1.39; 95% CI, 1.23-1.56). VTE risk was not significantly increased in women who reported being treated for depression or anxiety but no use of antidepressants or other psychotropic drugs (hazard ratio, 1.19; 95% CI, 0.95-1.49).Use of antidepressants is common in UK women and is associated with an increased risk of VTE.

BACKGROUND: Some carcinogenic viruses are known to be transmissible by blood transfusion. Intensive viral screening of transfused blood now exists in most countries. In the UK, high-sensitivity nucleic acid amplification tests for hepatitis C virus were introduced in 1999 and it was thought that this would reduce, and possibly eliminate, transfusion-related liver cancer. We aimed to investigate cancer risk in recipients of blood transfusion in 2000 or after. METHODS: A total of 1.3 million UK women recruited in 1998 on average were followed for hospital records of blood transfusion and for cancer registrations. After excluding women with cancer or precancerous conditions before or at the time of transfusion, Cox regression yielded adjusted relative risks of 11 site-specific cancers for women with compared to without prior blood transfusion. RESULTS: During follow up, 11 274 (0.9%) women had a first recorded transfusion in 2000 or after, and 1648 (14.6%) of them were subsequently diagnosed with cancer, a mean 6.8 years after the transfusion. In the first 5 years after transfusion there were significant excesses for most site-specific cancers examined, presumably because some had preclinical cancer. However, 5 or more years (mean 8 years) after blood transfusion, there were significant excess risks only for liver cancer (adjusted relative risk = 2.63, 95%CI 1.45-4.78) and for non-Hodgkin lymphoma (adjusted relative risk = 1.74, 1.21-2.51). When analyses were restricted to those undergoing hip or knee replacement surgery, the commonest procedure associated with transfusion, these relative risks were not materially altered. CONCLUSIONS: In a large cohort of UK women, transfusions in the 21st century were associated with long-term increased risks of liver cancer and non-Hodgkin lymphoma. Some of these malignancies may have been caused by carcinogenic agents that are not currently screened for in transfused blood.

Background: Some viruses are known to be transmissible by blood transfusion. Intensive viral screening of transfused blood now exists in most countries. In the UK, high-sensitivity nucleic acid amplification tests for hepatitis C virus were introduced in 1999 and it was thought that this would reduce, and possibly eliminate, transfusion-related liver cancer. We aimed to investigate cancer risk in recipient of blood transfusion in 2000 or after. Methods: 1.3 million UK women recruited in 1998, on average, were followed for hospital records of blood transfusion and for cancer registrations. After excluding women with cancer or precancerous conditions before or at the time of transfusion, Cox regression yielded adjusted relative risks of 11 site-specific cancers for women with compared to without prior blood transfusion. Results: During follow up, 11,274 (0.9%) women had a first recorded transfusion in 2000 or after, and 1648 (14.6%) of them were subsequently diagnosed with cancer, a mean 6.8 years after the transfusion. In the first 5 years after transfusion there were, as expected, significant excesses for most site-specific cancers examined, presumably because some had preclinical cancer. However, 5 or more years (mean 8 years) after blood transfusion there were significant excess risks only for liver cancer (relative risk=2.63, 95%CI 1.45-4.78) and for non-Hodgkin lymphoma (relative risk=1.74, 1.21-2.51). When analyses were restricted to those undergoing hip or knee replacement surgery, the commonest procedure associated with transfusion, these risks were not materially altered. Conclusions: In a large cohort of UK women, 21st century transfusions were associated with long-term increased risks of liver cancer and non-Hodgkin lymphoma. These findings suggest that some cases of liver cancer and non-Hodgkin lymphoma are caused by carcinogenic agents that are not currently screened for in transfused blood.

Objective:To compare associations of body mass index (BMI) with ischemic stroke and hemorrhagic stroke risk, and to review the worldwide evidence. Methods:We recruited 1.3 million previously stroke-free UK women between 1996 and 2001 (mean age 57 years [SD 5]) and followed them by record linkage for hospital admissions and deaths. We used Cox regression to estimate adjusted relative risks for ischemic and hemorrhagic (intracerebral or subarachnoid hemorrhage) stroke in relation to BMI. We conducted a meta-analysis of published findings from prospective studies on these associations. Results:During an average follow-up of 11.7 years, there were 20,549 first strokes, of which 9,993 were specified as ischemic and 5,852 as hemorrhagic. Increased BMI was associated with an increased risk of ischemic stroke (relative risk 1.21 per 5 kg/m2 BMI, 95% confidence interval 1.18-1.23, p < 0.0001) but a decreased risk of hemorrhagic stroke (relative risk 0.89 per 5 kg/m2 BMI, 0.86-0.92, p < 0.0001). The BMI-associated trends for ischemic and hemorrhagic stroke were significantly different (heterogeneity: p < 0.0001) but were not significantly different for intracerebral hemorrhage (n = 2,790) and subarachnoid hemorrhage (n = 3,062) (heterogeneity: p = 0.5). Published data from prospective studies showed consistently greater BMI-associated relative risks for ischemic than hemorrhagic stroke with most evidence (prior to this study) coming from Asian populations. Conclusions:In UK women, higher BMI is associated with increased risk of ischemic stroke but decreased risk of hemorrhagic stroke. The totality of the available published evidence suggests that BMI-associated risks are greater for ischemic than for hemorrhagic stroke.

Concern about possible increased risks for cancer associated with night work, circadian rhythm disruption, and impaired nocturnal melatonin production (Cohen et al, 1978; Stevens, 1987; Erren, 2002; Stevens, 2002; Straif et al, 2007; Wang et al, 2011) has prompted interest in cancer risk in relation to sleep behaviours and disturbance. Several studies have examined associations between sleep duration and breast cancer risk (Verkasalo et al, 2005; McElroy et al, 2006; Pinheiro et al, 2006; Kakizaki et al, 2008; Wu et al, 2008), but have not demonstrated a consistent association. Daytime fatigue and daytime napping are associated with sleep disturbance (Ursin et al, 2005), and cancer risk might therefore be related to daytime napping. Although there is a substantial literature on sleep problems and fatigue in cancer patients (Davidson et al, 2002; Stasi et al, 2003; Lee et al, 2004), including before treatment (Ancoli-Israel et al, 2006), little has been published on whether daytime napping is a marker of pre-clinical disease. The association between daytime napping and cancer mortality has been examined in two cohorts (Suzuki, 2007; Stone et al, 2009; Tanabe et al, 2010); one found increased liver cancer mortality among women who nap during the day (Suzuki, 2007). This is the first prospective study to investigate the association between daytime napping and cancer incidence.

Background:Previous research suggests associations of lower alcohol intake and higher tobacco consumption with increased risks of haematological malignancy. The prospective Million Women Study provides sufficient power for reliable estimates of subtype-specific associations in women.Methods: Approximately 1.3 million middle-aged women were recruited in the United Kingdom during 1996-2001 and followed for death, emigration and cancer registration until 2009 (mean 10.3 years per woman); potential risk factors were assessed by questionnaire. Adjusted relative risks were estimated by Cox regression.Results:During follow-up, 9162 incident cases of haematological malignancy were recorded, including 7047 lymphoid and 2072 myeloid cancers. Among predominantly moderate alcohol drinkers, higher intake was associated with lower risk of lymphoid malignancies, in particular diffuse large B-cell lymphoma (relative risk 0.85 per 10 g alcohol per day (95% confidence interval 0.75-0.96)), follicular lymphoma (0.86 (0.76-0.98)) and plasma cell neoplasms (0.86 (0.77-0.96)). Among never-and current smokers, higher cigarette consumption was associated with increased risk of Hodgkin lymphoma (1.45 per 10 cigarettes per day (1.22-1.72)), mature T-cell malignancies (1.38 (1.10-1.73)) and myeloproliferative/myelodysplastic disease (1.42 (1.31-1.55)).Conclusion: These findings confirm and extend existing evidence for associations of subtypes of haematological malignancy with two common exposures in women. © 2012 Cancer Research UK.

Background: Organically produced foods are less likely than conventionally produced foods to contain pesticide residues. Methods: We examined the hypothesis that eating organic food may reduce the risk of soft tissue sarcoma, breast cancer, non-Hodgkin lymphoma and other common cancers in a large prospective study of 623 080 middle-aged UK women. Women reported their consumption of organic food and were followed for cancer incidence over the next 9.3 years. Cox regression models were used to estimate adjusted relative risks for cancer incidence by the reported frequency of consumption of organic foods. Results: At baseline, 30%, 63% and 7% of women reported never, sometimes, or usually/always eating organic food, respectively. Consumption of organic food was not associated with a reduction in the incidence of all cancer (n=53 769 cases in total) (RR for usually/always vs never=1.03, 95% confidence interval (CI): 0.99–1.07), soft tissue sarcoma (RR=1.37, 95% CI: 0.82–2.27), or breast cancer (RR=1.09, 95% CI: 1.02–1.15), but was associated for non-Hodgkin lymphoma (RR=0.79, 95% CI: 0.65–0.96). Conclusions: In this large prospective study there was little or no decrease in the incidence of cancer associated with consumption of organic food, except possibly for non-Hodgkin lymphoma.

Risk factors for fracture of the neck of the femur are relatively well established, but those for fracture at other sites are little studied. In this large population study we explore the role of age, body mass index (BMI), and physical activity on the risk of fracture at seven sites in postmenopausal women. As part of the Million Women Study, 1,154,821 postmenopausal UK women with a mean age of 56.0 (SD 4.8) years provided health and lifestyle data at recruitment in 1996 to 2001. All participants were linked to National Health Service (NHS) hospital records for day-case or overnight admissions with a mean follow-up of 11 years per woman. Adjusted absolute and relative risks for seven site-specific incident fractures were calculated using Cox regression models. During follow-up, 4931 women had a fracture of the humerus; 2926 of the forearm; 15,883 of the wrist; 9887 of the neck of the femur; 1166 of the femur (not neck); 3199 a lower leg fracture; and 10,092 an ankle fracture. Age-specific incidence rates increased gradually with age for fractures of forearm, lower leg, ankle, and femur (not neck), and steeply with age for fractures of neck of femur, wrist, and humerus. When compared to women with desirable BMI (20.0 to 24.9 kg/m(2) ), higher BMI was associated with a reduced risk of fracture of the neck of femur, forearm, and wrist, but an increased risk of humerus, femur (not neck), lower leg, and ankle fractures (p

We thank Lin and colleagues for drawing attention to hypotheses about the possible role of heavy manual work and work-related stress in vascular disease. We previously reported associations between coronary heart disease, cerebrovascular disease, and venous thromboembolism risk and the frequency of strenuous activity and of any activity.1 We also assessed the associations between these diseases and walking, gardening, cycling, housework, and strenuous activity, which were reported for the first time ≈3 years after recruitment.1 At that time, women were asked about whether or not they were in paid work: about half (53%) reported that they were not in paid work. Findings for women not in paid work cannot be confounded by heavy manual work or stress at work. We therefore conducted further analyses for vascular disease risk associated with physical activity, restricted to the 376 732 women who reported not being in paid work, using the date at which they reported their employment status as the start of follow-up. Similar to our previous findings for all women,1 we again observed that the lowest risks were among women with a moderate frequency of physical activity, suggesting that these associations are not attributable to heavy manual work or stress at work. (There may, of course, be residual confounding with other factors, as discussed in our original article.) The results for the frequency of strenuous physical activity among women who reported not being in paid work are presented here, for comparison with our findings for all women. For coronary heart disease risk (20 861 cases), in comparison with inactive women, the women who were active at most once per week had a relative risk (RR) of 0.85 (95% confidence interval [CI], 0.82–0.87), women active 2 to 3 times per week had an RR of 0.80 (95% CI, 0.77–0.84), women active 4 to 6 times per week had an RR of 0.74 (95% CI, 0.67–0.81), and those active daily had an RR of 0.91 (95% CI, 0.84– 0.99). For cerebrovascular disease (7638 cases), the corresponding RRs and 95% CIs were 0.83 (0.78–0.88), 0.84 (0.78–0.90), 0.84 (0.74–0.97), and 0.92 (0.80–1.05), and for venous thromboembolism (5999 cases), the corresponding RRs and 95% CIs were 0.85 (0.80– 0.90), 0.82 (0.76–0.89), 0.86 (0.73–1.00), and 0.98 (0.84–1.13). The P values for heterogeneity across activity levels were significant (P

Objective:To explore the long-term effects of women's childbearing patterns on their body mass index.Design:Cross-sectional analysis.Setting:Population- based study of UK women.Participants:740 628 postmenopausal participants in the Million Women Study who reported their height, weight, reproductive histories and other relevant factors.Main Outcome Measures:Standardized mean BMI (kg m -2) in groups defined by their parity and breastfeeding history.Results:Women were aged 57.5 (s.d. 4) years on average, and had a mean BMI of 26.2 kg m -2 (s.d. 5); 88% were parous, with 2.1 (s.d. 1.2) children on average. The standardised mean BMI increased progressively with the number of births from 25.6 kg m -2 (95% confidence interval (CI): 25.5-25.6) in nulliparous women up to 27.2 kg m -2 (CI: 27.2-27.3) for women with four or more births, a difference of 1.7 kg m -2 (CI: 1.6-1.7). Among the parous women 70% had ever breastfed and their average total duration of breastfeeding was 7.7 (s.d. 8.8) months. At every parity level the standardised mean BMI was significantly lower among women who had breastfed than those who had not, decreasing by 0.22 kg m -2 (CI: 0.21-0.22) for every 6 months of breastfeeding, that is, women's mean BMI was 1% lower for every 6 months that they had breastfed. These associations were highly statistically significant (P

Summary. Background: Current use of menopausal hormone therapy (HT) increases the risk of venous thromboembolism (VTE) and the formulations used may affect risk. Methods: A total of 1 058 259 postmenopausal UK women were followed by record linkage to routinely collected National Health Service hospital admission and death records. HT use and risk of VTE was examined using Cox regression to estimate relative risks (RRs) and 95% confidence intervals (CIs). Results: During 3.3 million years of follow-up, 2200 women had an incident VTE, diagnosed, on average, 1.5 years after last reporting HT use. RRs in current vs. never users at last reporting varied by HT formulation: the risk was significantly greater for oral estrogen-progestin than oral estrogen-only therapy (RR = 2.07 [95%CI, 1.86–2.31] vs. 1.42 [1.21–1.66]), with no increased risk with transdermal estrogen-only therapy (0.82 [0.64–1.06]). Among users of oral estrogen-progestin, the risk from HT varied by progestin type, with significantly greater risks for preparations containing medroxyprogesterone acetate than other progestins (2.67 [2.25–3.17] vs. 1.91 [1.69–2.17]; Pheterogeneity = 0.0007). Current users of oral HT at last reporting had twice the risk of VTE in the first 2 years after starting HT than later (Pheterogeneity = 0.0006). Associations were similar for deep vein thrombosis with and without pulmonary embolism. Over 5 years, 1 in 660 who had never used HT were admitted to hospital for (or died from) pulmonary embolism, compared with 1 in 475 current users of oral estrogen-only HT,1 in 390 users of estrogen-progestin HT containing norethisterone/norgestrel, and 1 in 250 users of estrogen-progestin HT containing medroxyprogesterone acetate. Conclusions: The risk of VTE varied considerably by HT formulation, being greatest in users of oral estrogen-progestin HT, especially formulations containing medroxyprogesterone acetate.

BACKGROUND: Sleep disturbance, a correlate of which is daytime napping, has been hypothesised to be associated with risk of breast and other cancers. METHODS: We estimated relative risks (RR) of breast and other invasive cancers by the reported frequency of daytime napping in a large prospective cohort of middle-aged women in the UK. RESULTS: During an average of 7.4 years of follow-up, 20 058 breast cancers and 31 856 other cancers were diagnosed. Over the first 4 years of follow-up, daytime napping (sometimes/usually vs rarely/never) was associated with slightly increased risks of breast cancer (RR=1.10, 95% CI 1.06-1.15) and of other cancers (RR=1.12, 1.08-1.15), but the RRs decreased significantly with increasing follow-up time (P=0.001 and P=0.01, respectively, for trend). Four or more years after baseline, there was no elevated risk of breast cancer (RR=1.00, 0.96-1.05), and only marginally greater risk of other cancers (RR=1.04, 1.01-1.07). CONCLUSION: The effect of pre-clinical disease is a likely explanation for the short-term increased risk of breast and other cancers associated with daytime napping.

Little is known about how reproductive factors affect the risk of breast cancers of different histology. In an analysis of prospective data on 1.2 million middle-aged UK women, we used proportional hazards models to estimate the relative risks of six histological types in relation to menarche, childbearing and menopause. During 8.7 million person-years of follow-up, 17 923 ductal, 3332 lobular, 1062 tubular, 944 mixed ductal lobular, 330 mucinous and 117 medullary cancers were diagnosed. The effect of both age at menarche and age at first birth was greatest for lobular tumours; relative risks per 5-year increase in age at menarche for ductal, lobular, and tubular cancers were 0.93 (0.87-0.99), 0.65 (0.56-0.76), and 0.75 (0.57-0.98), respectively (P-value for heterogeneity=0.0001); and the relative risks per 5-year increase in age at first birth were 1.10 (1.07-1.12), 1.23 (1.17-1.29), and 1.13 (1.03-1.23), respectively (P-value for heterogeneity=0.0006). Increasing parity reduced the risk of each tumour type, except medullary cancers, but the reduction in risk was greater for mucinous cancers than for any other subtype considered (P

The role of spontaneous and induced abortion on breast cancer risk is examined among 267,361 women recruited into the European Prospective Investigation into Cancer and nutrition between 1992 and 2000. The data were collected from 20 centers, across 9 countries, and included information on a total of 4,805 women with breast cancer, of whom 1,657 reported having ever had any type of abortion. Overall, the relative risk of breast cancer in women who reported ever having had a spontaneous abortion was not significantly elevated when compared with women who reported never having had such an abortion (RR = 1.07, 95% CI = 0.99-1.14). However, there was some evidence of a slight increase in the risk of breast cancer among women who reported having had 2 or more spontaneous abortions (1.20, 1.07-1.35). The relative risk of breast cancer among women who reported ever having had an induced abortion when compared to women who reported never having had an induced abortion was 0.95 (0.87-1.03). Overall, the findings provide further unbiased evidence of the lack of an adverse effect of induced abortion on breast cancer risk. © 2006 Wiley-Liss, Inc.

Menopausal hormone therapy (MHT) is characterized by use of different constituents, regimens and routes of administration. We investigated the association between the use of different types of MHT and breast cancer risk in the EPIC cohort study. The analysis is based on data from 133,744 postmenopausal women. Approximately 133,744 postmenopausal women contributed to this analysis. Information on MHT was derived from country-specific self-administered questionnaires with a single baseline assessment. Incident breast cancers were identified through population cancer registries or by active follow-up (mean: 8.6 yr). Overall relative risks (RR) and 95% confidence interval (CI) were derived from country-specific Cox proportional hazard models estimates. A total of 4312 primary breast cancers were diagnosed during 1,153,747 person-years of follow-up. Compared with MHT never users, breast cancer risk was higher among current users of estrogen only (RR: 1.42, 95% CI 1.23-1.64) and higher still among current users of combined MHT (RR: 1.77, 95% CI 1.40-2.24; p = 0.02 for combined vs. estrogen-only). Continuous combined regimens conferred a 43% (95% CI: 19-72%) greater risk compared with sequential regimens. There was no significant difference between progesterone and testosterone derivatives in sequential regimens. There was no significant variation in risk linked to the estrogenic component of MHT, neither for oral vs. cutaneous administration nor for estradiol compounds vs. conjugated equine estrogens. Estrogen-only and combined MHT uses were associated with increased breast cancer risk. Continuous combined preparations were associated with the highest risk. Further studies are needed to disentangle the effects of the regimen and the progestin component.