Vitamin C may influence cancer progression through its antioxidant properties. However, the evidence from observational epidemiologic studies on vitamin C intake and survival following breast cancer diagnosis is not consistent, and the safety of vitamin C supplements following breast cancer diagnosis has not been extensively studied.
Using a food-frequency questionnaire we investigated whether vitamin C intake was associated with survival among 3405 women diagnosed with invasive breast cancer in the Swedish Mammography Cohort.
From 1987–2010, there were 1055 total deaths with 416 deaths from breast cancer. Women in the highest quartile of pre-diagnosis vitamin C intake had an adjusted HR (95% CI) of breast cancer death of 0.75 (0.57–0.99) compared with those in the lowest quartile (Ptrend=0.03). There was a borderline significant association between vitamin C intake and total mortality (HR=0.84; 95% CI=0.71–1.00; Ptrend=0.08). Among 717 breast cancer cases for whom post-diagnosis supplement use was available, there was no association between vitamin C supplement use (≈1000 mg) and breast cancer-specific mortality (HR=1.06; 95% CI=0.52–2.17).
Our findings suggest that dietary vitamin C intake before breast cancer diagnosis may be associated with breast cancer survival. In addition, post-diagnosis vitamin C supplementation at the level observed in our population was not associated with survival.
breast cancer; diet; epidemiology; vitamin C; supplements; survival
Coffee and black tea contain a mixture of compounds that have the potential to influence breast cancer risk and survival. However, epidemiologic data on the relation between coffee and black tea consumption and breast cancer survival are sparse.
We investigated the association between coffee and black tea consumption and survival among 3243 women with invasive breast cancer in the Swedish Mammography Cohort. Intake was estimated using a food frequency questionnaire. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs).
From 1987 to 2010 there were 394 breast cancer-specific deaths and 973 total deaths. Coffee and black tea were not associated with breast cancer-specific or overall mortality. Women consuming 4+ cups of coffee per day had a covariate and clinical characteristics-adjusted HR (95% CI) of death from breast cancer of 1.14 (0.71–1.83; ptrend=0.81) compared with those consuming <1 cup per day. Women consuming 2+ cups of black tea per day had a covariate and clinical characteristics-adjusted HR (95% CI) of death from breast cancer of 1.02 (0.67–1.55; ptrend=0.94) compared with non-tea drinkers. Caffeine was also not associated with breast cancer-specific (HR for top to bottom quartile=1.06; 95% CI=0.79–1.44; ptrend=0.71) or overall mortality.
Our findings suggest that coffee, black tea, and caffeine consumption before breast cancer diagnosis do not influence breast cancer-specific and overall survival.
breast cancer; epidemiology; coffee; tea; caffeine; survival
Alcohol intake has consistently been associated with increased breast cancer incidence in epidemiological studies. However, the relation between alcohol and survival after breast cancer diagnosis is less clear.
We investigated whether alcohol intake was associated with survival among 3146 women diagnosed with invasive breast cancer in the Swedish Mammography Cohort. Alcohol consumption was estimated using a food frequency questionnaire. Cox proportional hazard models were used to calculate hazard ratios (HRs) and 95% confidence intervals (95% CIs).
From 1987 to 2008 there were 385 breast cancer-specific deaths and 860 total deaths. No significant association was observed between alcohol intake and breast cancer-specific survival. Women who consumed 10 g per day (corresponding to approximately 0.75 to 1 drinks) or more of alcohol had an adjusted HR (95% CI) of breast cancer-specific death of 1.36 (0.82–2.26;ptrend=0.47) compared with non-drinkers. A significant inverse association was observed between alcohol and non-breast cancer deaths. Those who consumed 3.4–9.9 g per day of alcohol had a 33% lower risk of death compared with non-drinkers (95% CI 0.50–0.90;ptrend=0.04).
Our findings suggest that alcohol intake up to approximately one small drink per day does not negatively impact breast cancer-specific survival and a half drink per day is associated with a decreased risk of mortality from other causes.
alcohol; breast cancer; survival
Current guidelines recommend completion axillary lymph node dissection (cALND) in case of a sentinel lymph node (SLN) metastasis larger than 0.2 mm. However, in 50%–65% of these patients, the non-SLNs contain no further metastases and cALND provides no benefit. Several nomograms and scoring systems have been suggested to predict the risk of metastases in non-SLNs. We have evaluated the Tenon score.
Patients and Methods
In a retrospective review of the Swedish Sentinel Node Multicentre Cohort Study, risk factors for additional metastases were analysed in 869 SLN-positive patients who underwent cALND, using uni- and multivariate logistic regression models. A receiver operating characteristic (ROC) curve was drawn on the basis of the sensitivity and specificity of the Tenon score, and the area under the curve (AUC) was calculated.
Non-SLN metastases were identified in 270/869 (31.1%) patients. Tumour size and grade, SLN status and ratio between number of positive SLNs and total number of SLNs were significantly associated with non-SLN status in multivariate analyses. The area under the curve for the Tenon score was 0.65 (95% CI 0.61–0.69). In 102 patients with a primary tumour <2 cm, Elston grade 1–2 and SLN metastases ≤2 mm, the risk of non SLN metastasis was less than 10%.
The Tenon score performed inadequately in our material and we could, based on tumour and SLN characteristics, only define a very small group of patients in which negative non-sentinel nodes could be predicted.
breast cancer; sentinel node; metastases
Among the 51 823 postmenopausal women in the Swedish Mammography Cohort, we investigated breast cancer risk in relation to the FFQ-based estimated lignan intake by oestrogen receptor (ER) and progesterone receptor (PR) subtypes. A significant 17% risk reduction for breast cancer overall in the high lignan quartile was observed, especially among PMH user (Pinteraction<0.010), but no heterogeneity across ER/PR subtypes.
breast cancer; oestrogen receptor; progesterone receptor; dietary lignans; risk
Breast cancer is globally the most common malignancy in women. Her2-targeted monoclonal antibodies are established treatment modalities, and vaccines are in late-stage clinical testing in patients with breast cancer and known to promote tumour-killing through mechanisms like antibody-dependent cellular cytotoxicity. It is therefore increasingly important to study immunological consequences of conventional treatment strategies. In this study, functional tests and four-colour flow cytometry were used to detect natural killer (NK)-cell functions and receptors as well as T-cell signal transduction molecules and intracellular cytokines in preoperative breast cancer patients, and patients who had received adjuvant radiotherapy or adjuvant combined chemo-radiotherapy as well as in age-matched healthy controls. The absolute number of NK cells, the density of NK receptors as well as in vitro quantitation of functional NK cytotoxicity were significantly higher in preoperative patients than the post-treatments group and controls. A similar pattern was seen with regard to T-cell signalling molecules, and preoperative patients produced significantly higher amounts of cytokines in NK and T cells compared to other groups. The results indicate that functions of NK and T cells are well preserved before surgery but decrease following adjuvant therapy, which may speak in favour of early rather than late use of immunotherapeutic agents such as trastuzumab that may depend on intact immune effector functions.
breast cancer; Her-2; T-cell signalling proteins; cytokines; NK cytotoxicity
We examined the associations of body mass index (BMI), waist circumference, a history of diabetes, and cigarette smoking with risk of pancreatic cancer among 37 147 women and 45 906 men followed up during 560 666 person-years in the Swedish Mammography Cohort and the Cohort of Swedish Men; 136 incident cases of pancreatic cancer were diagnosed. The multivariate rate ratio (RR) of pancreatic cancer for obese women and men (BMI ⩾30 kg/m2) was 1.81 (95% CI: 1.04–3.15) compared to those with a BMI of 20–25 kg/m2. For a difference of 20 cm (about two standard deviations) in waist circumference, the multivariate RRs were 1.32 (95% CI: 0.73–2.37) among women and 1.74 (95% CI: 1.00–3.01) among men. Pancreatic cancer risk was associated with history of diabetes (multivariate RR: 1.88; 95% CI: 1.09–3.26) and cigarette smoking (multivariate RR for current compared with never smokers: 3.06; 95% CI: 1.99–4.72). Current smokers of ⩾40 pack-years had a five-fold elevated risk compared with never smokers. Risk among past smokers approached the RR for never smokers within 5–10 years following smoking cessation. Findings from this prospective study support positive relationships of overall obesity, abdominal adiposity, diabetes and smoking with risk of pancreatic cancer.
anthropometry; body mass index; cohort studies; diabetes mellitus; pancreatic neoplasms; obesity; prospective studies; smoking; smoking cessation
We examined prospectively the association between whole grain consumption and colorectal cancer risk in the population-based Swedish Mammography Cohort. A total of 61 433 women completed a food-frequency questionnaire at baseline (1987–1990) and, through linkage with the Swedish Cancer Registry, 805 incident cases of colorectal cancer were identified during a mean follow-up of 14.8 years. High consumption of whole grains was associated with a lower risk of colon cancer, but not of rectal cancer. The multivariate rate ratio (RR) of colon cancer for the top category of whole grain consumption (⩾4.5 servings day−1) compared with the bottom category (<1.5 servings day−1) was 0.67 (95% confidence interval (CI), 0.47–0.96; P-value for trend=0.06). The corresponding RR after excluding cases occurring within the first 2 years of follow-up was 0.65 (95% CI, 0.45–0.94; P-value for trend=0.04). Our findings suggest that high consumption of whole grains may decrease the risk of colon cancer in women.
cohort studies; colon cancer; epidemiology; dietary fibre; rye; whole grains
BACKGROUND—The presumed protective effect of coffee consumption on colorectal cancer, which is supported by case control studies, has not been confirmed in prospective cohort studies. Cohort studies are few in number however and often suffer from a small number of cases, limited attention to confounding variables, and a low percentage of heavy coffee drinkers.
METHODS—We examined data from a large population based cohort of Swedish women who were free from cancer at the start of follow up, with a wide range of coffee consumption, information on many potentially confounding variables, and a larger number of cases than any previous cohort study of coffee consumption and colorectal cancer.
RESULTS—During an average of 9.6 years of follow up of 61 463 women aged 40-74 years, we observed 460 incident cases of colorectal cancer (291 with colon cancer, 159 with rectal cancer, 10 with cancer at both sites). We found no association between coffee consumption and colorectal cancer risk. The risk ratio for drinking four or more cups per day compared with none was 1.04 (95% confidence interval 0.63—1.69; p for trend 0.84). The findings were similar for cancers of the distal and proximal colon and rectum.
CONCLUSIONS—The recently published affirmative conclusions regarding the protective effect of coffee consumption may be premature. For patients seeking advice about coffee consumption, the evidence suggests that moderate or even high consumption will probably not influence the risk of colorectal cancer.
Keywords: colorectal neoplasms; cohort studies; coffee drinking
Ductal breast carcinoma in situ (DCIS) is regarded as a precursor to invasive breast cancer. The progression from in situ to invasive cancer is however little understood. We compared some tumour markers in invasive and in situ breast carcinomas trying to find steps in this progression. We designed a semi-experimental setting and compared histopathological grading and tumour marker expression in pure DCIS (n = 194), small invasive lesions (n = 127) and lesions with both an invasive and in situ component (n = 305). Grading was done according to the Elston–Ellis and EORTC classification systems, respectively. Immunohistochemical staining was conducted for p53, c-erbB-2, Ki-67, ER, PR, bcl-2 and angiogenesis. All markers correlated with grade rather than with invasiveness. No marker was clearly associated with the progression from in situ to invasiveness. The expression of tumour markers was almost identical in the 2 components of mixed lesions. DCIS as a group showed a more ‘malignant picture' than invasive cancer according to the markers, probably, due to a higher proportion of poorly differentiated lesions. The step between in situ and invasive cancer seems to occur independently of tumour grade. The results suggest that well-differentiated DCIS progress to well-differentiated invasive cancer and poorly differentiated DCIS progress to poorly differentiated invasive cancer. © 2001 Cancer Research Campaign http://www.bjcancer.com
breast cancer; invasive; in situ; progression
The relation between relative body weight and colorectal cancer among women is unclear. In a large prospective cohort study, we found a positive association only for distal cancers among younger women that became attenuated at older ages. These results support previous reports in which results were stratified by age or colorectal cancer site. © 2001 Cancer Research Campaign http://www.bjcancer.com
colorectal neoplasms; body weight; insulin; menopause; cohort studies
OBJECTIVE: To determine the relative risk of developing endometrial neoplasia after treatment with oestrogens alone or in conjunction with progestogens. DESIGN: Prospective cohort follow up study, average observation period 5.7 years for each patient. To have a 90% chance of detecting a relative risk of 2.0 with 95% significance the study required 78,000 person years of observation. SETTING: Community based cohort. PATIENTS: Women aged over 35 who were prescribed non-contraceptive oestrogens in the Uppsala health care region during April 1977 to March 1980 were identified from pharmacy records. Of all prescriptions issued, 95% were identified. Patients from the cohort who developed endometrial neoplasia were identified from the cancer registry of the Uppsala health care region. Compliance, sociodemographic data, and lifetime exposures to oestrogen and cyclically added progestogen were assessed by questionnaire in a sample of the cohort. The final cohort consisted of 23,244 patients (133,373 person years). The prevalence of university education, oophorectomy, and hysterectomy was higher in the cohort than the general population; no other confounding factors were identified. MEASUREMENTS: The total number of person years was divided into exposure groups by inference from the data from the questionnaire. Compensation was made for the excess of hysterectomies. Specimens from all cases of endometrial neoplasia in the cohort and 90% of cases in the general population were studied blind histopathologically. Characteristics of treatment of all women who had endometrial neoplasia were assessed by questionnaire. Relative risks and 95% confidence intervals were calculated. RESULTS: Seventy four cases of carcinoma and 33 cases of premalignant lesions occurred in the cohort. The relative risk of endometrial carcinoma was 1.8 (95% confidence interval 1.1 to 3.2) after exposure to any oestrogen compound without progestogen for more than six years; 2.2 (1.2 to 4.4) after more than three years' exposure to conjugated oestrogens without progestogen; and 2.7 (1.4 to 5.1) after more than three years' exposure to oestradiol compounds without progestogen. When carcinoma and premalignant lesions were considered together the results were similar but the relative risk was higher. Risk of carcinoma did not increase when progestogens were cyclically added to oestrogens for the entire treatment period (relative risk 0.9 (0.4 to 2.0]. CONCLUSIONS: Use of oestrogens without progestogens is associated with a twofold to threefold increase in risk of endometrial neoplasia. Use of progestogens either removes this increased risk or delays its onset. A further follow up of the cohort is essential to analyse the risks with greater statistical power.
The association between breast and endometrial cancer was investigated in a cohort consisting of 60,065 subjects (99% of all women in whom a first breast cancer was diagnosed in Sweden in 1960-63 and 1968-81). Complete follow-up until 1981 revealed a total of 260 endometrial cancers, as against an expected number of 151.1 (relative risk (RR) = 1.72; 95% confidence limits (CL) 1.46; 1.87). RR increased steadily from close to unity in women younger than 50 at breast cancer diagnosis to 2.40 (CL 1.97; 2.93) in those 70 years of age and older. The excess number of endometrial cancers occurred primarily during the first five years of follow-up (RR = 2.07; CL 1.79; 2.38). A common causal agency for breast and endometrial cancer is more likely to lie in environmental than in genetic factors and other observations in the same population do not support that such factors are related to characteristics of the women's reproductive histories.