The natural history of type-specific human papillomavirus (HPV) infections was examined in a cohort of 331 women aged 18-35 years who self-referred for routine gynecological care. Participants underwent a gynecological examination at baseline and at approximately 4 and approximately 10 months after baseline. Cervical samples were collected for HPV testing and genotyping at each visit, as was information on reproductive, sexual, and medical histories. The rate of new HPV infections was 2.9% per month; the highest rates were observed for HPV types 16, 39, 84, and 51. Among women who tested negative for HPV at baseline, the cumulative probability of acquiring an oncogenic HPV strain during a 12-month follow-up period was 0.32, compared with 0.18 for nononcogenic strains. Women who had had >/=1 new male sex partner in the recent past were significantly more likely to acquire a new HPV infection (relative hazard, 2.39; 95% confidence interval, 1.20-4.76). The median time to clearance of infection was significantly longer for oncogenic strains (9.8 months) than for nononcogenic strains (4.3 months).

The purpose of this study is to investigate 1-year adherence rates to aromatase inhibitors (AI) and to determine risk factors for non-adherence among commercially insured post-menopausal breast cancer patients. A retrospective cohort of 13,593 commercially insured breast cancer patients with a prescription claim for an AI therapy (exemestane, anastrozole, and letrozole) in 2006 were identified using the MarketScan Commercial Claims and Encounters Database. Adherence was calculated by the medication possession ratio (MPR) for a 1-year period following the initial claim in 2006. The main outcome variable was non-adherence (<80% MPR) to AI therapy. Multivariate logistic regression was used to determine predictors of non-adherence. Over a 1-year period, 23% of patients were non-adherent with their AI therapy. AI non-adherence was associated with younger age, out-of-pocket costs ≥$30 per AI prescription, as well as with measures during the 12-month period prior to the initial 2006 AI claim of lower patient out-of-pocket total pharmacy costs, no mastectomy, and higher Charlson Comorbidity Index. Non-adherence to AI is a common occurrence. A number of factors were identified that influence patience non-adherence. These factors can be used to identifying patients at increased risk for non-adherence to better target and intervene to support medication taking behaviors.

Purpose Obesity increases risk for all-cause and breast cancer mortality and comorbidities in women who have been diagnosed and treated for breast cancer. The Exercise and Nutrition to Enhance Recovery and Good Health for You (ENERGY) study is the largest weight loss intervention trial among survivors of breast cancer to date. Methods In this multicenter trial, 692 overweight/obese women who were, on average, 2 years since primary treatment for early-stage breast cancer were randomly assigned to either a group-based behavioral intervention, supplemented with telephone counseling and tailored newsletters, to support weight loss or a less intensive control intervention and observed for 2 years. Weight and blood pressure were measured at 6, 12, 18, and 24 months. Longitudinal mixed models were used to analyze change over time. Results At 12 months, mean weight loss was 6.0% of initial weight in the intervention group and 1.5% in the control group (P < .001). At 24 months, mean weight loss in the intervention and control groups was 3.7% and 1.3%, respectively (P < .001). Favorable effects of the intervention on physical activity and blood pressure were observed. The weight loss intervention was more effective among women older than 55 years than among younger women. Conclusion A behavioral weight loss intervention can lead to clinically meaningful weight loss in overweight/obese survivors of breast cancer. These findings support the need to conduct additional studies to test methods that support sustained weight loss and to examine the potential benefit of intentional weight loss on breast cancer recurrence and survival.

Epidemiologic evidence points to obesity as a major risk factor for many cancers, including cancers of the breast, endometrium, colorectum, kidney, oesophagus and pancreas. Whether intentional weight loss might reduce this excess risk is not yet proven. We searched the medical literature for studies reporting changes in cancer risk following intentional weight loss, and for studies reporting changes in cancer-relevant risk factors of oestrogens, sex hormone binding globulin (SHBG), Insulin-like growth factor-I (IGF-I), IGF binding proteins and selected inflammatory markers [C-reactive protein (CRP), interleukin 6 (IL-6) and tumour necrosis factor-α (TNF-α)]. Observational cohort studies and randomized controlled trials of both dietary interventions and bariatric surgery all indicate fairly immediate reductions in cancer incidence following intentional weight loss. Oestrogen levels drop and SHBG levels increase coincident with intentional weight loss, with about a one-third reduction in free oestradiol to be expected from a 10% weight loss. CRP levels also drop substantially after weight loss at about this same 3 : 1 ratio. Reductions in TNF-α and IL-6 are consistently seen, but of a smaller magnitude, and IGF-I and IGFBP changes after weight loss are small and inconsistent. Because both cancer incidence and levels of circulating cancer biomarkers drop fairly rapidly following weight loss, intentional weight loss may well lead to meaningful reductions in cancer risk with a short latency time.

Adiposity has been recognized as a risk factor for colorectal adenoma, but the influence of weight gain, adipose tissue distribution, and possible differences between ethnic/racial and gender groups remains unanswered. The aim of this prospective study was to examine the association between adiposity and weight change and colorectal adenoma risk. Over f10-year period, anthropometric measures and other risk factors were measured at three time points in the multicenter multiethnic Insulin Resistance Atherosclerosis Study cohort. Colonoscopies were then conducted on 600 cohort participants regardless of symptoms whose mean age at colonoscopy was 64 years. Multivariate logistic regression analyses were used to assess the association between colorectal adenomas and measures of adiposity and weight change over the f10-year period before colonoscopy. Obesity was positively associated with risk of colorectal adenomas at the time of colonoscopy [adjusted odds ratio (OR adj ), 2.16; 95% confidence interval (95% CI), 1.13-4.14] and was stronger in women (OR adj , 4.42; 95% CI, 1.53-12.78) than in men (OR adj , 1.26; 95% CI, 0.52-3.07). The risk of adenomas increased among participants who gained weight compared with those who maintained weight over the f5 years (OR adj , 2.30; 95% CI, 1.25-4.22) and f10 years (OR adj , 2.12; 95% CI, 1.25-3.62). These associations were similar for both advanced and nonadvanced adenomas. These results suggest a positive association between obesity, weight gain, and colorectal adenoma risk. Stronger associations were observed when obesity was measured at the time of colonoscopy, suggesting that obesity may be a promoting factor in the growth of colorectal adenomas. (Cancer Epidemiol Biomarkers Prev 2007;16(3):526-31)

Breast cancer is the most common invasive cancer among women in developed countries. Obesity is a major risk factor for breast cancer recurrence and mortality in both pre-and postmenopausal women. Co-morbid medical conditions are common among breast cancer survivors. The Exercise and Nutrition to Enhance Recovery and Good Health for You (ENERGY) study is a 4-year randomized clinical trial of 693 overweight/obese women aged ≥21 years diagnosed with any early stage breast cancer (stages I[≥1 cm]-III) within the previous five years, designed to demonstrate the feasibility of achieving sustained weight loss and to examine the impact of weight loss on quality of life and co-morbidities, and to enable future exploration of biochemical mechanisms linking obesity to lower likelihood of disease-free survival. This trial is strategically designed as a vanguard for a fully-powered trial of women who will be evaluated for breast cancer recurrence and disease-free survival. Participants were recruited between 2010 and 2012 at four sites, had completed initial therapies, and had a body mass index between 25 and 45 kg/m2. The intervention featured a group-based cognitive-behavioral weight loss program with telephone counseling and tailored newsletters to support initial weight loss and subsequent maintenance, with the goal of 7% weight loss at two years. This study has high potential to have a major impact on clinical management and outcomes after a breast cancer diagnosis. This trial initiates the effort to establish weight loss support for overweight or obese breast cancer survivors as a new standard of clinical care.

Carrying excess body fat is a leading cause of cancer. Epidemiologic evidence gives strong clues about the mechanisms that link excess adiposity to risk for several cancer sites. For postmenopausal breast cancer and endometrial cancer, the hyper-estrogenic state that is induced by excess body fatness is the likely cause. For esophageal cancer and gallbladder cancer, chronic local inflammation induced by acid reflux and gallstones is the likely cause, and for liver cancer, local inflammation induced by hepatic fatty infiltration is the likely cause. However, for several other cancers known to be associated with excess adiposity, including cancers of the colon, pancreas, ovary, kidney, and prostate, specific causes are not known. Possible candidates include elevated systemic or local tissue inflammation induced by adiposity and effects of the elevated levels of leptin, insulin, IGFs, and depressed immune function that are seen with excess adiposity. There is growing evidence that intentional weight loss not only reduces circulating levels of cancer-associated factors but that it also reduces cancer incidence and recurrence. Better research is needed to understand the mechanisms that link excess body fat to cancer risk as well as to understand the amount of weight loss needed for substantial cancer risk reduction. Finally, as we develop better understanding of the mediators of the effects of excess body fatness on cancer risk, we should identify pharmacologic interventions that target those mediators so that they can be used to complement weight loss in order to reduce cancer risk.

This is the first study to demonstrate that smoking promotes early cervical carcinogenic events by increasing duration of oncogenic HPV infections and decreasing probability of clearing oncogenic infections.