Adult ovary transfer counteracts the callosal enlargement resulting from prepubertal ovariectomy

The rat corpus callosum (CC) is larger in males than females, and is sensitive to hormone manipulations during development. Previous research found that, in rats, CC sensitivity to testosterone ended by postnatal day 8 (P8). In contrast, more recent findings demonstrated that CC responsivity to ovarian hormones continued at least through P70. The current experiment extends these findings by showing that the female callosum is still sensitive to ovarian hormones as late as P130, well into adulthood.     

Polymorphisms and circulating levels in the insulin-like growth factor system and risk of breast cancer: a systematic review.

We reviewed all English-language articles on associations among circulating levels of the insulin-like growth factors (IGF) and their binding proteins (IGFBP), polymorphisms in their genes, and breast cancer risk. In premenopausal women, five of eight IGF-I studies and four of six IGFBP-3 studies of circulating levels found that women in the highest quantile had more than twice the risk of developing breast cancer of those in the lowest, although in some this effect was only apparent at young ages. In postmenopausal women, however, there was no consistent effect. A simple sequence length polymorphism 1 kb 5' to IGF-I was examined in relation to circulating levels of IGF-I (12 studies) or breast cancer risk (4 studies), but there was no convincing evidence of any effect. For an A/C polymorphism 5' to IGFBP-3, all three studies were consistent with a modest effect on circulating levels, but no evidence of a direct effect on breast cancer risk was seen in the only relevant study. Variation within the reference range of IGF-I and IGFBP-3 may confer only modest increases in breast cancer risk, and any single polymorphism may only account for a small proportion of that variation. Nevertheless, population attributable fractions for high circulating levels of IGF-I and IGFBP-3 and for common genetic variants could be substantial. Further large studies, or combined analysis of data from existing studies, are needed to quantify these effects more precisely.     

Cigarette smoking and risk of non-Hodgkin lymphoma: a pooled analysis from the International Lymphoma Epidemiology Consortium (interlymph).

BACKGROUND: The International Lymphoma Epidemiology Consortium (InterLymph) provides an opportunity to analyze the relationship between cigarette smoking and non-Hodgkin lymphoma with sufficient statistical power to consider non-Hodgkin lymphoma subtype. The results from previous studies of this relationship have been inconsistent, likely due to the small sample sizes that arose from stratification by disease subtype. To clarify the role of cigarette smoking in the etiology of non-Hodgkin lymphoma, we conducted a pooled analysis of original patient data from nine case-control studies of non-Hodgkin lymphoma conducted in the United States, Europe, and Australia. METHODS: Original data were obtained from each study and uniformly coded. Risk estimates from fixed-effects and two-stage random-effects models were compared to determine the impact of interstudy heterogeneity. Odds ratios (OR) and 95% confidence intervals (95% CI) were derived from unconditional logistic regression models, controlling for study center, age, sex, and race. RESULTS: In our pooled study population of 6,594 cases and 8,892 controls, smoking was associated with slightly increased risk estimates (OR, 1.07; 95% CI, 1.00-1.15). Stratification by non-Hodgkin lymphoma subtype revealed that the most consistent association between cigarette smoking and non-Hodgkin lymphoma was observed among follicular lymphomas (n = 1452). Compared with nonsmokers, current smokers had a higher OR for follicular lymphoma (1.31; 95% CI, 1.12-1.52) than former smokers (1.06; 95% CI, 0.93-1.22). Current heavy smoking (> or = 36 pack-years) was associated with a 45% increased OR for follicular lymphoma (1.45; 95% CI, 1.15-1.82) compared with nonsmokers. CONCLUSIONS: Cigarette smoking may increase the risk of developing follicular lymphoma but does not seem to affect risk of the other non-Hodgkin lymphoma subtypes we examined. Future research is needed to determine the biological mechanism responsible for our subtype-specific results.     

Vegetable and fruit intake and pancreatic cancer in a population-based case-control study in the San Francisco bay area.

Pancreatic cancer is one of the most devastating and rapidly fatal cancers, yet little is known about the primary cause and prevention of this disease. We conducted a population-based case-control study to investigate the association between vegetables and fruits and pancreatic cancer. Between 1995 and 1999, 532 cases and 1,701 age- and sex-matched controls completed direct interviews using a semiquantitative food-frequency questionnaire. No proxy interviews were conducted. We observed inverse associations between consumption of total and specific vegetables and fruits and the risk of pancreatic cancer. The odds ratio and 95% confidence interval for the highest versus the lowest quartile of total vegetable intake was 0.45 (0.32-0.62), trend P < 0.0001; and for total fruits and fruit juice was 0.72 (0.54-0.98), trend P = 0.06. Odds ratios and 95% confidence intervals for the highest versus the lowest quartile of specific vegetables and fruits were: 0.63 (0.47-0.83) for dark leafy vegetables, 0.76 (0.56-1.0) for cruciferous vegetables, 0.59 (0.43-0.81) for yellow vegetables, 0.56 (0.41-0.76) for carrots, 0.51 (0.38-0.70) for beans, 0.46 (0.33-0.63) for onions and garlic, and 0.78 (0.58-1.0) for citrus fruits and juice. Compared with less than five servings per day of total vegetables and fruits combined, the risk of pancreatic cancer was 0.49 (0.36-0.68) for more than nine servings per day. These results suggest that increasing vegetable and fruit consumption, already recommended for the prevention of several other chronic diseases, may impart some protection against developing pancreatic cancer.     

Research priorities to address polypharmacy in older adults with cancer

Polypharmacy poses a significant public health problem that disproportionately affects older adults (≥65 years) since this population represents the largest consumers of medications. Clinicians caring for older adults with cancer must rely on evidence to understand polypharmacy and its implications, not only to communicate with patients and other healthcare providers, but also because of the significant interplay between polypharmacy, cancer, cancer-related treatment, and clinical outcomes. Interest in polypharmacy is rising because of its prevalence, the origins and facilitating factors behind it, and the direct and indirect clinical outcomes associated with it. The growing body of publications focused on polypharmacy in older adults with cancer demonstrates that this is a significant area of research; however, limited evidence exists to guide medication use (e.g., prescribing, administration) in this population. Currently, research priorities aimed at polypharmacy in the field of geriatric oncology lack clarity. We identified current gaps in the literature in order to establish research priorities for polypharmacy in older adults with cancer. The five research priorities—Polypharmacy Methodology and Definitions, Suboptimal Medication Use, Comorbidities and Geriatric Syndromes, Underrepresented Groups, and Polypharmacy Interventions—highlight critical areas for future research to improve outcomes for older adults with cancer.