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Changes in epigenetic marks such as DNA methylation and histone acetylation are associated with a broad range of disease traits, including cancer, asthma, metabolic disorders, and various reproductive conditions. It seems plausible that changes in epigenetic state may be induced by environmental exposures such as malnutrition, tobacco smoke, air pollutants, metals, organic chemicals, other sources of oxidative stress, and the microbiome, particularly if the exposure occurs during key periods of development. Thus, epigenetic changes could represent an important pathway by which environmental factors influence disease risks, both within individuals and across generations. We discuss some of the challenges in studying epigenetic mediation of pathogenesis and describe some unique opportunities for exploring these phenomena.

Patients undergoing radiation treatment for Hodgkins's lymphoma are at increased risk of developing secondary malignancies with time. This genome-wide analysis identifies genetic polymorphisms associated with increased risk of secondary malignancies in treated children. The risk alleles result in decreased radiation-mediated induction of PRDM1, a tumor suppressor transcription factor, leading to impaired repression of oncogenic drivers such as MYC. Survivors of pediatric Hodgkin's lymphoma are at risk for radiation therapy–induced second malignant neoplasms (SMNs). We identified two variants at chromosome 6q21 associated with SMNs in survivors of Hodgkin's lymphoma treated with radiation therapy as children but not as adults. The variants comprise a risk locus associated with decreased basal expression of PRDM1 (encoding PR domain containing 1, with ZNF domain) and impaired induction of the PRDM1 protein after radiation exposure. These data suggest a new gene-exposure interaction that may implicate PRDM1 in the etiology of radiation therapy-induced SMNs.

While alcohol consumption is known to increase the risk of several types of cancer, evidence regarding the association between alcohol and melanoma is inconclusive. This pooled analysis was conducted to examine total alcohol consumption (grams per day), and type of alcohol consumed (beer, wine, beer and wine combined, and liquor) in relation to melanoma among women using original data from eight completed case–control studies (1886 cases and 2113 controls), with adjustment for the potential confounding effects of sun exposure-related factors. We found a positive association with ever consuming alcohol [adjusted pooled odds ratio (pOR) 1.3, 95 % confidence interval (CI) 1.1–1.5]. Specifically the pORs were 1.4 (95 % CI 1.1–1.8) for wine, 1.1 (95 % CI 0.9–1.5) for beer and 1.2 (95 % CI 1.0–1.4) for liquor. However, the pOR for the highest fourth of consumption compared with never consumption was 1.0 (95 % CI 0.7–1.3) without evidence of a trend with increasing amount of total alcohol, or separately with amount of beer, wine or liquor consumed. Stratifying by anatomic site of lesion, number of nevi, age group, or histologic subtype did not alter these results. Although the results showed a weak positive association between ever consuming alcohol and melanoma occurrence, our findings do not provide strong support for the hypothesis that alcohol consumption plays a role in the development of melanoma in women.

The incidence of breast cancer rises steeply between ages 25 and 50, and more slowly thereafter. In contrast, the incidence in the unaffected (contralateral) breast of women who have had breast cancer remains constant at about 0.7% per year for at least the next 20 years after diagnosis, irrespective of age at first diagnosis. The incidence in relatives of the patients seems to show a similar pattern. The incidence in a prospective study of monozygotic twins of patients was approximately constant at 1.3% per year (77 cases), again about 0.7% per breast. At ages older than a patient's age at diagnosis, her mother and sisters have an incidence of 0.3–0.4% per year. Above the index patient's age at diagnosis, the rate in relatives shows no temporal trend and is independent of the patient's age at diagnosis. A statistically simple explanation is that incidence in susceptible women increases to a high constant level by a predetermined age that varies between families, but this seems inconsistent with conventional models of carcinogenesis and susceptibility. The very high incidence in monozygotic twins of patients indicates that a high proportion, and perhaps the majority, of breast cancers arise in a susceptible minority of women.

Hodgkin's disease is likely to have different causes in young adulthood and old age. 1 The characteristic clinical presentation and histopathological appearance suggest that in young adults the disease is initiated by an environmental exposure, possibly to an infectious agent. The age-specific incidence during young adulthood varies over time and according to place and social class, much like that of infections. Those affected have a small average number of siblings, may not have had the common childhood infections, and are likely to have a history of infectious mononucleosis. 2 These findings have been interpreted to suggest that Hodgkin's disease may occur as . . .

•Glycemic index was associated with increased lung cancer risk.•Positive associations of glycemic index on adenocarcinoma and small cell carcinoma.•Stronger associations in individuals who had smoked, BMI < 25, and no diabetes history. Although there is some evidence of positive associations between both the glycemic index (GI) and glycemic load (GL) with cancer risk, the relationships with lung cancer risk remain largely unexplored. We evaluated the associations between GI and GL with lung cancer. The analyses were performed using data from a population-based case-control study recruited between 1999 and 2004 in Los Angeles County. Dietary factors were collected from 593 incident lung cancer cases and 1026 controls using a modified food frequency questionnaire. GI and GL were estimated using a food composition table. Adjusted odds ratios (ORs) and 95 % confidence intervals (CI) were estimated using unconditional logistic regression adjusting for potential confounders. Dietary GI was positively associated with lung cancer (OR for upper vs. lower tertile = 1.62; 95 % CI: 1.17, 2.25). For histologic subtypes, positive associations were observed between GI and adenocarcinoma (OR for upper vs. lower tertile = 1.82; 95 % CI: 1.22, 2.70) and small cell carcinoma (OR for upper vs. lower tertile = 2.68; 95 % CI: 1.25, 5.74). No clear association between GL and lung cancer was observed. These findings suggest that high dietary GI was associated with increased lung cancer risk, and the positive associations were observed for both lung adenocarcinoma and small cell lung carcinoma. Replication in an independent dataset is merited for a broader interpretation of our results.

This volume, the first of its kind ever, is designed to provide both laypersons and professionals with a detailed description of the occurrence of each common form of cancer in the ethnically, socially, and environmentally complex milieu of a modern urban complex. The place is Los Angeles County, and the patterns of 72 different malignancies are described according to race, age, sex, social class calendar time (since 1972) and most notably, individual neighborhood, using detailed maps of high risk.The book permits residents to screen the malignancies and identify those of special concern locally, and to identify other communities with similar concerns. The pattern of each malignancy is briefly discussed with reference to background knowledge of causation and the degree to which the observed pattern was expected on that basis. Persons residing outside Los Angeles County will identify patterns likely to prevail in their own communities.Physicians and scientific investigators in California and elsewhere can use the material provided to counsel patients and evaluate the consistency of any specific pattern of occurrence with each specific causal hypothesis. A detailed appendix describes the source of data, provides the basis for the choices made in the production of the volume, and gives a perspective on the search for \"clusters\" of malignancy. * Compares different types of cancers with respect to the degree of non-random occurrence* Contains numerous maps detailing the demographic and geographic pattern of cancer occurrence in Los Angeles County* Provides an empirical perspective to the search for disease \"clusters\"

Most epidemiologic studies employ a vacuum cleaner used by a trained technician to collect household allergens. This approach is labor intensive, equipment dependent, and impractical if study subjects reside over a wide geographic area. We examined the feasibility of a self-administered dust collection method, using an electrostatic cloth sent by conventional mail, to obtain allergen measurements. Thirty-two nonasthmatic twins from the California Twin Program wiped areas in the family room, kitchen, and bedroom, according to standardized instructions, and returned the cloths by mail. Allergen concentrations for Der-p-1, Der-f-1, Fel-d-1, and Bla-g-2 were determined using ELISA, and intrahouse and room-to-room concentrations were compared. Der-p-1 and Fel-d-1 were found in most homes, with highest concentrations in bedrooms and kitchens, respectively. Der-f-1 and Bla-g-2 were rarely found. Intrahouse Der-p-1 and Fel-d-1 concentrations were highly correlated and statistically significant (for Der-p-1, bedroom vs. kitchen, p = .0003, bedroom vs. family room, p = .0001, and family room vs. kitchen, p = .002; for Fel-d-1, bedroom vs. kitchen, p = .0004, bedroom vs. family room, p < .0001, and family room vs. kitchen, p = .0001). Reported cat ownership was strongly correlated with household Fel-d-1 concentrations (p < .005). In another comparison from different homes of children enrolled in the La Casa atopy prevention study, allergen concentrations measured from dust collected by a single operator from the left and right half of the same room in 21 homes were compared. Levels of Bla-g-2, Der-p-1, and Fel-d-1 concentrations collected from right and left halves of the same room were highly correlated, with r2 ranging from .7 to .9, and were highly statistically significant (all p values < .01). We conclude that nonintrusive and self-administered dust collection, using commercially available electrostatic dust cloths, sent by conventional mail services, is a promising alternative to technician-collected vacuumed dust for measuring indoor allergens in population-based studies, although further validation of the method is necessary.

This study involved more than 1900 pairs of twins in which one or both women had breast cancer. In monozygotic pairs in which both women had breast cancer, earlier puberty in one twin was a strong risk factor for an earlier diagnosis of breast cancer. Earlier puberty a strong risk factor in monozygotic pairs. Breast cancer can result from the actions of ovarian hormones 1 that stimulate cell proliferation 2 and that may increase the rate of genetic errors in ductal cells. This view is based on hormonal risk factors, a “breast-age” (hormonal) index that predicts age-specific incidence, 3 , 4 and differences in plasma estrogen levels between patients with cancer or their family members and controls. 5 , 6 Even perinatal 7 – 9 and environmental 10 – 12 risk factors have been attributed to hormonal differences. Genetic risk factors include those that regulate the production, transport, and metabolism of estrogens 13 ; determine the hormonal sensitivity of cells 14 ; or repair errors of . . .

The California Twin Program (CTP) is a population-based sample of over 52,000 twins in which a number of nested studies are ongoing. We outline our experience to date, providing estimates of crude response rates for a variety of different study designs and protocols. We have experienced very high response rates in our studies to date, even in studies with demanding protocols. Lowest response rates have occurred in studies among afflicted individuals, and in one with an unusual protocol. We have experienced some difficulty in locating original members of the cohort, despite efforts to trace individuals using a variety of sources of information. However, in most analyses, the participating sample of twins does not differ substantially from the underlying sample from the CTP. Future work will focus on improving methods of recontacting cohort members.