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Reynolds P.,Cancer Prevention Institute of California | Reynolds P.,Stanford University
Journal of Mammary Gland Biology and Neoplasia | Year: 2013

The potential role of smoking in breast cancer risk has been the subject of over 100 publications, numerous scientific reviews, and animated debate. Tobacco exposure is a well-established cause of lung cancer, and is thought to account for nearly one third of all cancer deaths. Tobacco smoke contains thousands of chemicals, many of which are known to be mammary carcinogens. Although not initially thought to be a tobacco-related cancer, over the last several decades evidence has been accumulating on the role of both active smoking and secondhand smoking in the etiology of breast cancer. The human health evidence has been systematically evaluated not only by several independent researchers but also by several expert agency panels including those of the U.S. Surgeon General, the International Agency for Research on Cancer, the California Environmental Protection Agency, and a coalition of Canadian health agencies. Although the assessments have varied with time and across reviewers, the most recent weight of the evidence has suggested a potentially casual role for active smoking and breast cancer, particularly for long-term heavy smoking and smoking initiation at an early age. The role of secondhand smoking and breast cancer is less clear, although there has been some suggestion for an increased risk for premenopausal breast cancer. Recent studies evaluating the possible modifying role of polymorphisms in genes involved in the metabolism of tobacco products, particularly NAT2, have contributed another dimension to these assessments, although to date that evidence remains equivocal. © 2012 Springer Science+Business Media New York.

Corbett B.A.,Vanderbilt University | Corbett B.A.,Vanderbilt Kennedy Center | Schupp C.W.,Cancer Prevention Institute of California
Hormones and Behavior | Year: 2014

Our ability to adapt to change is fundamental. The cortisol awakening response (CAR) is a sharp rise in cortisol 30min after waking to help prepare an individual for ensuing stress. Children with autism spectrum disorder (ASD) often have difficulty adapting to change. Exploration of the CAR is warranted; yet, the few studies investigating it are inconclusive. The CAR was investigated in 94 pre-pubertal male children 8-to-12years of age with ASD (46) and typical development (TD, 48). Salivary samples were collected over three diurnal cycles involving two morning samples: M1: Immediately upon Waking and M2: 30-min Post Waking (M2-M1=CAR). The magnitude of the CAR was measured by independent two sample t-tests, variability was measured using Levene's Test, the sequence of the CAR was analyzed by a linear mixed-effects model and proportion of children exhibiting a CAR by chi-square test of independence. There were no significant differences on the CAR between the groups based on magnitude (t(92)=-0.14, p=0.89, d=0.04), variability (F(45,47)=1.11, p=0.72, η2=0.11) or the sequence over three days (F(2,88)=0.26, p=0.77, η2=0.01). No significant differences were shown in the proportion of children exhibiting a CAR across the groups based on child (χ2(1)=0.02, p=0.89) or adult criterion (χ2(1)=1.82, p=0.18). Despite group differences in the regulation and responsivity of cortisol, the CAR is indistinguishable between children with and without ASD. Inconsistencies across studies may be due to age, criterion used, and diagnostic distinctions. © 2014 Elsevier Inc.

Rachakonda T.D.,University of Colorado at Denver | Schupp C.W.,Cancer Prevention Institute of California | Armstrong A.W.,University of Colorado at Denver
Journal of the American Academy of Dermatology | Year: 2014

Background Psoriasis is a chronic inflammatory disorder associated with significant morbidity and mortality. Up-to-date prevalence data on psoriasis provide the foundation for informing population research, education, and health policy. Objective We sought to determine the prevalence of psoriasis among US adults. Methods We performed a cross-sectional study using National Health and Nutrition Examination Survey 2009 through 2010 data to determine psoriasis prevalence rates. Results From 6218 participants older than 20 years of age, 6216 respondents provided complete information regarding a psoriasis diagnosis. The prevalence of psoriasis among US adults ages 20 years and older is 3.2% (95% confidence interval [CI] 2.6%-3.7%). A total of 7.2 million US adults had psoriasis in 2010; an estimated 7.4 million US adults were affected in 2013. When stratifying the sample by race among those between ages 20 and 59 years, the psoriasis prevalence was highest in Caucasians at 3.6% (95% CI 2.7%-4.4%), followed by African Americans (1.9%; 95% CI 1.0%-2.8%), Hispanics (1.6%; 95% CI 0.5%-2.8%), and others (1.4%; 95% CI 0.3%-2.6%). The prevalence of psoriasis among US adults has not changed significantly since 2003 to 2004 (P >.05). Limitations Dermatologist evaluation and skin photographs were unavailable for the 2009 through 2010 surveys. Conclusions In the United States, psoriasis remains a common, immune-mediated disease, affecting 7.4 million adults. Its prevalence has remained stable since the mid-2000s. © 2013 by the American Academy of Dermatology, Inc.

Gibson T.M.,St Jude Childrens Research Hospital | Morton L.M.,U.S. National Cancer Institute | Shiels M.S.,U.S. National Cancer Institute | Clarke C.A.,Cancer Prevention Institute of California | Engels E.A.,U.S. National Cancer Institute
AIDS | Year: 2014

Objective: HIV-infected people have greatly elevated risk of non-Hodgkin lymphoma (NHL), particularly the AIDS-defining NHL subtypes: diffuse large B-cell lymphoma, Burkitt lymphoma and primary lymphomas arising in the central nervous system. The goals of this analysis were to comprehensively describe risks of NHL subtypes, especially those not well studied, among HIV/AIDS patients; examine risks specifically in the HAART era; and distinguish risks in HIV-infected individuals prior to diagnosis with AIDS. Design: Population-based registry linkage study. Methods: We used data from the US HIV/AIDS Cancer Match Study from 1996 to 2010 (N=273 705) to calculate standardized incidence ratios (SIRs) comparing subtypespecific NHL risks in HIV-infected people to those in the general population, and used Poisson regression to test for differences in SIRs between the HIV-only and AIDS periods. Results: NHL risk was elevated 11-fold compared to the general population, but varied substantially by subtype. AIDS-defining NHL subtypes comprised the majority, and risks were high (SIRs >17), but risks were also increased for some T-cell lymphomas (SIRs=3.6-14.2), marginal zone lymphoma (SIR=2.4), lymphoplasmacytic lymphoma/ Waldenström macroglobulinemia (SIR=3.6), and acute lymphoblastic leukemia/ lymphoma (SIR=2.4). Conclusion: HIV-infected people in the HAART era continue to have elevated risk of AIDS-defining NHL subtypes, highlighting the contribution of moderate and severe immunosuppression to their cause. Whereas non-AIDS-defining subtypes are much less common, immunosuppression or other dysregulated immune states likely play a role in the cause of some T-cell lymphomas, marginal zone lymphoma, lymphoplasmacytic lymphoma/Waldenström macroglobulinemia, and acute lymphoblastic leukemia/lymphoma. © 2014 Wolters Kluwer Health - Lippincott Williams & Wilkins.

Corbett B.A.,Vanderbilt University | Schupp C.W.,Cancer Prevention Institute of California | Lanni K.E.,Veterans Affairs Northern California Healthcare System
Molecular Autism | Year: 2012

Background: Autism spectrum disorders (ASD) are defined by impairment in reciprocal social interaction and flexible adaptation to the environment. This study compared physiological stress in children with and without ASD exposed to two social stress protocols. We hypothesized that the ASD group would show heightened initial and enduring cortisol levels to the social stressors, which would be moderated by age and intelligence. Methods. Twenty-seven children with ASD and 32 with typical development (TYP) completed a standardized social-evaluative performance task and a validated paradigm of social play with peers. Physiological stress was measured by salivary cortisol at nine time points. Statistical approaches included repeated-measures linear mixed models and correlation analyses. Results: The average cortisol level of both groups during initial exposure to social situations was significantly greater than baseline levels (ASD, P = 0.018; TYP, P = 0.006). Stress responsivity was significantly different between the groups; the TYP group showed a significant reduction in cortisol over time (P = 0.023), whereas the ASD group maintained an elevated cortisol level (P >0.05). The ASD group evidenced greater variability in between-group, within-group and intra-individual analyses. Age was a positive moderator of stress for the ASD group (P = 0.047), whereas IQ was a negative moderator for the TYP group (P = 0.061). Conclusions: Initial stress to novel social scenarios is idiosyncratic and predictive of subsequent exposure. Amidst significant variability in cortisol, children with ASD show enhanced and sustained social stress that increases with age. Developmental and cognitive factors differentially moderate stress in children with ASD and TYP, respectively. A model of neuroendocrine reactivity is proposed. © 2012 Corbett et al.; licensee BioMed Central Ltd.

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