Cigarette smoking patterns among U.S. military service members before and after separation from the military.

U.S. military Service members have consistently smoked more than the general population and the prevalence of smoking is even higher among U.

Comparing self-reported physical activity and sedentary time to objective fitness measures in a military cohort.

Objectives: Regular vigorous physical activity (PA) and high levels of physical fitness (PF) confer health benefits. Conversely, sedentary time is a risk factor for chronic illness, independent of PA. We evaluated associations between self-reported PA, sedentary time, and objective PF measures in military Service members.

The Epidemiology of Irritable Bowel Syndrome in the US Military: Findings from the Millennium Cohort Study.

Objectives: Functional gastrointestinal disorders occur more frequently among deployed veterans, although studies evaluating the relative impact of risk factors, including stress and antecedent infectious gastroenteritis (IGE), are limited. We examined risk factors for new-onset irritable bowel syndrome (IBS) among active duty participants in the military's Millennium Cohort Study.

Methods: Medical encounter data from 2001 to 2009, limited to Cohort members on active duty, were used to identify incident IBS cases (any and highly probable).

Deployment-related depression screening, 2001-2008: comparing clinical versus research surveys.

Background: Potential adverse mental health effects of deployment, including depression, are an ongoing concern. Although a previous study assessed under-reporting of depression on post-deployment health assessments compared to anonymous surveys, those results were not examined at the individual level to identify demographic or military factors that may be associated with unwillingness to report depression symptoms.

Purpose: To compare self-reported depression symptoms on post-deployment health assessments with responses to the same depression questions on a research survey.

Comprehensive genetic analysis of cytarabine sensitivity in a cell-based model identifies polymorphisms associated with outcome in AML patients.

A whole-genome approach was used to investigate the genetic determinants of cytarabine-induced cytotoxicity. We performed a meta-analysis of genome-wide association studies involving 523 lymphoblastoid cell lines (LCLs) from individuals of European, African, Asian, and African American ancestry. Several of the highest-ranked single-nucleotide polymorphisms (SNPs) were within the mutated in colorectal cancers (MCC) gene.

Genetic determinants of UV-susceptibility in non-melanoma skin cancer.

A milieu of cytokines and signaling molecules are involved in the induction of UV-induced immune suppression and thus the etiology of non-melanoma skin cancer (NMSC). Targeting the UV-induced immunosuppression pathway, and using a large population based study of NMSC, we have investigated the risk associated with functional variants in 10 genes (IL10, IL4, IL4R, TNF, TNFR2, HTR2A, HRH2, IL12B, PTGS2, and HAL). The most prominent single genetic effect was observed for IL10.

Genome-wide local ancestry approach identifies genes and variants associated with chemotherapeutic susceptibility in African Americans.

Chemotherapeutic agents are used in the treatment of many cancers, yet variable resistance and toxicities among individuals limit successful outcomes. Several studies have indicated outcome differences associated with ancestry among patients with various cancer types. Using both traditional SNP-based and newly developed gene-based genome-wide approaches, we investigated the genetics of chemotherapeutic susceptibility in lymphoblastoid cell lines derived from 83 African Americans, a population for which there is a disparity in the number of genome-wide studies performed.

The role of TP53 and MDM2 polymorphisms in TP53 mutagenesis and risk of non-melanoma skin cancer.

P53 is a key regulatory molecule in the cellular response to ultraviolet radiation, and TP53 mutation is the most common alteration in non-melanoma skin cancer. The MDM2 oncogene negatively regulates p53 protein levels, and both genes have functional polymorphisms that may modify skin cancer risk. Furthermore, prior research suggests that TP53 mutations preferentially occur on the arginine allele to selectively inactivate the p63 pathway.

Pharmacogenomic discovery using cell-based models.

Quantitative variation in response to drugs in human populations is multifactorial; genetic factors probably contribute to a significant extent. Identification of the genetic contribution to drug response typically comes from clinical observations and use of classic genetic tools. These clinical studies are limited by our inability to control environmental factors in vivo and the difficulty of manipulating the in vivo system to evaluate biological changes.

CTLA4 variants, UV-induced tolerance, and risk of non-melanoma skin cancer.

Although skin tumors are highly immunogenic, exposure to UV radiation is known to suppress immune responses via regulatory T cells. Specifically, the activity of cytotoxic lymphocyte-associated antigen-4 (CTLA-4) is integral in regulating the development of UV-induced tolerance and, concomitantly, skin cancers. Due to the inverse relationship between tumor surveillance and autoimmunity, we hypothesize that the same genetic variant in the CTLA4 locus that increases risk for autoimmune diseases is associated with decreased risk of non-melanoma skin cancer (NMSC).

A role for ultraviolet radiation immunosuppression in non-melanoma skin cancer as evidenced by gene-environment interactions.

The genotoxic effects of ultraviolet (UV) radiation are well-known causes of skin cancers; however, UV radiation also suppresses the immune system, decreasing the body's surveillance for tumor cells. In experimental systems, UV radiation immunosuppression is at least partially mediated through urocanic acid (UCA), an UV radiation-absorbing molecule in the stratum corneum. We tested the hypothesis that genetic variation in the histidase gene (HAL), which catalyzes the formation of UCA in the skin, modifies risk of basal cell carcinoma (BCC) and squamous cell carcinoma (SCC) in a population-based study (914 BCC, 702 SCC and 848 controls).