Sanjay Shete

University of Texas MD Anderson Cancer Center, Houston, Texas, United States

Are you Sanjay Shete?

Claim your profile

Publications (182)942.15 Total impact


  • No preview · Article · Feb 2016 · Cancer Epidemiology Biomarkers & Prevention
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Decades of research have established only a few etiological factors for glioma, which is a rare and highly fatal brain cancer. Common methodological challenges among glioma studies include small sample sizes, heterogeneity of tumor subtypes, and retrospective exposure assessment. Here, we briefly describe the Glioma International Case-Control (GICC) Study (recruitment, 2010–2013), a study being conducted by the Genetic Epidemiology of Glioma International Consortium that integrates data from multiple data collection sites, uses a common protocol and questionnaire, and includes biospecimen collection. To our knowledge, the GICC Study is the largest glioma study to date that includes collection of blood samples, which will allow for genetic analysis and interrogation of gene-environment interactions.
    Full-text · Article · Dec 2015 · American journal of epidemiology
  • Source

    Full-text · Article · Nov 2015 · Neuro-Oncology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We examined cross-sectional associations of health literacy (HL) with smoking and other established health indicators among 1,467 African American adults. Data emanated from a longitudinal cohort study designed to investigate cancer risk factors among church-going African American adults. We conducted linear and logistic regression analyses to assess associations between HL and health indicators. HL was assessed using an established single-item screening question. Outcomes included indicators of poor physical health (cigarette smoking, self-rated general and physical health) and mental health (self-rated mental health, depressive symptoms, perceived stress). Nearly 19% of participants had low HL. Low HL was significantly associated with current smoking, poorer self-rated general and physical health, and higher perceived stress (ps < .05) even after we controlled for demographic variables (i.e., age, gender, relationship status) and indicators of socioeconomic status (i.e., education, income, insurance status). Low HL appears to be an independent risk factor for smoking and other indicators of poor physical and mental health in a large sample of African American adults. Future directions and clinical implications are discussed.
    Preview · Article · Oct 2015 · Journal of Health Communication
  • [Show abstract] [Hide abstract]
    ABSTRACT: The prevalence and effect of single-parent families in childhood-onset essential hypertension (EH) is unknown. Children with EH and age-, sex-, and ethnicity-matched controls were enrolled. Family structure data were obtained by in-person interview. A total of 148 families (76 hypertension probands, 72 control probands; median 14 years) were prospective-ly enrolled in the study. Single-parent status was seen in 42% of the families--with and without EH (38% vs 46%, P=.41; odds ratio, 0.7; 95% confidence interval, 0.4-1.4). After multivariable analysis, a statistically significant sociofamilial contributor to the development of childhood-onset EH was not identified. A significant number of single-parent families (42%), the majority with single mothers, were found in our pedigree study. Sociofamilial factors are known to contribute to the expression of adult-onset EH, but findings in our study suggest that they appear to contribute less in the expression of childhood-onset EH.
    No preview · Article · Oct 2015 · Journal of Clinical Hypertension
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Host genetic variability has been implicated in chemotherapy-induced peripheral neuropathy (CIPN). A dose-limiting toxicity for chemotherapy agents, CIPN is also a debilitating condition that may progress to chronic neuropathic pain. We utilized a bioinformatics approach, which captures the complexity of intracellular and intercellular interactions, to identify genes for CIPN. Using genes pooled from the literature as a starting point, we used Ingenuity Pathway Analysis (IPA) to generate gene networks for CIPN. We performed IPA core analysis for genes associated with platinum-, taxane- and platinum-taxane-induced neuropathy. We found that IL6, TNF, CXCL8, IL1B and ERK1/2 were the top genes in terms of the number of connections in platinum-induced neuropathy and TP53, MYC, PARP1, P38 MAPK and TNF for combined taxane-platinum-induced neuropathy. Neurotoxicity is common in cancer patients treated with platinum compounds and anti-microtubule agents and CIPN is one of the debilitating sequela. The bioinformatic approach helped identify genes associated with CIPN in cancer patients.
    Full-text · Article · Aug 2015 · BioData Mining

  • No preview · Article · Aug 2015 · Cancer Research
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Addictions to alcohol and tobacco, known risk factors for cancer, are complex heritable disorders. Addictive behaviors have a bidirectional relationship with pain. We hypothesize that the associations between alcohol, smoking, and opioid addiction observed in cancer patients have a genetic basis. Therefore, using bioinformatics tools, we explored the underlying genetic basis and identified new candidate genes and common biological pathways for smoking, alcohol, and opioid addiction. Results Literature search showed 56 genes associated with alcohol, smoking and opioid addiction. Using Core Analysis function in Ingenuity Pathway Analysis software, we found that ERK1/2 was strongly interconnected across all three addiction networks. Genes involved in immune signaling pathways were shown across all three networks. Connect function from IPA My Pathway toolbox showed that DRD2 is the gene common to both the list of genetic variations associated with all three addiction phenotypes and the components of the brain neuronal signaling network involved in substance addiction. The top canonical pathways associated with the 56 genes were: 1) calcium signaling, 2) GPCR signaling, 3) cAMP-mediated signaling, 4) GABA receptor signaling, and 5) G-alpha i signaling. Conlusions Cancer patients are often prescribed opioids for cancer pain thus increasing their risk for opioid abuse and addiction. Our findings provide candidate genes and biological pathways underlying addiction phenotypes, which may be future targets for treatment of addiction. Further study of the variations of the candidate genes could allow physicians to make more informed decisions when treating cancer pain with opioid analgesics. Electronic supplementary material The online version of this article (doi:10.1186/s12918-015-0167-x) contains supplementary material, which is available to authorized users.
    Full-text · Article · Jun 2015 · BMC Systems Biology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Despite well-established negative health consequences of smokeless tobacco use (STU), the number and variety of alternative non-combustible tobacco products on the market have increased tremendously over the last 10 years, as has the market share of these products relative to cigarettes. While STU among non-Hispanic white youth has decreased over the last 10 years, the prevalence has remained constant among Hispanic youth. Here we examine demographic, psychosocial, and genetic risk associated with STU among Mexican heritage youth. Participants (50.5 % girls) reported on psychosocial risk factors in 2008-09 (n = 1,087, mean age = 14.3 years), and smokeless tobacco use in 2010-11 (mean age = 16.7 years). Participants provided a saliva sample that was genotyped for genes in the dopamine, serotonin and opioid pathways. Overall 62 (5.7 %) participants reported lifetime STU. We identified five single nucleotide polymorphisms that increased the risk for lifetime use. Specifically, rs2023902 on SERGEF (OR = 1.93; 95 % CI: 1.05-3.53), rs16941667 on ALDH2 (OR = 3.14; 95 % CI: 1.65-5.94), and rs17721739 on TPH1 (OR = 1.71; 95 % CI: 1.00-2.91) in the dopamine pathway, rs514912 on TRH-DE (OR = 1.84; 95 % CI: 1.25-2.71) in the serotonin pathway, and rs42451417 on the serotonin transporter gene, SLC6A4 (OR = 3.53; 95 % CI: 1.56-7.97). After controlling for genetic risk, being male (OR = 1.86; 95 % CI: 1.02-3.41), obesity status (OR = 2.22; 95 % CI: 1.21-4.09), and both higher levels of anxiety (OR = 1.04; 95 % CI: 1.01-1.08) and social disinhibition (OR = 1.26; 95 % CI: 1.07-1.48) were associated with increased use. High subjective social status (OR = 0.78; 95 % CI: 0.64-0.93) was protective against use, while higher parental education (OR = 2.01; 95 % CI: 1.03-3.93) was associated with increased use. These data suggest that use of genetic risk, along with psychosocial, demographic, and behavioral risk factors may increase our ability to identify youth at increased risk for STU, which in turn may improve our ability to effectively target prevention messages to Mexican heritage youth.
    Full-text · Article · Jun 2015 · BMC Medical Genetics
  • [Show abstract] [Hide abstract]
    ABSTRACT: http://onlinelibrary.wiley.com/enhanced/doi/10.1002/bdra.23385/ Birth defects are a major cause of morbidity and mortality worldwide. There has been much progress in understanding the genetic basis of familial and syndromic forms of birth defects. However, the etiology of nonsydromic birth defects is not well-understood. Although there is still much work to be done, we have many of the tools needed to accomplish the task. Advances in next-generation sequencing have introduced a sea of possibilities, from disease-gene discovery to clinical screening and diagnosis. These advances have been fruitful in identifying a host of candidate disease genes, spanning the spectrum of birth defects. With the advent of CRISPR-Cas9 gene editing, researchers now have a precise tool for characterizing this genetic variation in model systems. Work in model organisms has also illustrated the importance of epigenetics in human development and birth defects etiology. Here we review past and current knowledge in birth defects genetics. We describe genotyping and sequencing methods for the detection and analysis of rare and common variants. We remark on the utility of model organisms and explore epigenetics in the context of structural malformation. We conclude by highlighting approaches that may provide insight into the complex genetics of birth defects.
    No preview · Article · May 2015 · Birth Defects Research Part A Clinical and Molecular Teratology
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background and Objectives To assess tobacco use among lesbian, gay, bisexual, and transgender (LGBT) individuals from the 2014 Houston Pride Parade and Festival in Houston, Texas (TX).Methods Cross-sectional study using convenience sample of LGBT individuals (n = 99) examining tobacco use, sexual orientation, and other socio-demographic factors through survey participation.ResultsFindings showed a high prevalence of tobacco and electronic cigarettes use. White LGBT individuals had greater odds of using any type of tobacco product.Discussion and Conclusions Despite a high smoking prevalence among the surveyed LGBT individuals, this study sample did not identify tobacco use as a health issue.Scientific SignificanceSupports the need for further investigation on tobacco-related disparities among LGBT individuals in Houston, TX.
    No preview · Article · May 2015 · American Journal on Addictions
  • Source
    Rajesh Talluri · Sanjay Shete
    [Show abstract] [Hide abstract]
    ABSTRACT: Epistasis helps to explain how multiple single-nucleotide polymorphisms (SNPs) interact to cause disease. A variety of tools have been developed to detect epistasis. In this article, we explore the strengths and weaknesses of an information theory approach for detecting epistasis and compare it to the logistic regression approach through simulations. We consider several scenarios to simulate the involvement of SNPs in an epistasis network with respect to linkage disequilibrium patterns among them and the presence or absence of main and interaction effects. We conclude that the information theory approach more efficiently detects interaction effects when main effects are absent, whereas, in general, the logistic regression approach is appropriate in all scenarios but results in higher false positives. We compute epistasis networks for SNPs in the FSD1L gene using a two-phase head and neck cancer genome-wide association study involving 2,185 cases and 4,507 controls to demonstrate the practical application of the methods.
    Preview · Article · Feb 2015 · Cancer informatics
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Glioma is a rare, but highly fatal, cancer that accounts for the majority of malignant primary brain tumors. Inherited predisposition to glioma has been consistently observed within non-syndromic families. Our previous studies, which involved non-parametric and parametric linkage analyses, both yielded significant linkage peaks on chromosome 17q. Here, we use data from next generation and Sanger sequencing to identify familial glioma candidate genes and variants on chromosome 17q for further investigation. We applied a filtering schema to narrow the original list of 4830 annotated variants down to 21 very rare (<0.1% frequency), non-synonymous variants. Our findings implicate the MYO19 and KIF18B genes and rare variants in SPAG9 and RUNDC1 as candidates worthy of further investigation. Burden testing and functional studies are planned.
    Full-text · Article · Feb 2015 · Scientific Reports
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Gliomas are the most common brain tumor, with several histological subtypes of various malignancy grade. The genetic contribution to familial glioma is not well understood. Using whole exome sequencing of 90 individuals from 55 families, we identified two families with mutations in POT1 (p.G95C, p.E450X), a member of the telomere shelterin complex, shared by both affected individuals in each family and predicted to impact DNA binding and TPP1 binding, respectively. Validation in a separate cohort of 264 individuals from 246 families identified an additional mutation in POT1 (p.D617Efs), also predicted to disrupt TPP1 binding. All families with POT1 mutations had affected members with oligodendroglioma, a specific subtype of glioma more sensitive to irradiation. These findings are important for understanding the origin of glioma and could have importance for the future diagnostics and treatment of glioma. © The Author 2014. Published by Oxford University Press. All rights reserved. For Permissions, please e-mail: journals.permissions@oup.com.
    Full-text · Article · Jan 2015 · JNCI Journal of the National Cancer Institute
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: BACKGROUND: Although familial susceptibility to glioma is known, the genetic basis for this susceptibility remains unidentified in the majority of glioma-specific families. An alternative approach to identifying such genes is to examine cancer pedigrees that include glioma as one of several cancer phenotypes to determine whether common chromosomal modifications might account for the familial aggregation of glioma and other cancers. METHODS: Germline rearrangements in 146 glioma families from the Gliogene Consortium (http://www.gliogene.org/) with at least two glioma cases verified and a third reported or verified in the same family or two glioma cases in the family with at least one family member affected with melanoma, colon or breast cancer were examined using Multiplex Ligation dependent Probe Amplification (MLPA). The genomic areas covering TP53, CDKN2A, MLH1 and MSH2 were selected as these genes have previously been reported to be associated with cancer pedigrees known to include glioma. RESULTS: We detected a single structural rearrangement, a deletion of exons 1-6 in MSH2, in the proband of one family with 3 cases with glioma and 1 relative with colon cancer. CONCLUSIONS: Large deletions and duplications are rare events in familial glioma cases even in families with a strong family history with cancers that may be involved in known cancer syndromes.
    Preview · Article · Sep 2014 · Neuro-Oncology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The underlying ethos of dbGaP is that access to these data by secondary data analysts facilitates advancement of science. NIH has required that genome-wide association study data be deposited in the Database of Genotypes and Phenotypes (dbGaP) since 2003. In 2013, a proposed updated policy extended this requirement to next-generation sequencing data. However, recent literature and anecdotal reports suggest lingering logistical and ethical concerns about subject identifiability, informed consent, publication embargo enforcement, and difficulty in accessing dbGaP data. We surveyed the International Genetic Epidemiology Society (IGES) membership about their experiences. One hundred and seventy five (175) individuals completed the survey, a response rate of 27%. Of respondents who received data from dbGaP (43%), only 32% perceived the application process as easy but most (75%) received data within five months. Remaining challenges include difficulty in identifying an institutional signing official and an overlong application process. Only 24% of respondents had contributed data to dbGaP. Of these, 31% reported local IRB restrictions on data release; an additional 15% had to reconsent study participants before depositing data. The majority of respondents (56%) disagreed that the publication embargo period was sufficient. In response, we recommend longer embargo periods and use of varied data-sharing models rather than a one-size-fits-all approach.
    Full-text · Article · Aug 2014 · International Journal of Environmental Research and Public Health
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: Smoking experimentation in Mexican American youth is problematic. In light of the research showing that preventing smoking experimentation is a valid strategy for smoking prevention, there is a need to identify Mexican American youth at high risk for experimentation. Methods: A prospective population-based cohort of 1179 adolescents of Mexican descent was followed for 5 years starting in 2005-06. Participants completed a baseline interview at a home visit followed by three telephone interviews at intervals of approximately 6 months and additional interviews at two home visits in 2008-09 and 2010-11. The primary end point of interest in this study was smoking experimentation. Information regarding social, cultural, and behavioral factors (e.g., acculturation, susceptibility to experimentation, home characteristics, household influences) was collected at baseline using validated questionnaires. Results: Age, sex, cognitive susceptibility, household smoking behavior, peer influence, neighborhood influence, acculturation, work characteristics, positive outcome expectations, family cohesion, degree of tension, ability to concentrate, and school discipline were found to be associated with smoking experimentation. In a validation dataset, the proposed risk prediction model had an AUC of 0.719 (95% confidence interval, 0.637 to 0.801) for predicting absolute risk for smoking experimentation within 1 year. Conclusions: The proposed risk prediction model is able to quantify the risk of smoking experimentation in Mexican American adolescents. Impact: Accurately identifying Mexican American adolescents who are at higher risk for smoking experimentation who can be intervened will substantially reduce the incidence of smoking and thereby subsequent health risks.
    Full-text · Article · Jul 2014 · Cancer Epidemiology Biomarkers & Prevention
  • [Show abstract] [Hide abstract]
    ABSTRACT: Unlabelled: Survival outcomes in patients with squamous cell carcinoma of the head and neck (HNSCC) vary by extent of disease, behavioral factors, and socioeconomic factors. We assessed the extent to which pretreatment pain influences survival in 2,340 newly diagnosed patients with HNSCC, adjusting for disease stage, symptoms, pain medications, comorbidities, smoking, alcohol consumption, age, sex, and race/ethnicity. Patients rated their pain at presentation to the cancer center (0 = "no pain" and 10 = "pain as bad as you can imagine"). Survival time was calculated from the date of diagnosis to the date of death of any cause or last follow-up. Five-year overall survival was calculated for all the variables assessed in the study. Severe pain (≥7) was most prevalent among those with oral cancer (20.4%; pharynx = 18.8%; larynx = 16.1%) and significantly varied by tumor stage, fatigue severity, smoking status, comorbid lung disease, and race (all P < .05) across cancer diagnoses. Overall 5-year survival varied by pain for oral (severe pain = 31% vs nonsevere pain = 52%; P < .001) and pharyngeal cancer (severe pain = 33% vs nonsevere pain = 53%; P < .001). Multivariable analyses showed that pain persisted as an independent prognostic factor for survival. Pain reported prior to treatment should be considered in understanding survival outcomes in HNSCC patients. Perspective: Pretreatment pain was an independent predictor of survival in a large sample of HNSCC patients even after accounting for tumor node metastasis stage, fatigue, age, race/ethnicity, smoking, and alcohol intake. Therefore, symptoms at presentation and before cancer treatment are important factors to be considered in understanding survival outcomes in HNSCC patients.
    No preview · Article · Jul 2014 · Journal of Pain
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Genome-wide association studies (GWAS) have mapped risk alleles for at least 10 distinct cancers to a small region of 63 000 bp on chromosome 5p15.33. This region harbors the TERT and CLPTM1L genes; the former encodes the catalytic subunit of telomerase reverse transcriptase and the latter may play a role in apoptosis. To investigate further the genetic architecture of common susceptibility alleles in this region, we conducted an agnostic subset-based meta-analysis (association analysis based on subsets) across six distinct cancers in 34 248 cases and 45 036 controls. Based on sequential conditional analysis, we identified as many as six independent risk loci marked by common single-nucleotide polymorphisms: five in the TERT gene (Region 1: rs7726159, P = 2.10 × 10−39; Region 3: rs2853677, P = 3.30 × 10−36 and PConditional = 2.36 × 10−8; Region 4: rs2736098, P = 3.87 × 10−12 and PConditional = 5.19 × 10−6, Region 5: rs13172201, P = 0.041 and PConditional = 2.04 × 10−6; and Region 6: rs10069690, P = 7.49 × 10−15 and PConditional = 5.35 × 10−7) and one in the neighboring CLPTM1L gene (Region 2: rs451360; P = 1.90 × 10−18 and PConditional = 7.06 × 10−16). Between three and five cancers mapped to each independent locus with both risk-enhancing and protective effects. Allele-specific effects on DNA methylation were seen for a subset of risk loci, indicating that methylation and subsequent effects on gene expression may contribute to the biology of risk variants on 5p15.33. Our results provide strong support for extensive pleiotropy across this region of 5p15.33, to an extent not previously observed in other cancer susceptibility loci.
    Full-text · Article · Jul 2014 · Human Molecular Genetics
  • Source
    Jian Wang · Robert Yu · Sanjay Shete
    [Show abstract] [Hide abstract]
    ABSTRACT: X-chromosome inactivation (XCI) is the process in which one of the two copies of the X-chromosome in females is randomly inactivated to achieve the dosage compensation of X-linked genes between males and females. That is, 50% of the cells have one allele inactive and the other 50% of the cells have the other allele inactive. However, studies have shown that skewed or nonrandom XCI is a biological plausibility wherein more than 75% of cells have the same allele inactive. Also, some of the X-chromosome genes escape XCI, i.e., both alleles are active in all cells. Current statistical tests for X-chromosome association studies can either account for random XCI (e.g., Clayton's approach) or escape from XCI (e.g., PLINK software). Because the true XCI process is unknown and differs across different regions on the X-chromosome, we proposed a unified approach of maximizing likelihood ratio over all biological possibilities: random XCI, skewed XCI, and escape from XCI. A permutation-based procedure was developed to assess the significance of the approach. We conducted simulation studies to compare the performance of the proposed approach with Clayton's approach and PLINK regression. The results showed that the proposed approach has higher powers in the scenarios where XCI is skewed while losing some power in scenarios where XCI is random or XCI is escaped, with well-controlled type I errors. We also applied the approach to the X-chromosomal genetic association study of head and neck cancer.
    Full-text · Article · Jul 2014 · Genetic Epidemiology

Publication Stats

7k Citations
942.15 Total Impact Points

Institutions

  • 2002-2015
    • University of Texas MD Anderson Cancer Center
      • • Department of Biostatistics
      • • Department of Epidemiology
      Houston, Texas, United States
  • 2014
    • University of Texas Health Science Center at Houston
      Houston, Texas, United States
  • 2010
    • Baylor College of Medicine
      • Department of Pediatrics
      Houston, Texas, United States
  • 2004-2008
    • University of Houston
      Houston, Texas, United States
  • 2001
    • Cedars-Sinai Medical Center
      • Cedars Sinai Medical Center
      Los Ángeles, California, United States
  • 2000
    • Case Western Reserve University
      • Rammelkamp Center for Education and Research
      Cleveland, Ohio, United States