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Linda M Liao,
Kendra Schwartz,
Michael Pollak,
Barry I Graubard,
Zhen Li,
Julie Ruterbusch,
Nathaniel Rothman, Faith Davis,
Sholom Wacholder,
Joanne Colt,
Wong-Ho Chow,
Mark P Purdue
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ABSTRACT: OBJECTIVE: The incidence of renal cell carcinoma (RCC) has increased rapidly in the U.S., particularly among African Americans. Despite a well-established link between obesity and RCC, the mechanism through which obesity increases cancer risk has yet to be established. Adipokines, such as leptin and adiponectin, may link obesity and cancer, with different quantitative effects by race. DESIGN AND METHODS: We evaluated the association between leptin and adiponectin concentrations and RCC risk among Caucasians (581 cases, 558 controls) and African Americans (187 cases, 359 controls) in a case-control study conducted in Detroit and Chicago. Odds ratios (ORs) and 95% confidence intervals (95%CIs) were estimated using unconditional logistic regression. RESULTS: Among controls, Caucasians had higher median adiponectin than African Americans (males: 8.2 vs. 7.0 μg/ml, P = 0.001; females: 13.4 vs. 8.4 μg/ml, P < 0.0001), and lower median leptin than African Americans (males: 11.8 vs. 14.1 ng/ml, P = 0.04; females: 28.3 vs. 45.9 ng/ml, P < 0.0001). Among Caucasians, the ORs for RCC comparing the highest (Q4) to the lowest (Q1) sex-specific quartile of leptin were 3.2 (95% CI: 1.9-5.2) for males and 4.7 (95% CI: 2.6-8.6) for females. Serum leptin was not significantly associated with RCC among African American males (OR 1.5, 95% CI: 0.7-3.1) or females (OR 2.1, 95% CI: 0.8-5.5). Higher adiponectin was associated with RCC risk among African American males (Q4 vs. Q1: OR 2.3, 95% CI: 1.1-4.6) and females (OR 2.1, 95% CI: 1.2-6.7), but not significantly among Caucasian males (OR 1.6, 95% CI: 0.99-2.7) and females (OR 1.6, 95% CI: 0.9-3.1). CONCLUSION: We observed an association between both leptin and adiponectin concentrations and risk of RCC, which may differ by race. Confirmation in further investigations is needed.
Obesity 11/2012; · 4.28 Impact Factor
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Xiangqing Sun,
Jaime Vengoechea,
Robert Elston,
Yanwen Chen,
Christopher I Amos,
Georgina Armstrong,
Jonine L Bernstein,
Elizabeth B Claus, Faith Davis,
Richard S Houlston, [......],
Joellen M Schildkraut,
Sanjay S Shete,
Robert Yu,
Nicholas A Vick,
Ryan Merrell,
Margaret R Wrensch,
Ping Yang,
Beatrice Melin,
Melissa L Bondy,
Jill S Barnholtz-Sloan
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ABSTRACT: BACKGROUND: We propose a two-step model-based approach, with correction for ascertainment, to linkage analysis of a binary trait with variable age of onset and apply it to a set of multiplex pedigrees segregating for adult glioma. METHODS: First, we fit segregation models by formulating the likelihood for a person to have a bivariate phenotype, affection status and age of onset, along with other covariates, and from these we estimate population trait allele frequencies and penetrance parameters as a function of age (N=281 multiplex glioma pedigrees). Second, the best fitting models are used as trait models in multipoint linkage analysis (N=74 informative multiplex glioma pedigrees). To correct for ascertainment, a prevalence constraint is used in the likelihood of the segregation models for all 281 pedigrees. Then the trait allele frequencies are re-estimated for the pedigree founders of the subset of 74 pedigrees chosen for linkage analysis. RESULTS: Using the best fitting segregation models in model-based multipoint linkage analysis, we identified two separate peaks on chromosome 17; the first agreed with a region identified by Shete et al. (1) who used model-free affected-only linkage analysis, but with a narrowed peak: and the second agreed with a second region they found but had a larger maximum LOD. Conclusions/Impact: Our approach has the advantage of not requiring markers to be in linkage equilibrium unless the minor allele frequency is small (markers which tend to be uninformative for linkage), and of using more of the available information for LOD-based linkage analysis.
Cancer Epidemiology Biomarkers & Prevention 09/2012; · 4.12 Impact Factor
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Yanhong Liu,
Beatrice S Melin,
Preetha Rajaraman,
Zhaoming Wang,
Martha Linet,
Sanjay Shete,
Christopher I Amos,
Ching C Lau,
Michael E Scheurer,
Spiridon Tsavachidis, [......],
Robert B Jenkins,
Daniel LaChance,
Nicholas A Vick,
Margaret Wrensch, Faith Davis,
Bridget J McCarthy,
Ulrika Andersson,
Patricia A Thompson,
Stephen Chanock,
Melissa L Bondy
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ABSTRACT: The risk of glioma has consistently been shown to be increased twofold in relatives of patients with primary brain tumors (PBT). A recent genome-wide linkage study of glioma families provided evidence for a disease locus on 17q12-21.32, with the possibility of four additional risk loci at 6p22.3, 12p13.33-12.1, 17q22-23.2, and 18q23. To identify the underlying genetic variants responsible for the linkage signals, we compared the genotype frequencies of 5,122 SNPs mapping to these five regions in 88 glioma cases with and 1,100 cases without a family history of PBT (discovery study). An additional series of 84 familial and 903 non-familial cases were used to replicate associations. In the discovery study, 12 SNPs showed significant associations with family history of PBT (P < 0.001). In the replication study, two of the 12 SNPs were confirmed: 12p13.33-12.1 PRMT8 rs17780102 (P = 0.031) and 17q12-21.32 SPOP rs650461 (P = 0.025). In the combined analysis of discovery and replication studies, the strongest associations were attained at four SNPs: 12p13.33-12.1 PRMT8 rs17780102 (P = 0.0001), SOX5 rs7305773 (P = 0.0001) and STKY1 rs2418087 (P = 0.0003), and 17q12-21.32 SPOP rs6504618 (P = 0.0006). Further, a significant gene-dosage effect was found for increased risk of family history of PBT with these four SNPs in the combined data set (P(trend) <1.0 × 10(-8)). The results support the linkage finding that some loci in the 12p13.33-12.1 and 17q12-q21.32 may contribute to gliomagenesis and suggest potential target genes underscoring linkage signals.
Human Genetics 06/2012; 131(9):1507-17. · 5.07 Impact Factor
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Summer S Han,
Meredith Yeager,
Lee E Moore,
Ming-Hui Wei,
Ruth Pfeiffer,
Ousmane Toure,
Mark P Purdue,
Mattias Johansson,
Ghislaine Scelo,
Charles C Chung, [......],
James D McKay,
Joseph F Fraumeni,
Nilanjan Chatterjee,
Philip S Rosenberg,
Nathaniel Rothman,
Paul Brennan,
Wong-Ho Chow,
Margaret A Tucker,
Stephen J Chanock,
Jorge R Toro
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ABSTRACT: In follow-up of a recent genome-wide association study (GWAS) that identified a locus in chromosome 2p21 associated with risk for renal cell carcinoma (RCC), we conducted a fine mapping analysis of a 120 kb region that includes EPAS1. We genotyped 59 tagged common single-nucleotide polymorphisms (SNPs) in 2278 RCC and 3719 controls of European background and observed a novel signal for rs9679290 [P = 5.75 × 10(-8), per-allele odds ratio (OR) = 1.27, 95% confidence interval (CI): 1.17-1.39]. Imputation of common SNPs surrounding rs9679290 using HapMap 3 and 1000 Genomes data yielded two additional signals, rs4953346 (P = 4.09 × 10(-14)) and rs12617313 (P = 7.48 × 10(-12)), both highly correlated with rs9679290 (r(2) > 0.95), but interestingly not correlated with the two SNPs reported in the GWAS: rs11894252 and rs7579899 (r(2) < 0.1 with rs9679290). Genotype analysis of rs12617313 confirmed an association with RCC risk (P = 1.72 × 10(-9), per-allele OR = 1.28, 95% CI: 1.18-1.39) In conclusion, we report that chromosome 2p21 harbors a complex genetic architecture for common RCC risk variants.
Human Molecular Genetics 11/2011; 21(5):1190-200. · 7.64 Impact Factor
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ABSTRACT: Renal cell carcinoma and hypertension (a well-established renal cancer risk factor) are both more frequent among blacks than whites in the United States. The association between hypertension and renal cell carcinoma has not been examined in black Americans. We investigated the hypertension-renal cancer association by race, and we assessed the role of hypertension in the racial disparity of renal cancer incidence.
Participants were enrolled in a population-based case-control study in Detroit and Chicago during 2002-2007 (number of cases: 843 whites, 358 blacks; number of controls: 707 whites, 519 blacks). Participants reported their history of hypertension and antihypertensive drug use. We used unconditional logistic regression to calculate odds ratios (ORs) and 95% confidence intervals (CIs), adjusted for demographic characteristics, smoking, body mass index, and family history of cancer.
Hypertension doubled renal cancer risk (OR = 2.0 [CI = 1.7-2.5]) overall. For whites, the OR was 1.9 (CI = 1.5-2.4), whereas for blacks it was 2.8 (2.1-3.8) (P for interaction = 0.11). ORs increased with time after hypertension diagnosis (P for trend <0.001), reaching 4.1 (CI = 2.3-7.4) for blacks and 2.6 (CI = 1.7-4.1) for whites after 25 years. ORs for poorly controlled hypertension were 4.5 (CI = 2.3-8.8) for blacks and 2.1 (CI = 1.2-3.8) for whites. If these estimates correctly represent causal effects and if, hypothetically, hypertension could be prevented entirely among persons aged 50-79 years, the black/white disparity in renal cancer could be reversed among women and reduced by two-thirds among men.
Hypertension is a risk factor for renal cancer among both blacks and whites, and might explain a substantial portion of the racial disparity in renal cancer incidence. Preventing and controlling hypertension might reduce renal cancer incidence, adding to the known benefits of blood pressure control for heart disease and stroke reduction, particularly among blacks.
Epidemiology (Cambridge, Mass.) 08/2011; 22(6):797-804. · 5.51 Impact Factor
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ABSTRACT: Renal cell carcinoma (RCC) incidence is higher among blacks than whites in the United States and has been associated with the frequency and timing of childbirth among women in some epidemiologic studies. We investigated whether reproductive factors are associated with RCC, overall and by race, within a population-based case-control study.
Between 2002 and 2007, 497 female cases of incident RCC (136 black, 361 white) and 546 female controls (273 black, 273 white) within the Detroit and Chicago metropolitan areas were enrolled. Information on reproductive history and other factors was collected through in-person interviews. Multivariate-adjusted odds ratios (OR) and 95% confidence intervals (CI) were computed using unconditional logistic regression.
Reduced RCC risk was observed among women aged ≥30 years at first live birth, relative to an age of <20 years (OR 0.5, 95% CI 0.3-0.9). This association was present among both white (OR 0.4, 95% CI 0.2-0.9) and, though not statistically significant, black women (OR 0.6, 95% CI 0.2-1.8). In analyses restricted to clear cell adenocarcinoma, the most common RCC histological subtype, the association was particularly strong (OR 0.3, 95% CI 0.2-0.8). We did not observe clear evidence of association with RCC for other reproductive factors.
Our findings further support an association between late maternal age at first birth and reduced RCC risk, and suggest that the association may be particularly strong for clear cell adenocarcinoma.
Cancer Causes and Control 08/2011; 22(11):1537-44. · 2.88 Impact Factor
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Daniel H Lachance,
Ping Yang,
Derek R Johnson,
Paul A Decker,
Thomas M Kollmeyer,
Lucie S McCoy,
Terri Rice,
Yuanyuan Xiao,
Francis Ali-Osman,
Frances Wang, [......], Faith Davis,
Bridget McCarthy,
Amanda L Rynearson,
Joel B Worra,
Brooke L Fridley,
Brian Patrick O'Neill,
Jan C Buckner,
Dora Il'yasova,
Robert B Jenkins,
Margaret R Wrensch
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ABSTRACT: Glioma risk has consistently been inversely associated with allergy history but not with smoking history despite putative biologic plausibility. Data from 855 high-grade glioma cases and 1,160 controls from 4 geographic regions of the United States during 1997-2008 were analyzed for interactions between allergy and smoking histories and inherited variants in 5 established glioma risk regions: 5p15.3 (TERT), 8q24.21 (CCDC26/MLZE), 9p21.3 (CDKN2B), 11q23.3 (PHLDB1/DDX6), and 20q13.3 (RTEL1). The inverse relation between allergy and glioma was stronger among those who did not (odds ratio(allergy-glioma) = 0.40, 95% confidence interval: 0.28, 0.58) versus those who did (odds ratio(allergy-glioma) = 0.76, 95% confidence interval: 0.59, 0.97; P(interaction) = 0.02) carry the 9p21.3 risk allele. However, the inverse association with allergy was stronger among those who carried (odds ratio(allergy-glioma) = 0.44, 95% confidence interval: 0.29, 0.68) versus those who did not carry (odds ratio(allergy-glioma) = 0.68, 95% confidence interval: 0.54, 0.86) the 20q13.3 glioma risk allele, but this interaction was not statistically significant (P = 0.14). No relation was observed between glioma risk and smoking (odds ratio = 0.92, 95% confidence interval: 0.77, 1.10; P = 0.37), and there were no interactions for glioma risk of smoking history with any of the risk alleles. The authors' observations are consistent with a recent report that the inherited glioma risk variants in chromosome regions 9p21.3 and 20q13.3 may modify the inverse association of allergy and glioma.
American journal of epidemiology 07/2011; 174(5):574-81. · 5.59 Impact Factor
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ABSTRACT: High-dose ionizing radiation is an established risk factor for glioma, but it remains unknown whether moderate- and low-dose radiation increase glioma risk. In this analysis, we assessed the evidence that self-reported exposures to diagnostic ionizing radiation, including computerized tomography (CT) scans, is associated with increased risk of adult glioma. While no independent association was observed for CT scans alone (3+ scans compared to none P = 0.08 and 1-2 scans compared to none P = 0.68), our findings suggest an increased risk of adult gliomas with cumulative exposure to three or more CT scans to the head and neck region (OR = 1.97, 95% CI: 0.92-4.23) limited to those who reported a family history of cancer: the P value for the interaction between having three or more CT scans and family history of cancer was 0.08. The stratum-specific adjusted OR for those with family history of cancer was more than three times that for the sub-group without family history of cancer. While there is some potential for symptom-related bias, one might expect this to be present for all diagnostic procedures rather than specific to one procedure. The interaction between CT scans and glioma with family history of cancer supports the biological plausibility of our findings, because similar results have been found for breast cancer and radiation. This observational data will increase awareness about potential risks associated with CT scans and the need to minimize the use of unnecessary examinations.
Radiation Research 04/2011; 175(6):790-6. · 2.68 Impact Factor
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ABSTRACT: Allergies have been associated with decreased risk of glioma; but, associations between duration and timing of allergies, and antihistamine use and glioma risk have been less consistent. The objective was to investigate this association by analyzing types, number, years since diagnosis, and age at diagnosis of allergies, and information on antihistamine usage, including type, duration, and frequency of exposure.
Self-report data on medically diagnosed allergies and antihistamine use were obtained for 419 glioma cases and 612 hospital-based controls from Duke University and NorthShore University HealthSystem.
High- and low-grade glioma cases were statistically significantly less likely to report any allergy than controls (OR = 0.66, 95% CI: 0.49-0.87 and OR = 0.44, 95% CI: 0.25-0.76, respectively). The number of types of allergies (seasonal, medication, pet, food, and other) was inversely associated with glioma risk in a dose-response manner (P value for trend < 0.05). Age at diagnosis and years since diagnosis of allergies were not associated with glioma risk. Oral antihistamine use was statistically significantly inversely associated with glioma risk, but when stratified by allergy status, remained significant only for those with high-grade glioma and no medically diagnosed allergy.
All types of allergies appear to be protective with reduced risk for those with more types of allergies. Antihistamine use, other than in relationship with allergy status, may not influence glioma risk.
A comprehensive study of allergies and antihistamine use using standardized questions and biological markers will be essential to further delineate the biological mechanism that may be involved in brain tumor development.
Cancer Epidemiology Biomarkers & Prevention 03/2011; 20(2):370-8. · 4.12 Impact Factor
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Lindsay B Robertson,
Georgina N Armstrong,
Bianca D Olver,
Amy L Lloyd,
Sanjay Shete,
Ching Lau,
Elizabeth B Claus,
Jill Barnholtz-Sloan,
Rose Lai,
Dora Il'yasova, [......],
Nicholas A Vick,
Christoffer Johansen,
Hanne Bødtcher,
Siegal Sadetzki,
Revital Bar-Sade Bruchim,
Galit Hirsh Yechezkel,
Ulrika Andersson,
Beatrice S Melin,
Melissa L Bondy,
Richard S Houlston
Familial Cancer 06/2010; · 1.30 Impact Factor
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Lindsay B Robertson,
Georgina N Armstrong,
Bianca D Olver,
Amy L Lloyd,
Sanjay Shete,
Ching Lau,
Elizabeth B Claus,
Jill Barnholtz-Sloan,
Rose Lai,
Dora Il'yasova, [......],
Nicholas A Vick,
Christoffer Johansen,
Hanne Bødtcher,
Siegal Sadetzki,
Revital Bar-Sade Bruchim,
Galit Hirsh Yechezkel,
Ulrika Andersson,
Beatrice S Melin,
Melissa L Bondy,
Richard S Houlston
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ABSTRACT: There is increasing recognition of familial propensity to glioma as a distinct clinical entity beyond a few rare syndromes; however its genetic basis is poorly understood. The role of p16(INK4A)/p14(ARF) and p53 mutations in sporadic glioma provides a strong rationale for investigating germline mutations in these genes as a cause of familial glioma. To survey the familial glioma phenotype and examine the contribution of germline mutation in p16(INK4A)/p14(ARF) and p53 to the disease we have analyzed a series of 101 index familial cases collected through the GLIOGENE Consortium (http://braintumor.epigenetic.org/). There was little evidence for within family correlations for tumour histology, suggesting generic susceptibility to glial tumors. We did not detect any functional mutations in p16(INK4A) or p14(ARF). One index case with glioblastoma multiforme (GBM) diagnosed at age 54 and had a family history comprised of a paternal aunt with GBM at age 55, carried the p53 R158H mutation, which is predicted to be functional and has previously been implicated as a cause of Li-Fraumeni syndrome. Our findings provide no evidence that p16(INK4A)/p14(ARF) and p53 mutations contribute significantly to familial glioma.
Familial Cancer 05/2010; 9(3):413-21. · 1.30 Impact Factor
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Lee E Moore,
Paul Brennan,
Sara Karami,
Idan Menashe,
Sonja I Berndt,
Linda M Dong,
Allison Meisner,
Meredith Yeager,
Stephen Chanock,
Joanne Colt, [......],
Hellena Kollarova,
Vladimir Bencko,
Marie Navratilova,
Neonilia Szeszenia-Dabrowska,
Dana Mates,
Ivana Holcatova,
Paolo Boffetta,
Wong-Ho Chow,
Philip S Rosenberg,
Nathaniel Rothman
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ABSTRACT: Lipid peroxidation is considered a unifying mechanistic pathway through which known risk factors induce renal cell carcinoma (RCC). We hypothesized that genes selected a priori for their role in lipid peroxidation would modify cancer risk. We genotyped 635 single nucleotide polymorphisms (SNP) in 38candidate genes in 777 Caucasian RCC cases and 1,035 controls enrolled in a large European case-control study. Top candidate SNPs were confirmed among 718 Caucasian cases and 615 controls in a second study in the United States. Two of the three SNPs (rs8106822 and rs405509) that replicated in the U.S. study were within a regulatory region of the APOE promoter. The OR for rs8106822 A>G variant was 1.22(AG) and 1.41(GG) (P(trend) = 0.01) in the European study, 1.05(AG) and 1.51(GG) (P(trend) = 0.03) in the U.S. study, and 1.15(AG) and 1.44(GG) (P(trend) = 0.001) among 1,485 cases and 1,639 controls combined. The rs405509 G>T variant was associated with risk in the European (OR, 0.87(TG); OR, 0.71(TT); P(trend) = 0.02), the U.S. (OR, 0.68(TG); OR, 0.71(TT); P(trend) = 0.02), and both studies combined (OR(TG), 0.79; OR(TT), 0.71; P(trend) = 0.001), as was the G-G haplotype (r(2) = 0.64; P= 4.7 x 10(-4)). This association is biologically plausible as SNP rs405509 was shown to modify protein binding and transcriptional activity of the APOE protein in vitro and is in linkage disequilibrium with key known variants defining the e2, e3, and e4 alleles that modify risk of atherosclerosis, Alzheimer's disease risk, and progression to AIDS. In two large case-control studies, our findings further define a functional region of interest at the APOE locus that increases RCC susceptibility.
Cancer Research 10/2009; 69(20):8001-8. · 7.86 Impact Factor
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ABSTRACT: Because glioma etiology is largely unknown, the inverse association of glioma risk with atopic conditions is promising and deserves close scrutiny. We examined the association between a history of allergies, asthma, and eczema, and glioma risk using sibling, friend, and clinic-based controls. This analysis included 388 incident glioma cases and 80 sibling, 191 friend, and 177 clinic-based controls. Each subject's medical history was assessed via a Web-based or telephone survey. Odds ratios (OR) and their 95% confidence intervals (CI) for the associations with allergies, asthma, eczema, and the overall number of these conditions were calculated from conditional (for sibling and friend controls) and unconditional (for clinic-based controls) logistic models. Allergies were consistently inversely associated with the glioma: ORs were 0.53 (95% CI, 0.15-1.84), 0.54 (95% CI, 0.28-1.07), and 0.34 (95% CI, 0.23-0.50) with sibling, friend, and clinic-based controls, respectively. Asthma showed an inverse association only in the comparison with sibling controls (OR, 0.43; 95% CI, 0.19-1.00). Eczema showed an inverse association only in the comparison with friend controls (OR, 0.42; 95% CI, 0.15-1.18). The overall number of these conditions (ordinal score 0, 1, 2, 3) was inversely associated with glioma: The risk decreased 31% to 45% with each addition of an atopic condition. These estimates were the most stable when different control groups were considered. Comparing the prevalence of these conditions in the three control groups with published data, we note that clinic-based controls generally better approximate the prevalence data for population-based groups. These controls seem to present a reasonable choice for clinic-centered case-control studies.
Cancer Epidemiology Biomarkers & Prevention 05/2009; 18(4):1232-8. · 4.12 Impact Factor
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Linda M Dong,
Paul Brennan,
Sara Karami,
Rayjean J Hung,
Idan Menashe,
Sonja I Berndt,
Meredith Yeager,
Stephen Chanock,
David Zaridze,
Vsevolod Matveev, [......],
Marie Navratilova,
Neonila Szeszenia-Dabrowska,
Dana Mates,
Joanne S Colt,
Ivana Holcatova,
Paolo Boffetta,
Nathaniel Rothman,
Wong-Ho Chow,
Philip S Rosenberg,
Lee E Moore
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ABSTRACT: We conducted a case-control study of renal cancer (987 cases and 1298 controls) in Central and Eastern Europe and analyzed genomic DNA for 319 tagging single-nucleotide polymorphisms (SNPs) in 21 genes involved in cellular growth, differentiation and apoptosis using an Illumina Oligo Pool All (OPA). A haplotype-based method (sliding window analysis of consecutive SNPs) was used to identify chromosome regions of interest that remained significant at a false discovery rate of 10%. Subsequently, risk estimates were generated for regions with a high level of signal and individual SNPs by unconditional logistic regression adjusting for age, gender and study center. Three regions containing genes associated with renal cancer were identified: caspase 1/5/4/12(CASP 1/5/4/12), epidermal growth factor receptor (EGFR), and insulin-like growth factor binding protein-3 (IGFBP3). We observed that individuals with CASP1/5/4/12 haplotype (spanning area upstream of CASP1 through exon 2 of CASP5) GGGCTCAGT were at higher risk of renal cancer compared to individuals with the most common haplotype (OR:1.40, 95% CI:1.10-1.78, p-value = 0.007). Analysis of EGFR revealed three strong signals within intron 1, particularly a region centered around rs759158 with a global p = 0.006 (GGG: OR:1.26, 95% CI:1.04-1.53 and ATG: OR:1.55, 95% CI:1.14-2.11). A region in IGFBP3 was also associated with increased risk (global p = 0.04). In addition, the number of statistically significant (p-value<0.05) SNP associations observed within these three genes was higher than would be expected by chance on a gene level. To our knowledge, this is the first study to evaluate these genes in relation to renal cancer and there is need to replicate and extend our findings. The specific regions associated with risk may have particular relevance for gene function and/or carcinogenesis. In conclusion, our evaluation has identified common genetic variants in CASP1, CASP5, EGFR, and IGFBP3 that could be associated with renal cancer risk.
PLoS ONE 01/2009; 4(3):e4895. · 4.09 Impact Factor
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ABSTRACT: To determine whether a Web-based survey was an acceptable method of data collection for a clinic-based case-control study of adult brain cancer, the authors compared the reliability of paired responses to a main and resurvey for participants completing surveys by telephone (n=74) or self-administered on the Web (n=465) between 2003 and 2006.
Recruitment of cases was done at the Evanston Northwestern Healthcare Kellogg Cancer Care Center and the Duke University Medical Center Cancer Control division, and controls were friends and siblings of cases. Twenty-five variables were examined, including smoking, oral contraceptive and residential histories, water sources, meat preparation, fruit and vegetable consumption, and pesticide use. Weighted and simple kappa's were estimated for categorical and binary variables, respectively.
The number of concordant paired responses was summed for use in linear regression. Respondents were 97% White and 85% had postsecondary education. Kappa's for individual questions ranged from 0.31 (duration of residence in a single family house) to 0.96 (ever smoked), with a median of 0.57 (95% confidence interval, 0.47-0.64). The median number of concordant responses was 16.2 (range, 5-22). Reliability was greater for controls than cases, Web-based versus telephone responders, females, and higher-income responders. Frequency of e-mail and Internet use was not associated with reliability.
A self-administered, Web-based survey was a feasible and appropriate mode of interview in this study. The comparable reliability of Web compared with telephone responses suggest that Web-based self-interviews could be a cost-effective alternative to traditional modes of interview.
Cancer Epidemiology Biomarkers & Prevention 11/2008; 17(10):2639-46. · 4.12 Impact Factor
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Beatrice Malmer,
Phyllis Adatto,
Georgina Armstrong,
Jill Barnholtz-Sloan,
Jonine L Bernstein,
Elizabeth Claus, Faith Davis,
Richard Houlston,
Dora Il'yasova,
Robert Jenkins, [......],
Ching Lau,
Bridget McCarthy,
Hanne Nielsen,
Sara H Olson,
Siegal Sadetzki,
Sanjay Shete,
Fredrik Wiklund,
Margaret Wrensch,
Ping Yang,
Melissa Bondy
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ABSTRACT: Evidence for familial aggregation of glioma has been documented in both case-control and cohort studies and occurs apart from the well-described rare inherited genetic syndromes involving glioma: neurofibromatosis type 1 and 2, tuberous sclerosis, Turcot's syndrome, and Li-Fraumeni syndrome. Nonsyndromic glioma families have been studied but no genes have been identified in the two published linkage studies of familial glioma probably due to the small number of families. Because glioma is a rare but devastating cancer, and a family history of glioma has been observed in approximately 5% of the cases, we initiated an international consortium to identify glioma families not affected by syndromes to better understand the inherited factors related to this disease. The international consortium GLIOGENE is an acronym for "glioma gene" and includes 15 research groups in North America, Europe, and Israel to study familial glioma. The overarching goal is to characterize genes in glioma families using a genome-wide single-nucleotide polymorphism approach and conducting linkage analysis to identify new genomic regions or loci that could harbor genes important for gliomagenesis. Here, we review the rationale for studying familial glioma and our proposed strategy for the GLIOGENE study.
Cancer Epidemiology Biomarkers & Prevention 10/2007; 16(9):1730-4. · 4.12 Impact Factor
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ABSTRACT: This study quantifies the risk of second primary tumors following a diagnosis of meningioma. 12,012 meningiomas and 926 second primary cancers were identified (ICD7, path code 461) between 1958 and 1997 using Swedish Cancer Registry data. Standardized incidence ratios (SIRs) and exact 95% confidence intervals (CIs) were calculated. An elevated risk of any second primary cancer diagnosis (SIR = 1.2, 95% CI = 1.1-1.3) was observed. Elevated and statistically significant SIRs were observed for renal cancer (SIR = 1.6), melanoma (SIR = 1.7), thyroid cancer (SIR = 2.6) and brain tumors (SIR = 2.6). A consistent pattern of risk over time supports the evaluation of common risk factor profiles for renal, melanoma and thyroid cancers. Radiation exposures increase the risk of these rare tumors, so quantifying the cumulative and shared effects of environmental and treatment exposures is of further interest.
Neuroepidemiology 02/2007; 29(1-2):101-6. · 2.31 Impact Factor
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ABSTRACT: The aims of this study were to describe causes of death during the 10-year period between 1995 and 2004 in a large urban jail in Chicago; to compare disease specific mortality rates between the jail population and the general population; to explore demographic and incarceration characteristics of the inmates who died in the jail by cause of death; and to examine gender difference in demographic characteristics, incarceration patterns, and causes of death. A total of 178 deaths occurring in the jail over a 10-year period (1995-2004) were reviewed. Age-adjusted disease-specific mortality rates were computed for the jail population and compared with the rates in the US general population. Cause of death, demographic variables, and incarceration related factors were retrieved from multiple computerized databases. Descriptive analyses were performed to examine demographic and incarceration-related patterns by cause of death and gender. Heart disease was the most frequent cause of death in the jail population, followed by cerebrovascular disease and suicide. Mortality rates for heart diseases, infectious/inflammatory conditions and suicide were higher for jail inmates than the general population. Black inmates accounted for the majority of deaths due to illnesses and homicide, and a much higher proportion of white and Hispanic inmates were involved in suicide deaths. Deaths due to drug overdose or withdrawal were disproportionately higher among female inmates compared with male inmates. Consistent review of mortality rates and causes of deaths in jail can be a useful tool to better understand health issues and needs of jail inmates. Surveillance of acute and chronic illnesses and strategic reengineering of jail health care is a key to quality improvement for incarcerated populations for whom the jail system becomes their primary care provider.
Journal of Urban Health 02/2007; 84(1):70-84. · 2.13 Impact Factor
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ABSTRACT: Meningiomas occur more commonly in females. The coincidence between meningioma and breast cancer and case reports of tumor growth during pregnancy support a hormonal hypothesis. A case control study was conducted to investigate this. Female subjects treated between 1987 and 1992 were identified from 3 hospitals in the Chicago area. Female spouses of male back pain patients were recruited as controls. A self-administered mail questionnaire focused on exogenous, endogenous and other hormonal factors, personal and family medical history as well as radiation exposures. Odds ratios and 95% confidence intervals were estimated using crude, stratified and multivariable logistic models including 219 cases and 260 controls. Participation rates were 86% among cases and 75% among controls. An increased odds ratio (OR) was observed comparing African Americans to Caucasians [OR = 2.4, 95% confidence interval (CI) = 1.0-6.1]. A protective effect was observed for pregnancy, which increased with number and age at first pregnancy. The odds ratio for 3 or more pregnancies compared to none was 0.3 (95% CI = 0.2-0.6). Age at menarche or total period of hormonal activity was not protective. Ever smokers showed a decreased odds ratio for meningioma (OR = 0.6, 95% CI = 0.4-0.9). The increased odds ratios with African Americans was retained in post-menopausal women, while the protective odds ratios for pregnancy, smoking and oral contraceptives (OCs) became stronger in pre-menopausal women. The pattern by duration and timing of use does not suggest an etiologic role for OCs or hormone replacement therapy. These data add to the evidence that factors known to influence endogenous hormones (pregnancy and indirectly smoking) may have protective effects for meningiomas primarily in premenopausal women.
International Journal of Cancer 10/2006; 119(5):1152-7. · 5.44 Impact Factor
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ABSTRACT: Participants in epidemiology studies are often asked to complete an interview and to provide biospecimens. In a population-based case-control study of kidney cancer involving an interview and optional biospecimens, we examined whether mentioning the biospecimens in the initial contact letter adversely affects willingness to be interviewed.
Eligible cases (n = 434) and controls (n = 775) in Detroit were alternately assigned to receive one of two versions of the contact letter. Both explained that the study involves an interview with 100 dollars compensation plus an optional component with additional compensation; only one disclosed that the optional component involved biospecimens.
There were no meaningful differences between the groups in willingness to be interviewed. However, among 303 cases and 351 controls already interviewed, the proportion providing biospecimens was higher in the fully informed group: for blood, the differences were 10.8 (95% CI, 2.0, 19.5) for cases and 6.7% (95% CI, -1.7, 15.1) for controls. Findings were similar for saliva.
In a study involving an interview and optional biospecimens, informing people about the samples in the contact letter seems preferable to a non-specific reference to a second study component. Both approaches yielded similar interview participation rates, but biospecimen participation rates were higher among those informed about the samples in the contact letter.
Annals of Epidemiology 11/2005; 15(9):700-4. · 3.21 Impact Factor
