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  • American Association for Cancer Research (AACR)  (7)
  • 1
    Online Resource
    Online Resource
    Gastrointestinal Cancer Survival and Radiation Exposure among Atomic Bomb Survivors: The Life Span Study
    American Association for Cancer Research (AACR) ; 2021
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 30, No. 2 ( 2021-02-01), p. 412-418
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 30, No. 2 ( 2021-02-01), p. 412-418
    Abstract: Radiation exposure is an established risk factor for the development of several forms of cancer, including gastrointestinal cancers. However, few studies have investigated the relationship between prediagnostic radiation exposure and survival after cancer diagnosis. Methods: Participants in the Life Span Study (LSS) of atomic bomb survivors who were diagnosed with a first primary invasive stomach, colon, or rectal cancer between 1958 and 2009 were followed for mortality during 1958–2014. Cox regression models were used to calculate HRs and 95% confidence intervals (CI) for associations of radiation dose from atomic bomb exposure with survival (cancer-specific and overall) after cancer diagnosis. Analyses were adjusted for city of primary exposure, sex, age at diagnosis, and year of diagnosis. Results: We identified 7,728 eligible patients with cancer for analysis. We observed no statistically significant associations between radiation dose and cancer-specific survival among LSS participants with a gastrointestinal cancer. Higher radiation doses (≥1 Gy) were suggestively, but not significantly, associated with modestly poorer cancer-specific survival for colon cancer only (HR, 1.38; 95% CI, 0.90–2.12), and were associated with poorer overall survival regardless of cancer site. Conclusions: Although radiation exposure is associated with increased risk of gastrointestinal cancer incidence and mortality, study results are inconclusive about an association between prediagnostic radiation exposure and survival after gastrointestinal cancer diagnosis. Impact: Radiation exposure from the atomic bomb before gastrointestinal cancer diagnosis was not associated with cancer survival, but should be evaluated in relation to survival for other cancer types.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-20-1239
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 2
    Online Resource
    Online Resource
    Risk of Meningioma and Common Variation in Genes Related to Innate Immunity
    American Association for Cancer Research (AACR) ; 2010
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 19, No. 5 ( 2010-05-01), p. 1356-1361
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 19, No. 5 ( 2010-05-01), p. 1356-1361
    Abstract: Background: The etiology of meningioma, the second most common type of adult brain tumor in the United States, is largely unknown. Prior studies indicate that history of immune-related conditions may affect the risk of meningioma. Methods: To identify genetic markers for meningioma in genes involved with innate immunity, we conducted an exploratory association study of 101 meningioma cases and 330 frequency-matched controls of European ancestry using subjects from a hospital-based study conducted by the National Cancer Institute. We genotyped 1,407 “tag” single nucleotide polymorphisms (SNP) in 148 genetic regions chosen on the basis of an r2 & gt; 0.8 and minor allele frequency of & gt;5% in Caucasians in HapMap1. Risk of meningioma was estimated by odds ratios and 95% confidence intervals. Results: Seventeen SNPs distributed across 12 genetic regions (NFKB1 (3), FCER1G (3), CCR6 (2), VCAM1, CD14, TNFRSF18, RAC2, XDH, C1D, TLR1/TLR10/TLR6, NOS1, and DEFA5) were associated with the risk of meningioma with P & lt; 0.01. Although individual SNP tests were not significant after controlling for multiple comparisons, gene region–based tests were statistically significant (P & lt; 0.05) for TNFRSF18, NFKB1, FCER1G, CD14, C1D, CCR6, and VCAM1. Conclusions and Impact: Our results indicate that common genetic polymorphisms in innate immunity genes may be associated with risk of meningioma. Given the small sample size, replication of these results in a larger study of meningioma is needed. Cancer Epidemiol Biomarkers Prev; 19(5); 1356–61. ©2010 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-09-1151
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2010
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 3
    Online Resource
    Online Resource
    Benign Breast and Gynecologic Conditions, Reproductive and Hormonal Factors, and Risk of Thyroid Cancer
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Prevention Research Vol. 7, No. 4 ( 2014-04-01), p. 418-425
    Details
    In: Cancer Prevention Research, American Association for Cancer Research (AACR), Vol. 7, No. 4 ( 2014-04-01), p. 418-425
    Abstract: The higher incidence of thyroid cancer in women compared with men suggests an influence of sex steroid hormones in the etiology of this malignancy. We investigated a comprehensive set of potential indicators of lifetime sex steroid hormone exposure in relation to thyroid cancer risk. Using data from the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, which enrolled 70,047 women, 50 to 78 years old, we prospectively examined associations of self-reported history of benign breast and gynecologic conditions, reproductive factors, and exogenous sex hormone use with thyroid cancer risk. Multivariable-adjusted HRs and 95% confidence intervals (CI) were calculated in models using age as the time metric. During follow-up (median, 11 years), 127 women were diagnosed with first primary thyroid cancer. Older age at natural menopause (≥55 vs. & lt;50 years; HR, 2.24; 95% CI, 1.20–4.18), greater estimated lifetime number of ovulatory cycles (≥490 vs. & lt;415 cycles; HR, 2.40; 95% CI, 1.33–4.30), greater number of live births (≥5 vs. 1–2; HR, 1.72; 95% CI, 1.05–2.82), and history of uterine fibroids (HR, 1.72; 95% CI, 1.18–2.50) were associated with an increased risk of thyroid cancer. Earlier age at menarche, greater number of reproductive years, history of a tubal ligation, and history of ovarian cysts were nonsignificantly associated with increased thyroid cancer risk. No associations were observed for oral contraceptive use, menopausal hormone therapy, or history of benign breast disease or endometriosis. In general, we found that factors reflecting a greater length of exposure to endogenous hormones, particularly during the reproductive years, were associated with risk of postmenopausal thyroid cancer. Cancer Prev Res; 7(4); 418–25. ©2014 AACR.
    Type of Medium: Online Resource
    ISSN: 1940-6207 , 1940-6215
    URL: Article
    DOI: 10.1158/1940-6207.CAPR-13-0367
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2422346-3
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  • 4
    Online Resource
    Online Resource
    Common Variation in Genes Related to Innate Immunity and Risk of Adult Glioma
    American Association for Cancer Research (AACR) ; 2009
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 18, No. 5 ( 2009-05-01), p. 1651-1658
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 18, No. 5 ( 2009-05-01), p. 1651-1658
    Abstract: Current evidence suggests that immune system alterations contribute to the etiology of adult glioma, the most common adult brain tumor. Although previous studies have focused on variation in candidate genes in the adaptive immune system, the innate immune system has emerged as a critical avenue for research given its known link with carcinogenesis. To identify genetic markers in pathways critical to innate immunity, we conducted an association study of 551 glioma cases and 865 matched controls of European ancestry to investigate “tag” single nucleotide polymorphisms (SNP) in 148 genetic regions. Two independent U.S. case-control studies included were as follows: a hospital-based study conducted by the National Cancer Institute (263 cases, 330 controls) and a community-based study conducted by the National Institute for Occupational Safety and Health (288 cases, 535 controls). Tag SNPs (1,397) chosen on the basis of an r2 of & gt;0.8 and minor allele frequency of & gt;5% in Caucasians in HapMap1 were genotyped. Glioma risk was estimated by odds ratios. Nine SNPs distributed across eight genetic regions (ALOX5, IRAK3, ITGB2, NCF2, NFKB1, SELP, SOD1, and STAT1) were associated with risk of glioma with P value of & lt;0.01. Although these associations were no longer statistically significant after controlling for multiple comparisons, the associations were notably consistent in both studies. Region-based tests were statistically significant (P & lt; 0.05) for SELP, SOD, and ALOX5. Analyses restricted to glioblastoma (n = 254) yielded significant associations for the SELP, DEFB126/127, SERPINI1, and LY96 genetic regions. We have identified a promising set of innate immunity-related genetic regions for further investigation. (Cancer Epidemiol Biomarkers Prev 2009;18(5):1651–8)
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-08-1041
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2009
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 5
    Online Resource
    Online Resource
    Abstract 2544: Associations between RET/PTC rearrangements, BRAF and RAS mutations and radiation dose, age at exposure, and latency in post-Chernobyl thyroid cancer
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Research Vol. 72, No. 8_Supplement ( 2012-04-15), p. 2544-2544
    Details
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 72, No. 8_Supplement ( 2012-04-15), p. 2544-2544
    Abstract: Introduction: Childhood exposure to I-131 from the Chernobyl accident was associated with a dramatic increase in incidence of papillary thyroid cancer (PTC). PTCs are characterized by several genetic alterations including RET/PTC rearrangements and point mutations of BRAF and RAS. Association between mutations and radiation doses has not been studied in post-Chernobyl tumors. Design: We analyzed 70 PTCs diagnosed in a Ukrainian-American cohort who were & lt; 18 y.o. at the time of Chernobyl and received 0.008-8.6 Gy of I-131 to the thyroid. Thyroid doses were estimated based on radioactivity measurements taken shortly after the accident, environmental transport models, and interview data. BRAF and RAS mutations were identified by melting curve analysis and RET/PTC1 and RET/PTC3 by real-time RT-PCR. All mutations were confirmed by sequencing. Results: Identified mutations and patient characteristics are shown in Table 1. Logistic regression analysis demonstrated a significant decrease in I-131 dose for both BRAF and RAS mutations (p=0.005 and 0.026). There were highly statistically significant (p & lt;0.001) differences between the trends with dose for BRAF and RAS vs RET/PTC. Comparing with BRAF and RAS mutations, the age at exposure was lower in cases with RET/PTC (p=0.001). RET/PTC3 was associated with a shorter latency period as compared to other mutations (p & lt;0.02). Table 1. Genetic alterations and corresponding patient characteristics Conclusions: Our results demonstrate for the first time that prevalence of BRAF or RAS point mutations in post-Chernobyl tumors significantly decreases with increasing radiation dose, in contrast to the lack of decrease for RET/PTC. RET/PTC rearrangements are associated with younger age at exposure than point mutations of BRAF and RAS. These data provide support for the potential relationship between chromosomal rearrangements, but not point mutations, and radiation exposure. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2544. doi:1538-7445.AM2012-2544
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    URL: Article
    DOI: 10.1158/1538-7445.AM2012-2544
    RVK:
    XA 36000
    RVK:
    XA 10000
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036785-5
    detail.hit.zdb_id: 1432-1
    detail.hit.zdb_id: 410466-3
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  • 6
    Online Resource
    Online Resource
    Common Obesity-Related Genetic Variants and Papillary Thyroid Cancer Risk
    American Association for Cancer Research (AACR) ; 2012
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 21, No. 12 ( 2012-12-01), p. 2268-2271
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 21, No. 12 ( 2012-12-01), p. 2268-2271
    Abstract: Background: Epidemiologic studies have shown consistent associations between obesity and increased thyroid cancer risk, but, to date, no studies have investigated the relationship between thyroid cancer risk and obesity-related single-nucleotide polymorphisms (SNP). Methods: We evaluated 575 tag SNPs in 23 obesity-related gene regions in a case–control study of 341 incident papillary thyroid cancer (PTC) cases and 444 controls of European ancestry. Logistic regression models, adjusted for attained age, year of birth, and sex were used to calculate ORs and 95% confidence intervals (CI) with SNP genotypes, coded as 0, 1, and 2 and modeled continuously to calculate Ptrend. Results: Nine of 10 top-ranking SNPs (Ptrend & lt; 0.01) were located in the FTO (fat mass and obesity associated) gene region, whereas the other was located in INSR (insulin receptor). None of the associations were significant after correcting for multiple testing. Conclusions: Our data do not support an important role of obesity-related genetic polymorphisms in determining the risk of PTC. Impact: Factors other than selected genetic polymorphisms may be responsible for the observed associations between obesity and increased PTC risk. Cancer Epidemiol Biomarkers Prev; 21(12); 2268–71. ©2012 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-12-0790
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2012
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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  • 7
    Online Resource
    Online Resource
    Personal History of Diabetes, Genetic Susceptibility to Diabetes, and Risk of Brain Glioma: A Pooled Analysis of Observational Studies
    American Association for Cancer Research (AACR) ; 2014
    In:  Cancer Epidemiology, Biomarkers & Prevention Vol. 23, No. 1 ( 2014-01-01), p. 47-54
    Details
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 23, No. 1 ( 2014-01-01), p. 47-54
    Abstract: Background: Brain glioma is a relatively rare and fatal malignancy in adulthood with few known risk factors. Some observational studies have reported inverse associations between diabetes and subsequent glioma risk, but possible mechanisms are unclear. Methods: We conducted a pooled analysis of original data from five nested case–control studies and two case–control studies from the United States and China that included 962 glioma cases and 2,195 controls. We examined self-reported diabetes history in relation to glioma risk, as well as effect modification by seven glioma risk-associated single-nucleotide polymorphisms (SNP). We also examined the associations between 13 diabetes risk-associated SNPs, identified from genome-wide association studies, and glioma risk. Odds ratios (OR) and 95% confidence intervals (CI) were calculated using multivariable-adjusted logistic regression models. Results: We observed a 42% reduced risk of glioma for individuals with a history of diabetes (OR = 0.58; 95% CI, 0.40–0.84). The association did not differ by sex, study design, or after restricting to glioblastoma, the most common histological subtype. We did not observe any significant per-allele trends among the 13 diabetes-related SNPs examined in relation to glioma risk. Conclusion: These results support an inverse association between diabetes history and glioma risk. The role of genetic susceptibility to diabetes cannot be excluded, and should be pursued in future studies together with other factors that might be responsible for the diabetes–glioma association. Impact: These data suggest the need for studies that can evaluate, separately, the association between type 1 and type 2 diabetes and subsequent risk of adult glioma. Cancer Epidemiol Biomarkers Prev; 23(1); 47–54. ©2013 AACR.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    URL: Article
    DOI: 10.1158/1055-9965.EPI-13-0913
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2014
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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