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  • American Association for Cancer Research (AACR)  (15)
  • 1
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 2484-2484
    Abstract: The zinc finger protein Zc3h8 is overexpressed in many mouse and human solid tumors. We have shown that increased expression of Zc3h8 in cultured mouse mammary cells is associated with increased proliferation rate, increased motility and invasiveness, increased capacity for growth in three dimensions, and increased capacity for tumor formation. Partial knockdown of Zc3h8 expression from mouse mammary tumor cells has the opposite effect. The Zc3h8 protein localizes to both PML bodies and Cajal bodies in the nucleus and features of this localization are altered by treatment of cells with a casein kinase 2 inhibitor, TBB. We have embarked upon an analysis of the contributions of structural features of the Zc3h8 protein through mutagenesis of the gene at key positions. The casein kinase 2 phosphorylation site at position T32 was mutated to either an alanine to prevent phosphorylation, or to glutamic acid to mimic constitutive phosphorylation. Each of the three zinc fingers in the C-terminal region was mutated to replace one cysteine residue. The mutations were introduced into a variant of the zc3h8 gene that has 6 mutations introduced at synonymous positions in order to escape knockdown by RNAi, although the protein sequence generated is identical to the original Zc3h8. Each of the mutant constructs was introduced into mouse mammary tumor cells with knockdown of the endogenous Zc3h8. Mutation of the phosphorylation site T32A led to the formation of fewer, although larger PML bodies, with continued ZC3h8 co-localization. The T32E mutant, with constitutive negative charge at this position led to the formation of a large number of small nuclear foci. Mutant constructs were stably transfected into tumor cells with knockdown of endogenous Zc3h8, and behavior of the mutants was compared to the behavior of cells transfected with the synonymously mutated gene construct. Disruption of each of the zinc fingers individually led to decreased proliferation rate, decreased growth as spheroids or in soft agar, and decreased invasion through Matrigel relative to the synonymous Zc3h8. Tumor cells with Zc3h8 knockdown failed to form tumors in syngeneic BALB/c mice within 10 weeks, while cells transfected with a negative control vector formed tumors in all animals. Rescue of Zc3h8 expression with the synonymous mutant led to tumor formation in 50% of the animals, while no tumors formed from cells transfected with zinc finger mutants. We conclude that the zinc fingers contribute to aggressive tumor cell behavior while the T32 phosphorylation site is essential for proper localization to nuclear bodies. Citation Format: John A. Schmidt, Emily R. Duffner, Emily M. Harris, Tyler Doan, Emanuel Irizarry, Keith G. Danielson, Janice E. Knepper. Structural analysis of features contributing to the oncogenic phenotype conferred by the zinc finger nuclear body protein Zc3h8 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 2484.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 2
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    American Association for Cancer Research (AACR) ; 2018
    In:  Cancer Research Vol. 78, No. 13_Supplement ( 2018-07-01), p. 14-14
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 78, No. 13_Supplement ( 2018-07-01), p. 14-14
    Abstract: A key component of tumor progression and metastasis is the hypoxic response. The hypoxic response regulates angiogenesis, tumor invasion, and metabolism. The Hypoxia Inducible Factor (HIF) is the transcriptional system responsible for the hypoxic response. The inhibition of the hypoxic response via inhibition of the HIF-1 pathway by disrupting its association with the transcriptional coactivator p300 presents a potential therapeutic target for multiple cancers where HIF is upregulated. To that end, we describe the preclinical development of previously described novel marine pyrroloiminoquinone alkaloids found using a HIF-1α/p300 assay in a high throughput screen of extracts from the National Cancer Institute's Natural Products Repository. Pyrroloiminoquinone alkaloids are a novel class of HIF-1α inhibitors, which interrupt the protein−protein interaction between HIF-1α and p300 and consequently reduce HIF-related transcription. The 2 lead candidates, discorhabdin L and H were assessed in inhibition of angiogenesis in an in vitro HUVEC assay and ex vivo rat aortic ring assay. The compounds were also evaluated for in vivo efficacy in prostate cancer cell tumor xenografts. Results show that development of these compounds for clinical use is warranted and may prevent the progression of multiple tumor types. Citation Format: Jonathan D. Strope, Emily M. Harris, Shaunna L. Beedie, Cindy H. Chau, Kristina M. Cook, Christopher J. Schofield, Kirk R. Gustafson, William D. Figg. Preclinical evaluation of novel HIF-1α/P300 binding inhibitors [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2018; 2018 Apr 14-18; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2018;78(13 Suppl):Abstract nr 14.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2018
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  • 3
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 30, No. 1 ( 2021-01-01), p. 217-228
    Abstract: Accumulating evidence suggests a relationship between endometrial cancer and ovarian cancer. Independent genome-wide association studies (GWAS) for endometrial cancer and ovarian cancer have identified 16 and 27 risk regions, respectively, four of which overlap between the two cancers. We aimed to identify joint endometrial and ovarian cancer risk loci by performing a meta-analysis of GWAS summary statistics from these two cancers. Methods: Using LDScore regression, we explored the genetic correlation between endometrial cancer and ovarian cancer. To identify loci associated with the risk of both cancers, we implemented a pipeline of statistical genetic analyses (i.e., inverse-variance meta-analysis, colocalization, and M-values) and performed analyses stratified by subtype. Candidate target genes were then prioritized using functional genomic data. Results: Genetic correlation analysis revealed significant genetic correlation between the two cancers (rG = 0.43, P = 2.66 × 10−5). We found seven loci associated with risk for both cancers (PBonferroni & lt; 2.4 × 10−9). In addition, four novel subgenome-wide regions at 7p22.2, 7q22.1, 9p12, and 11q13.3 were identified (P & lt; 5 × 10−7). Promoter-associated HiChIP chromatin loops from immortalized endometrium and ovarian cell lines and expression quantitative trait loci data highlighted candidate target genes for further investigation. Conclusions: Using cross-cancer GWAS meta-analysis, we have identified several joint endometrial and ovarian cancer risk loci and candidate target genes for future functional analysis. Impact: Our research highlights the shared genetic relationship between endometrial cancer and ovarian cancer. Further studies in larger sample sets are required to confirm our findings.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2021
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  • 4
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 79, No. 3 ( 2019-02-01), p. 505-517
    Abstract: DNA methylation is instrumental for gene regulation. Global changes in the epigenetic landscape have been recognized as a hallmark of cancer. However, the role of DNA methylation in epithelial ovarian cancer (EOC) remains unclear. In this study, high-density genetic and DNA methylation data in white blood cells from the Framingham Heart Study (N = 1,595) were used to build genetic models to predict DNA methylation levels. These prediction models were then applied to the summary statistics of a genome-wide association study (GWAS) of ovarian cancer including 22,406 EOC cases and 40,941 controls to investigate genetically predicted DNA methylation levels in association with EOC risk. Among 62,938 CpG sites investigated, genetically predicted methylation levels at 89 CpG were significantly associated with EOC risk at a Bonferroni-corrected threshold of P & lt; 7.94 × 10−7. Of them, 87 were located at GWAS-identified EOC susceptibility regions and two resided in a genomic region not previously reported to be associated with EOC risk. Integrative analyses of genetic, methylation, and gene expression data identified consistent directions of associations across 12 CpG, five genes, and EOC risk, suggesting that methylation at these 12 CpG may influence EOC risk by regulating expression of these five genes, namely MAPT, HOXB3, ABHD8, ARHGAP27, and SKAP1. We identified novel DNA methylation markers associated with EOC risk and propose that methylation at multiple CpG may affect EOC risk via regulation of gene expression. Significance: Identification of novel DNA methylation markers associated with EOC risk suggests that methylation at multiple CpG may affect EOC risk through regulation of gene expression.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2019
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  • 5
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 5 ( 2020-03-01), p. 1210-1218
    Abstract: Repeated exposure to the acute proinflammatory environment that follows ovulation at the ovarian surface and distal fallopian tube over a woman's reproductive years may increase ovarian cancer risk. To address this, analyses included individual-level data from 558,709 naturally menopausal women across 20 prospective cohorts, among whom 3,246 developed invasive epithelial ovarian cancer (2,045 serous, 319 endometrioid, 184 mucinous, 121 clear cell, 577 other/unknown). Cox models were used to estimate multivariable-adjusted HRs between lifetime ovulatory cycles (LOC) and its components and ovarian cancer risk overall and by histotype. Women in the 90th percentile of LOC ( & gt;514 cycles) were almost twice as likely to be diagnosed with ovarian cancer than women in the 10th percentile ( & lt;294) [HR (95% confidence interval): 1.92 (1.60–2.30)]. Risk increased 14% per 5-year increase in LOC (60 cycles) [(1.10–1.17)] ; this association remained after adjustment for LOC components: number of pregnancies and oral contraceptive use [1.08 (1.04–1.12)]. The association varied by histotype, with increased risk of serous [1.13 (1.09–1.17)] , endometrioid [1.20 (1.10–1.32)], and clear cell [1.37 (1.18–1.58)] , but not mucinous [0.99 (0.88–1.10), P-heterogeneity = 0.01] tumors. Heterogeneity across histotypes was reduced [P-heterogeneity = 0.15] with adjustment for LOC components [1.08 serous, 1.11 endometrioid, 1.26 clear cell, 0.94 mucinous]. Although the 10-year absolute risk of ovarian cancer is small, it roughly doubles as the number of LOC rises from approximately 300 to 500. The consistency and linearity of effects strongly support the hypothesis that each ovulation leads to small increases in the risk of most ovarian cancers, a risk that cumulates through life, suggesting this as an important area for identifying intervention strategies. Significance: Although ovarian cancer is rare, risk of most ovarian cancers doubles as the number of lifetime ovulatory cycles increases from approximately 300 to 500. Thus, identifying an important area for cancer prevention research.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 6
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 73, No. 24 ( 2013-12-15), p. 7222-7231
    Abstract: Ovarian cancer is a clinically and molecularly heterogeneous disease. The driving forces behind this variability are unknown. Here, we report wide variation in the expression of the DNA cytosine deaminase APOBEC3B, with elevated expression in the majority of ovarian cancer cell lines (three SDs above the mean of normal ovarian surface epithelial cells) and high-grade primary ovarian cancers. APOBEC3B is active in the nucleus of several ovarian cancer cell lines and elicits a biochemical preference for deamination of cytosines in 5′-TC dinucleotides. Importantly, examination of whole-genome sequence from 16 ovarian cancers reveals that APOBEC3B expression correlates with total mutation load as well as elevated levels of transversion mutations. In particular, high APOBEC3B expression correlates with C-to-A and C-to-G transversion mutations within 5′-TC dinucleotide motifs in early-stage high-grade serous ovarian cancer genomes, suggesting that APOBEC3B-catalyzed genomic uracil lesions are further processed by downstream DNA "repair" enzymes including error-prone translesion polymerases. These data identify a potential role for APOBEC3B in serous ovarian cancer genomic instability. Cancer Res; 73(24); 7222–31. ©2013 AACR.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
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    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2013
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  • 7
    In: Cancer Research, American Association for Cancer Research (AACR), Vol. 80, No. 16_Supplement ( 2020-08-15), p. 1180-1180
    Abstract: Purpose. Although the incidence of epithelial ovarian cancer is highest among non-Hispanic white women, African-American women have the worst survival of all racial/ethnic groups. We hypothesize that differences in the prevalence of known and suspected ovarian cancer risk factors may explain a portion of the differences in incidence of epithelial ovarian cancer between white and African-American women. Methods. We used data from seven U.S. studies in the Ovarian Cancer in Women of African Ancestry (OCWAA) consortium, the North Carolina Ovarian Cancer Study (NCOCS), the Los Angeles Ovarian Cancer Study (LACOCS), the African-American Cancer Epidemiology Study (AACES), the Cook County Case-Control Study (CCCCS), the Black Women's Health Study (BWHS), the Women's Health Initiative (WHI), and the Multiethnic Cohort Study (MEC). The association between each known or suspected ovarian cancer risk factor (age, parity, oral contraceptive use, tubal ligation, body mass index (BMI), family history of ovarian and breast cancer, menopausal status, education, hysterectomy, aspirin use, talcum powder applied to genital areas, endometriosis, and age at menarche) was estimated using logistic regression with study site interactions to capture heterogeneity across studies. Using the Bruzzi method, population attributable risks (PAR) were calculated by race for each risk factor individually and collectively for all risk factors. Results. The comparison of 3,249 white ovarian cancer cases and 9,650 controls to 1,054 African-American cases and 2,410 controls revealed notable differences in the PAR of several risk factors by race. African-American women had a statistically significantly higher PAR for family history of breast cancer and BMI ≥30kg/m2compared to white women (10.0% vs. 2.5% and 8.9% vs. 0.4%, respectively). Although not statistically significant, white women had a higher PAR for oral contraceptive use (duration & lt;5 years) and not having had a tubal ligation than African-American women. When evaluating all risk factors collectively, the overall PAR was 63.9% for African-American women and 48.0% for white women. We also calculated overall PARs excluding WHI due to differences in the inclusion criteria for WHI compared to the other population-based studies in OCWAA: 65.7% for African-American women and 57.8% for white women. Conclusions. Our findings suggest that the known and suspected ovarian cancer risk factors investigated in this study may be partially responsible for differences in ovarian cancer incidence between white and African-American women. Although important across both racial groups, collectively, the factors studied accounted for slightly more of the ovarian cancer risk among African-American women than white women. Citation Format: Lauren C. Peres, Tareq F. Camacho, Elisa V. Bandera, Traci N. Bethea, Charlotte E. Joslin, Anna H. Wu, Alicia Beeghly-Fadiel, Emily K. Cloyd, Holly R. Harris, Patricia G. Moorman, Evan Myers, Heather M. Ochs-Balcom, Will L. Rosenow, Veronica W. Setiawan, Lynn Rosenberg, Joellen M. Schildkraut. Estimating the contribution of epidemiologic risk factors to racial differences in epithelial ovarian cancer incidence [abstract]. In: Proceedings of the Annual Meeting of the American Association for Cancer Research 2020; 2020 Apr 27-28 and Jun 22-24. Philadelphia (PA): AACR; Cancer Res 2020;80(16 Suppl):Abstract nr 1180.
    Type of Medium: Online Resource
    ISSN: 0008-5472 , 1538-7445
    RVK:
    RVK:
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 8
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 29, No. 6_Supplement_2 ( 2020-06-01), p. C070-C070
    Abstract: Objective: Obesity disproportionately affects African American (AA) women, and there is some suggestion that its association with ovarian cancer risk may be stronger among AA compared to white women, but no study to date has been adequately powered to compare risk between the two populations. The Ovarian Cancer in Women of African Ancestry (OCWAA) Consortium provided a unique opportunity to evaluate the association between body mass index (BMI) and invasive epithelial ovarian cancer (EOC) risk in AA and white women and to estimate the contribution of obesity to ovarian cancer risk in both racial groups. Methods: The OCWAA Consortium is a collaboration of six of the largest epidemiologic studies of ovarian cancer in the United States that include AA women: four case-control and two case-control studies nested within cohort studies. The six studies are the Chicago Case-Control Study, the North Carolina Ovarian Cancer Study, the Los Angeles Ovarian Cancer Case-Control Studies, the African American Cancer Epidemiology Study, the Black Women’s Health Study, and the Multiethnic Cohort. BMI before diagnosis was available in all the studies and data on BMI and relevant confounders were harmonized for analyses. There were 1,144 AA cases, 2,910 AA controls, 3,174 white cases, and 9,160 white controls included. Adjusted odds ratios (ORs) and 95% confidence intervals (CIs) were computed using random-effects multi-level logistic regression models separately by race and histotype with control for relevant covariates, which included study, age, education, parity, oral contraceptive use, age at menarche and family history of breast/ovarian cancer. Multinomial regression was used for histotype analyses. Population attributable risk (PAR) estimates were computed by race and histotype. Results: The prevalence of obesity (BMI≥30 kg/m2) was higher in AAs compared to white women for both cases (53.2% vs 21.4%) and controls (45.7% vs. 18.4%). For EOC, there was little evidence of an association with obesity for white women. For AAs, risk was elevated for BMI≥30 kg/m2 (ORBMI 30-34=1.37, 95% CI: 1.12, 1.69; ORBMI≥35 = 1.26, 95% CI: 0.74, 2.15) relative to BMI 18.5- & lt;25 kg/m2. There was an elevated risk for non-high-grade serous EOC for both AA and white women (for AA women, ORBMI 30-34=1.67, 95% CI: 1.14, 2.44 and ORBMI≥35 = 1.76; 95% CI: 0.84, 3.69; for white women, ORBMI ≥35 = 1.39; 95% CI: 1.06, 1.82), but not for high-grade serous EOC. The PAR for BMI≥30 was 7.1% (95% CI: 2.4, 15.6) for AAs and 2.6% (95% CI: -0.3, 5.4) for whites for all EOC. For non-high-grade serous EOC, the PAR was 16.5% (95% CI: 3.4, 28.2) for AAs and 6.4% (95% CI: 2.2, 10.3) for whites. Conclusions: Obesity was a contributor to overall EOC risk among AA women but not among white women. Obesity did not contribute to the risk of high-grade serous EOC for AAs or whites, but it was associated with non-high-grade serous cases among both AA and white women. The association with non-high-grade serous EOC was greater among AAs than whites. Citation Format: Elisa V Bandera, Fabian Camacho, Deanna Chyn, Emily K Cloyd, Traci N Bethea, Alicia Beeghly-Fadiel, Charlotte E Joslin, Evan Myers, Patricia G Moorman, Heather M Ochs-Balcom, Holly R Harris, Lauren C Peres, Veronica Wendy Setiawan, Anna H Wu, Lynn Rosenberg, Joellen M Schildkraut. Racial disparities in body mass index and ovarian cancer risk in the OCWAA Consortium [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr C070.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 9
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 29, No. 6_Supplement_2 ( 2020-06-01), p. C038-C038
    Abstract: Background: Family history of ovarian and breast cancers is a well-established risk factor for ovarian cancer and recent findings suggest that the risk of ovarian cancer may be higher for African American (AA) women compared to other racial/ethnic groups. Few studies have been able to examine this association in both AA and White participants taking into account histotype. Methods: The Ovarian Cancer in Women of African Ancestry Consortium harmonized data from four case-control studies and two case-control studies nested within cohort studies. Each study collected self-reported first-degree family history of ovarian and breast cancers; the four case-control studies also collected self-reported data on second-degree family history of ovarian and breast cancers. For cases, data on age at diagnosis, tumor grade, and tumor histology were abstracted from medical records and cancer registry reports. Race-specific odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multilevel logistic regression with control for covariates. Results: Our sample included 1,052 AA cases, 2,328 AA controls, 2,380 White cases, and 3,982 White controls. The prevalence of first-degree history of ovarian or breast cancer was higher among AA than White ovarian cancer cases (28% vs. 21%) and similar among AA and White controls (15% vs. 16%). The prevalence of second-degree family history of ovarian or breast cancer was similar among AA and White ovarian cancer cases (38% vs. 34%) and among AA and White controls (28% vs. 32%). First-degree family history of ovarian cancer was significantly associated with high-grade serous ovarian cancer in both AA (OR=2.33; 95% CI: 1.48, 3.69) and White participants (OR=2.86; 95% CI: 2.03, 4.02). In AA women, first-degree family history of breast cancer was associated with increased risk of high-grade serous ovarian cancer (OR=1.80; 95% CI: 1.38, 2.34) and all other histotypes combined (OR=1.62; 95% CI: 1.16, 2.25). In White women, first degree family history of breast cancer was associated with high-grade serous ovarian cancer only (OR=1.40; 95% CI: 1.16, 1.68). Second-degree family history of ovarian cancer was associated with high-grade serous ovarian cancer among White women (OR=1.95; 95% CI: 1.32, 2.90) and second-degree family history of breast cancer was associated with high-grade serous ovarian cancer in AA women (OR=1.48; 95% CI: 1.11, 1.98). Second-degree family history of ovarian or breast cancer was not associated with the other histotypes. Estimates across studies were compatible with overall estimates (pheterogeneity & gt;0.05). Conclusion: First-degree family history of ovarian cancer may be more strongly associated with high-grade serous ovarian cancer than other histotypes in AA and White women. Second-degree family history of cancer may differ by race in the associations with ovarian cancer, but potential underreporting of second-degree family history and inability to account for family size limit interpretation of these data. Citation Format: Traci N. Bethea, Heather M. Ochs-Balcom, Elisa V. Bandera, Alicia Beeghly-Fadiel, Fabian Camancho, Emily K. Cloyd, Holly R. Harris, Charlotte E. Joslin, Evan Myers, Patricia G. Moorman, Lauren C. Peres, Veronica W. Setiawan, Anna H. Wu, Lynn Rosenberg, Joellen M. Schildkraut. First- and second-degree family history of ovarian and breast cancers in relation to risk of invasive ovarian cancer in African American and White women [abstract]. In: Proceedings of the Twelfth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2019 Sep 20-23; San Francisco, CA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(6 Suppl_2):Abstract nr C038.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
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  • 10
    In: Cancer Epidemiology, Biomarkers & Prevention, American Association for Cancer Research (AACR), Vol. 29, No. 12_Supplement ( 2020-12-01), p. PO-180-PO-180
    Abstract: PURPOSE: To date, the epidemiology of epithelial ovarian cancer (EOC) among African-American women has been severely understudied. It remains unclear to what extent variation in the prevalence of EOC risk factors may explain incidence disparities between African-American and white women. Genital powder use is more common among African-American women; however, studies of genital power use and EOC risk have been conducted predominantly in white populations, and histotype specific analyses among African-American populations are limited. The objective of this study was to evaluate the association between genital powder use and EOC risk among African-American and white women, overall and by histotype. METHODS: We used data from four ovarian cancer case-control studies in the Ovarian Cancer in Women of African Ancestry (OCWAA) consortium: the African American Cancer Epidemiology Study, the Los Angeles County Ovarian Cancer Study, the Cook County Case-Control Study, and the North Carolina Ovarian Cancer Study. Participants included 601 African-American cases, 1,012 African-American controls, 2,225 white cases, and 3,086 white controls who answered questions on genital powder use prior to 2014. The association between genital powder use and EOC risk was estimated using logistic regression. Pooled histotype specific odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated using polytomous logistic regression. The population attributable risk (PAR) by race was calculated using the Bruzzi method. RESULTS: The prevalence of reporting ever genital powder use was 66% among African-American women and 44% among white women. African- American women who ever used genital powder were 29% more likely to develop EOC compared to African-American women who reported no use (OR=1.29, 95% CI=0.98-1.71). White women who ever used genital powder were 36% more likely to develop EOC compared to white women reporting no use (OR=1.36, 95% CI=1.12- 1.52). The associations were similar when examined by histotype. Among African- American women, the ORs were 1.29 (95% CI=0.94-1.76) for high grade serous (HGS) and 1.38 (95% CI=0.87-2.19) for non-HGS. For white women, the corresponding ORs were 1.27 (95% CI=1.06-1.52) and 1.21 (95% CI=0.96-1.56), respectively. The PAR for genital powder use was slightly higher, but not statistically significantly different, in African-American women (PAR=10.7, 95% CI=3.7-17.5) compared to white women (PAR=7.8, 95% CI=4.9-10.7). CONCLUSION: While the prevalence of ever genital body powder use was higher among African-American women, the associations between genital powder use and ovarian cancer risk were similar between African-American and white women, and did not materially vary by histotype. Further analyses incorporating additional OCWAA studies and using more refined exposure categories (e.g., frequency and duration of powder use, age at first application) are currently being conducted. Citation Format: Colette P. Davis, Elisa V. Bandera, Traci N. Bethea, Tareq F. Camacho, Charlotte E. Joslin, Anna H. Wu, Alicia Beeghly-Fadiel, Emily K. Cloyd, Patricia G. Moorman, Evan Myers, Heather M. Ochs-Balcom, Lauren C. Peres, Will L. Rosenow, Veronica W. Setiawan, Lynn Rosenberg, Joellen M Schildkraut, Holly R. Harris. Genital powder use and risk of epithelial ovarian cancer in the Ovarian Cancer in Women of African Ancestry Consortium [abstract]. In: Proceedings of the AACR Virtual Conference: Thirteenth AACR Conference on the Science of Cancer Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; 2020 Oct 2-4. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2020;29(12 Suppl):Abstract nr PO-180.
    Type of Medium: Online Resource
    ISSN: 1055-9965 , 1538-7755
    Language: English
    Publisher: American Association for Cancer Research (AACR)
    Publication Date: 2020
    detail.hit.zdb_id: 2036781-8
    detail.hit.zdb_id: 1153420-5
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