bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A77: Walking and vigorous exercise and risk of breast cancer in African American women
Authors: Gong zhihong , Hong Chi-Chen , Bandera Elisa , Adams-Campbell Lucile , Park Song-Yi , Zirpoli Gary , Olshan Andrew , Ambrosone Christine , Palmer Julie , Rosenberg Lynn 
Published: May 2016

Abstract
The relationship between physical activity and breast cancer risk has been extensively studied among women of European descent, with most studies reporting an inverse association. However, data on African American (AA) women and by tumor subtypes are sparse. Thus, we examined associations of vigorous exercise and walking for exercise and breast cancer risk overall and by estrogen receptor (ER) status in the African American Breast Cancer Epidemiology and Risk (AMBER) Consortium. We pooled data on AA women from four large studies, the Black Women's Health Study, Carolina Breast Cancer Study, Multiethnic Cohort Study and Women's Circle of Health Study, for 2,482 ER+ cases, 1,374 ER- cases and 16,959 controls. Multivariable logistic regression was used to compute odds ratios (OR) and 95% confidence intervals (CI) for the risk of overall breast cancer, and polytomous logistic regression was used to model the risk of ER+ and ER- cancer. Based on all four studies, for recent vigorous exercise (reported by 29% of controls), the OR was 0.88 (95% CI: 0.81-0.96) for breast cancer overall, 0.88 (95% CI: 0.80-0.98) for ER+ breast cancer and 0.93 (95% CI: 0.82-1.06) for ER- breast cancer. There was a statistically significant trend across hours per week of vigorous activity for breast cancer overall (p for trend=0.006) and for ER+ cancer (p for trend=0.02), but there was not a clear dose response relationship, with the strongest reduced risk in the 1-2 and 3-4 hours/week categories. Data on walking for exercise, as the most frequently reported activity among adults who meet guidelines for regular physical activity (53% in controls), was available from two studies. Any walking for exercise was associated with reduced risk of breast cancer overall (OR=0.88, 95% CI: 0.80-0.97) and ER+ cancer (OR=0.87, 95% CI: 0.77-0.98), but not ER- cancer (OR=0.95, 95 CI: 0.81-1.12). There was a significant trend across hours per week of walking for breast cancer overall (p for trend=0.008) and ER+ breast cancer (p for trend=0.02), with the strongest reduced risk in the 5+ hours/week category. Our results from this large pooling study of AA women provide evidence that vigorous exercise and walking for exercise are associated with reduced risk of breast cancer, specifically ER+ cancer.
Citation Format: zhihong Gong, Chi-Chen Hong, Elisa Bandera, Lucile Adams-Campbell, Song-Yi Park, Gary Zirpoli, Andrew Olshan, Christine Ambrosone, Julie Palmer, Lynn Rosenberg. Walking and vigorous exercise and risk of breast cancer in African American women. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr A77.
Abstract A81: Relationship between out-of-pocket cost and use of tyrosine kinase inhibitors for the treatment of chronic myeloid leukemia
Authors: McDougall Jean A. , Bennette Caroline S. , Ramsey Scott D. , Sullivan Sean D. 
Published: May 2016

Abstract
Targeting tyrosine kinase activity in cancer cells represents one of the greatest innovations in cancer treatment. Yet the high cost of tyrosine kinase inhibitors (TKIs) and the cumulative financial burden to patients associated with their use may lead to disparities in medication adherence. This study investigated the relationship between out-of-pocket cost and adherence to TKIs among a cohort of commercially insured chronic myeloid leukemia (CML) patients. The Truven Health Marketscan database was used to identify prevalent cases of CML with &gt;1 prescription claim for a guideline-recommended first-line TKI, imatinib, nilotinib, or dasatinib. Out-of-pocket cost was calculated longitudinally using any amount paid by the patient towards a deductible, copayment, and coinsurance. Adherence was assessed using the medication possession ratio (MPR), calculated between the first and last TKI claims occurring between 2011 and 2013, and conditional on continuous insurance plan enrolment. Nonadherence was classified as an MPR &lt;80%. In addition to out-of-pocket cost, insurance plan, region, and area-level socioeconomic variables were assessed as determinants of adherence using logistic regression modeling to calculate and odds ratio (OR) and 95% confidence interval (CI). A total of 5,669 CML patients were identified from the Marketscan database between 2011 and 2013. Over that time period out-of-pocket costs for a 30-day supply of TKIs ranged from $0 to $1800, with means of $60 for dasatinib, $65 for imatinib, and $72 for nilotinib. Patients with relatively higher out-of-pocket costs (highest 75th percentile) were 27% more likely (OR 1.27, 95% 1.22 – 1.32) to be nonadherent to TKI therapy than patients with lower out-of-pocket costs. With the possibility of a generic version of imatinib on the horizon, understanding the association between out-of-pocket costs and adherence may have important implications for reducing disparities in adherence to TKIs for the treatment of CML.
Citation Format: Jean A. McDougall, Caroline S. Bennette, Scott D. Ramsey, Sean D. Sullivan. Relationship between out-of-pocket cost and use of tyrosine kinase inhibitors for the treatment of chronic myeloid leukemia. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr A81.
Abstract A89: Estimating potential years of life lost and productivity lost due to avoidable premature colorectal cancer deaths in U.S. counties with lower educational attainment
Authors: Weir Hannah K. , Li Chunyu , Henley Jane , Joseph Djenaba 
Published: May 2016

Abstract
Background: Measures of socioeconomic status (SES) are inversely associated with colorectal cancer (CRC) mortality. This study aims to estimate potential years of life lost and productivity lost due to premature cancer deaths among United States residents of lower SES areas, as measured by percentage of high school graduates. Methods: 2008-2012 mortality and population data were used to estimate the number of expected CRC deaths between the ages of 50-74 years by applying the mortality rate from higher SES areas (≥85% high school graduation) to lower SES areas, by race/ethnicity, age, and gender. Excess deaths (observed minus expected deaths) were used to estimate the years of potential life lost (YPLL) and the human capital method was used to estimate productivity lost due to YPLL. Results: Risk of CRC deaths was inversely associated with SES among non-Hispanic whites, non-Hispanic blacks and Hispanics. Of the 85,484 CRC deaths during 2008-2012 in lower SES groups, 16.8% (n=14,398) were potentially preventable if the CRC mortality rates in all areas were the same as higher SES areas. Eliminating avoidable CRC deaths would result in $4.2 billion in productivity gains in men and $2.2 billion in women based on a 3% discount rate. Conclusion: A substantial number of CRC deaths are potentially preventable through routine colorectal screening. SES disparities represent a large number of these deaths and result in a large economic burden in lower SES areas. Eliminating educational disparities could help decrease CRC cancer deaths and associated productivity lost in the US. These estimates do not include the costs to diagnose, treat and care for CRC patients.
Citation Format: Hannah K. Weir, Chunyu Li, Jane Henley, Djenaba Joseph. Estimating potential years of life lost and productivity lost due to avoidable premature colorectal cancer deaths in U.S. counties with lower educational attainment. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr A89.
Abstract B51: An interferon λ 4 genotype is linked to a gene expression signature in prostate tumors of African American men
Authors: Jordan Symone , Tang Wei , Wallace Tiffany , Dorsey Tiffany , Yi Ming , Stephens Robert , Prokunina-Olsson Ludmila , Ambs Stefan 
Published: May 2016

Abstract
Not all segments of the U.S. population have equally benefited from the advances in our knowledge and treatment of cancer. As a result, African-American (AA) men still have the highest prostate cancer mortality among all U.S. racial and ethnic groups. In a recent study, we examined the tumor biology of prostate cancer comparing AA patients with European-American (EA) patients using large scale gene expression profiling and found significant differences in gene expression that are consistent with race/ethnic differences in the tumor microenvironment and immunobiology. Intriguingly, an interferon gene signature was detected in AA prostate that may relate to an unknown etiologic agent in disease pathology. This signature occurred commonly in AA men in two independent patient cohorts and may influence therapeutic outcome because it is analogous to a recently discovered interferon-related DNA damage resistance signature (termed IRDS), which predicts resistance to chemotherapy and radiation in breast cancer and perhaps other epithelial cancers. Here, we assessed whether the development of this signature could be functionally linked to a germline variant allele (rs368234815-ΔG) that is frequently found in subjects of African ancestry (~65% allele frequency) but is less common in subjects of European ancestry (~30% allele frequency). Carriers of ΔG can express a recently discovered interferon, termed interferon lambda 4 (IFNL4), while the rs368234815-TT allele eliminates expression. We genotyped DNA from tumors that have previously been characterized for presence of the interferon signature and found that the ability to generate IFNL4 (in carriers of the ΔG allele) was significantly associated with the presence of this signature (P &lt; 0.001, n = 44), indicating that IFNL4 expression may be involved. In summary, our study links a germline genetic variant in IFNL4 to the occurrence of a clinically relevant interferon signature in prostate tumors of African-American men. Future research will assess how this genetic variant may influence disease outcome.
Citation Format: Symone Jordan, Wei Tang, Tiffany Wallace, Tiffany Dorsey, Ming Yi, Robert Stephens, Ludmila Prokunina-Olsson, Stefan Ambs. An interferon λ 4 genotype is linked to a gene expression signature in prostate tumors of African American men. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr B51.
Abstract C51: Ethnic differences in the relationship between diabetes, early age adiposity, and mortality among breast cancer survivors: The Breast Cancer Health Disparities Study
Authors: Connor Avonne E. , Visvanathan Kala , Baumgartner Kathy B. , Baumgartner Richard N. , Boone Stephanie D. , Hines Lisa M. , Giuliano Anna R. , Wolff Roger K. , John Esther M. , Slattery Martha L. 
Published: May 2016

Abstract
Hispanic women have a high prevalence of type 2 diabetes and obesity. Breast cancer (BC) has become the leading cause of death among Hispanic women. Limited information exists on the relationship between diabetes, obesity, and mortality in Hispanic women diagnosed with BC. In a multicenter study we examined the associations between diabetes, obesity measures and survival outcomes. The study included 1,180 Hispanic and 1,298 non-Hispanic white (NHW) women who were diagnosed with incident invasive BC from the San Francisco Bay Area, New Mexico, Utah, Colorado and Arizona. Adjusted hazard ratios (HR) and 95% confidence intervals (CI) were calculated by Cox proportional hazards regression models. The median follow-up time from BC diagnosis to death was 10.8 years and 267 of 466 deaths that occurred were from BC. Diabetes was significantly associated with BC-specific mortality (HR, 1.63 95% CI 1.08-2.47), with a stronger association among Hispanics (HR, 1.85 95% CI 1.11-3.09) compared to NHWs (HR, 1.33 95% CI 0.67-2.62). Among diabetic Hispanic women with estrogen receptor negative tumors, BC-specific mortality was increased three-fold (HR, 2.93 95% CI 1.09-7.88). In contrast, obesity at age 30 years was positively associated with BC-specific mortality in NHW women after adjusting for diabetes and known prognostic factors (HR, 2.33 95% CI 1.36-3.97, p interaction&lt; 0.05), but not in Hispanics. In conclusion, we observed differences in the prognostic significance of diabetes and obesity by ethnicity among women with BC. Larger prospective studies are needed to evaluate ethnic differences in associations between diabetes and mortality for less common BC subtypes.
Citation Format: Avonne E. Connor, Kala Visvanathan, Kathy B. Baumgartner, Richard N. Baumgartner, Stephanie D. Boone, Lisa M. Hines, Anna R, Giuliano, Roger K. Wolff, Esther M. John, Martha L. Slattery. Ethnic differences in the relationship between diabetes, early age adiposity, and mortality among breast cancer survivors: The Breast Cancer Health Disparities Study. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C51.
Abstract C63: Elucidating the role of AIB1 in triple-negative breast cancer cell lines
Authors: Saenz Francisco R. , Riegel Anna T. 
Published: May 2016

Abstract
Triple negative breast cancer (TNBC) patients do not benefit from directed therapy because these tumors do not express targetable molecules; such as, hormone or growth factor receptors (ER, PR and HER2). This subtype represents 15-20% of all breast cancer cases diagnosed in women in the United States. Higher incidence of TNBC affects, particularly, young African American women compared with other women. Clinically, TNBC patients often present an advanced stage disease. These tumors exhibit an increased inflammatory signal and an aggressive phenotype that leads to an increased frequency of metastasis. These patients have a poor survival outcome. Coincidentally, expression of the amplified in breast cancer 1 (AIB1) oncogene has also been reported in higher grade, inflammatory and invasive breast cancer. AIB1 is a nuclear coactivator that regulates transcription of several genes through hormone and/or growth factor signaling. Here we demonstrate that cell lines derived from tumors in African American women representing different TNBC subtypes have varying degree of sensitive to AIB1 shRNA by lentiviral infection. AIB1 knockdown has a considerable effect on viability of all the TNBC subtypes; however, we observed the presence of a small fraction of cells that proliferate independent of AIB1. Interestingly, these cells that retain the AIB1 knockdown following sub-culture for 3-4 passages are comparable to the initial TNBC cells as regards to cell cycle and apoptosis. Intriguingly, these TNBC cells that proliferate independent of AIB1 show increase in the percentage of cells expressing CD44+/CD24- cell surface markers indicating a selection of tumor initiating cells. Concomitantly, there is a decrease in the percentage of CD44-/CD24- cells suggesting that AIB1 may regulate tumor initiating cell differentiation upon external stresses such as those caused by chemotherapeutic agents during treatment. We will further study the chemo sensitivity of TNBC cells resistant to AIB1 loss and assess whether these cells represent a model of cancer cell dormancy associated to recurrence in TNBC patients.
Citation Format: Francisco R. Saenz, Anna T. Riegel. Elucidating the role of AIB1 in triple-negative breast cancer cell lines. [abstract]. In: Proceedings of the Eighth AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 13-16, 2015; Atlanta, GA. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2016;25(3 Suppl):Abstract nr C63.
Abstract A05: BRCA1 promoter hypermethylation loss in recurrent high-grade serous carcinoma.
Authors: Bisogna Maria , Dao Fanny , Olvera Narciso , Bacares Ruben , Zhang Liying , Levine Douglas A. 
Published: May 2016

Abstract
Objective: BRCA1 germline mutations are associated with improved ovarian cancer survival, yet secondary revertant mutations that impair chemo-sensitivity can develop after platinum-based therapy. BRCA1 promoter hypermethylation, present in ~10% of all high-grade serous carcinomas (HGSCs), is associated with reduced gene and protein expression. We hypothesize that BRCA1 promoter hypermethylation decreases in recurrent HGSCs compared with matched primary samples.
Methods: Primary, untreated HGSCs with known BRCA1 promoter methylation status and matched recurrent samples were macrodissected from archival slides. After DNA was extracted and bisulfite treated, pyrosequencing was performed across 11 CpG sites within the BRCA1 promoter to quantify methylation using a CLIA-approved assay. The methylation percentage was calculated from allele frequencies and 10% or greater is considered hypermethylated. Validation data were obtained from The Cancer Genome Atlas (TCGA) substudy of paired primary and recurrent HGSCs.
Results: Eleven patients with matched primary and recurrent tumors were evaluated. Six patients had hypermethylated primary tumors, with methylation percentages ranging from 35-69%. We found that BRCA1 promoter methylation decreased 16-95% in five recurrent samples compared to their primary tumors. One patient with a demethylated recurrent tumor had platinum refractory disease clinically and died 12 months after diagnosis. In contrast, the only patient with an increase (74%) in promoter methylation between primary and recurrent specimens is a long-term survivor alive with disease 14 years after diagnosis. There was negligible change in promoter methylation between primary and recurrent cases for the five unmethylated samples. Three of 17 paired samples from the ovarian TCGA substudy had BRCA1 promoter hypermethylation and showed a 20-50% decrease between primary and recurrent samples with a corresponding increase in BRCA1 gene expression.
Conclusion: BRCA1 promoter hypermethylation generally decreases between primary and recurrent HGSCs and can be associated with remarkable clinical outcomes. BRCA1 promoter methylation may be a marker of platinum response in the recurrent disease setting and can be assessed in prospective clinical trials. In addition to BRCA1 somatic revertant mutations, loss of BRCA1 promoter methylation may be another mechanism to restore BRCA1 function in recurrent disease.
Citation Format: Maria Bisogna, Fanny Dao, Narciso Olvera, Ruben Bacares, Liying Zhang, Douglas A. Levine. BRCA1 promoter hypermethylation loss in recurrent high-grade serous carcinoma. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr A05.
Abstract A39: FOXO1 is a key determinant of progesterone receptor isoform-specific senescence programming in ovarian cancer cells.
Authors: Diep Caroline H. , Knutson Todd P. , Mauro Laura J. , Lange Carol A. 
Published: May 2016

Abstract
Progesterone promotes proliferation and pro-survival in the breast, but inhibits growth in the reproductive tract and ovaries. Herein, using progesterone receptor (PR) isoform-specific ovarian cancer models, we show that PR-A and PR-B promote expression of distinct gene sets that differ from PR-driven genes in breast cancer cells. In ovarian cancer models, PR-A primarily regulates genes independently of progestin, while PR-B is the dominant ligand-dependent isoform. Notably, FOXO1 and the PR/FOXO1 target-gene p21 are repressed by PR-A, but induced by PR-B. In the presence of progestin, PR-B, but not PR-A, robustly induced cellular senescence via FOXO1-dependent induction of p21 and p15. ChIP assays performed on PR-isoform specific cells demonstrated that while each isoform is recruited to the same PRE-containing region of the p21 promoter in response to progestin, only PR-B elicits active chromatin. Overexpression of constitutively active FOXO1 (FOXO1-AAA) in PR-A-only expressing cells conferred robust ligand-dependent upregulation of the PR-B-target genes GZMA, IGFBP1, and p21, and induced cellular senescence. Similar results were observed when PR-A was titrated into PR-B-containing cells. PR isoform-specific regulation of the FOXO1/p21 axis recapitulated in human primary ovarian tumor explants treated with progestin. Our data indicate a key requirement for FOXO1 (a PR-B-induced, but PR-A-repressed gene) in progesterone signaling to cellular senescence in ovarian cancer cells and reveal a novel mechanism for PR-target gene (FOXO1) control of hormone sensitivity. Ultimately, harnessing PR isoform-specific gene regulation in hormone-driven cancers may provide a means to therapeutically induce the protective actions of progesterone while blocking unwanted proliferative and pro-survival effects.
Citation Format: Caroline H. Diep, Todd P. Knutson, Laura J. Mauro, Carol A. Lange. FOXO1 is a key determinant of progesterone receptor isoform-specific senescence programming in ovarian cancer cells. [abstract]. In: Proceedings of the AACR Special Conference on Advances in Ovarian Cancer Research: Exploiting Vulnerabilities; Oct 17-20, 2015; Orlando, FL. Philadelphia (PA): AACR; Clin Cancer Res 2016;22(2 Suppl):Abstract nr A39.