bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract A76: MicroRNA mediated negative regulation of caveolin 1 as a biological mechanism driving breast cancer disparities
Authors: Guo Qi Jin , King Brooke , Blake Bobbie , LaRue Amanda C. , Salley Judith D. , Ford Marvella E. , Evans-Knowell Ashley , Findlay Victoria J. 
Published: October 2015

Abstract
Although rates of breast cancer incidence are lower in African American (AA) women, the mortality rates are significantly higher compared to non-Hispanic white (WNH) women. This shocking statistic illustrates the racial disparities in breast cancer, as AA women have a poorer prognosis compared to WNH women. While this may be due in part to socioeconomic and standard of care issues, increasing evidence suggests that the racial disparity exists independent of these issues and could also be attributed to poorly understood inherent genetic and molecular characteristics within racial specific tumors. Caveolin-1 (Cav1) is a scaffolding protein with a tumor suppressor role. Loss of Cav1 in the tumor stromal compartment has emerged as a novel biomarker for predicting poor clinical outcome in all of the most common subtypes of human breast cancer, including the more lethal triple negative subtype which is significantly more common in AA women. While the loss of stromal Cav1 is becoming well established as a marker of poor outcome in breast cancer, the mechanism of this loss is still unknown. We propose that differences in microRNA mediated stromal Cav1 loss between AA and WNH women is driving the racial disparity in breast cancer. MicroRNAs (miRNAs) are short, endogenous, non-coding RNA that function as negative regulators of gene expression. miR-510 is an oncogenic miRNA that has been shown to be elevated in breast tumors. Cav1 is a predicted target of miR-510 and therefore miR-510 mediated negative regulation may be a novel mechanism of Cav1 loss in the tumor stroma. Our research shows that Cav1 is directly targeted by miR-510 by luciferase reporter assay and that overexpression of miR-510 leads to downregulation of Cav1 protein expression, specifically in the stromal compartment. Tumor epithelium and stroma co-culture assays demonstrate that epithelial derived miR-510 may be transferred to neighboring stromal cells and negatively regulate Cav1 expression in the stromal compartment. This may be racially significant as our supporting studies also show that miR-510 levels are elevated and Cav1 levels are reduced in AA breast cancer patients compared to their white counterparts. Our results suggest that the difference in miR-510 mediated regulation of stromal Cav1 is driving racial disparity in breast cancer.
Citation Format: Qi Jin Guo, Brooke King, Bobbie Blake, Amanda C. LaRue, Judith D. Salley, Marvella E. Ford, Ashley Evans-Knowell, Victoria J. Findlay. MicroRNA mediated negative regulation of caveolin 1 as a biological mechanism driving breast cancer disparities. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr A76.
Abstract A80: p53 protects against MG132-induced apoptosis in a cell state-dependent manner
Authors: Legesse-Miller Aster , Cheng Jacky Ho Wa 
Published: October 2015

Abstract
Since the approval of proteasome inhibitor, Bortezomib, for use in multiple myeloma in 2003, pharmacological proteasome inhibitors has been shown to be an important strategy for treating many types of cancer. While proteasome inhibitors induce apoptosis in certain rapidly proliferating cancer cells, some cells enters quiescence and survives. The mechanism by which quiescent cells become resistant to proteasome inhibitors is largely unknown. The tumor suppressor protein p53 plays an essential role in establishing and maintain quiescence in human cells. It also regulates several cell survival mechanisms, including cell cycle arrest, autophagy, and activation of reactive oxygen detoxifying enzymes. Here, we investigated the role of p53 in establishing resistance against proteasome inhibitors in quiescent cells. We found that MG132 (a know proteasome inhibitor) treatment induces the accumulation of p53 and its downstream target p21 more in quiescent cells than in proliferating primary human fibroblasts. shRNA mediated down-regulation of p53 sensitizes both proliferating and quiescent fibroblasts to MG132-mediated apoptosis and cell death, suggesting that p53 plays a protective role in all cell states. Additional experiments demonstrated that proliferating fibroblasts are susceptible to inhibition of cytoplasmic p53 activity, whereas quiescent fibroblasts are sensitive to inhibition of nuclear p53 activity. These findings suggest that p53 induces different protective mechanisms against MG132-mediated cell death, depending of the proliferative state of the cells. Autophagy, an alternative degradation pathway regulated by p53, is also induced in both cell states upon MG132 treatment. Identification of p53-mediated regulatory mechanisms that are activated in quiescent cells in response to proteasome inhibition may help to suggest strategies for improving the effectiveness of proteasome inhibitors in treating cancer.
Citation Format: Aster Legesse-Miller, Jacky Ho Wa Cheng. p53 protects against MG132-induced apoptosis in a cell state-dependent manner. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr A80.
Abstract A87: Cardiovascular disease (CVD) and hospitalization costs among lung cancer patients: Examining the effect of race and gender
Authors: Husaini Baqar , Selove Rebecca , Williams Elizabeth , Novotny Meggan , Emerson Janice , Cain Van , Whalen Margaret , Levine Robert 
Published: October 2015

Abstract
Objective: Delineate race and gender variations in cardiovascular disease associated with lung cancer and hospitalization cost of Tennessee lung cancer patients in 2008.
Methods: We examined Tennessee Hospital Discharge Database for2008 for patients (aged 20+) discharged with a primary diagnosis of lung cancer (LC). The LC patient sample (n= 6665) included black males (BM; n=494), white males (WM; n=3286), black females (BF; n=387); and white females (WF; n=2498). For each patient, we extracted data on cardiovascular risk factors and hospitalization costs for the entire year of 2008. Age-adjusted hospitalization rate for lung cancer (LC) per 100K 2000 US population for white and black as well as male & female groups were developed per CDC methodology. To delineate CVD risk factors, multivariate logistic models were used for each group separately to determine CVD risk factors of LC.
Results: Our analyses revealed four major trends: (i) Age-adjusted LC rates were higher for blacks and males compared to white and females; (ii) LC patients had an average of 3 co-morbid conditions which varied from 3 conditions among WM, to 2.86 among BF, 2.75 among BM, and 2.70 among WF; (iii) Regression analyses revealed COPD predicted LC for all four groups. In addition, BM had cardiac arrhythmia and high cholesterol, The same factors were associated with LC among both WM and WF. Among BF, hypertension and COPD predicted higher rates of LC; and (iv) hospitalization cost for the year was highest among BF ($97,085) and lowest among WF ($66,758). Among males, the cost was higher among BM compared to WM ($91,384 vs. 71,716, p&lt;.001). Hospitalization costs were higher among blacks compared to whites ($94,235 vs. 69,237, p&lt;.001), in part, due to longer hospitalization compared to whites.
Conclusion: Lung cancer rates and hospitalization costs are higher for blacks. While males have higher LC rate compared to females, the hospitalization costs are similar among them. COPD, cardiac arrhythmia, and high cholesterol are CVD factors that are associated with lung cancer and need to be aggressive managed through intensive population-based education programs in the minority populations.
Citation Format: Baqar Husaini, Rebecca Selove, Elizabeth Williams, Meggan Novotny, Janice Emerson, Van Cain, Margaret Whalen, Robert Levine. Cardiovascular disease (CVD) and hospitalization costs among lung cancer patients: Examining the effect of race and gender. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr A87.
Abstract B02: DNA promoter methylation of HIST1H2BB as a potential early detection biomarker to reduce ovarian cancer disparities in the United States
Authors: Valle Blanca L. , Kuhn Elisabetta , Sidransky David , Guerrero-Preston Rafael 
Published: October 2015

Abstract
Background: Ovarian cancer disproportionately affects African American women in the United States (US) at all stages of the disease, from presentation through treatment, and ultimately leads to increased mortality and decreased survival, compared to non-Hispanic White women. Till recently, epithelial ovarian cancers were thought to arise from the ovarian surface epithelial cells. However, recent studies suggest that the majority of high-grade serous carcinomas (HGSCs) arise from lesions in the fallopian tubes. DNA promoter hypermethylation of certain genes is often an early event in tumorigenesis, and it can be detected in blood and other bodily fluids, making it a feasible biomarker strategy for early detection of tumors.
Purpose of study: Therefore, we sought to determine the methylation profile of HGSCs as compared to fallopian tube epithelium. Using the Infinium HumanMethylation 450 Array, that permits to quantitatively assess over 450,000 methylation sites, within and outside of CpG islands and more than 20,000 genes per sample, at single-nucleotide resolution, we have obtained the genome-wide methylation profile of HGSC and fallopian tubal epithelium. We conducted a pilot study by comparing the global methylation status in 12 HGSC tissue samples to 15 fallopian tube epithelium samples. In addition, we compared the methylation profile among long-term survivors (more than 5 years) and short-term survivors (2-3 years) of HGSCs.
Results: Our results identified the HIST1H2BB promoter as the most differentially methylated region when comparing HGSC with normal fallopian tube samples. Furthermore, we also found that HIST1H2BB is differentially methylated in HGSC patients with long-term survival when compared to patients with short-term survival.
Conclusions: Taken together, these results support the potential use of HIST1H2BB promoter methylation as a diagnostic and prognostic biomarker for ovarian cancer. Our findings could lead to the development of a biomarker for the diagnosis and/or prognosis of ovarian cancer. An early detection biomarker for ovarian cancer could contribute to the reduction and eventual elimination of ovarian cancer health disparities in the US.
Citation Format: Blanca L. Valle, Elisabetta Kuhn, David Sidransky, Rafael Guerrero-Preston. DNA promoter methylation of HIST1H2BB as a potential early detection biomarker to reduce ovarian cancer disparities in the United States. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr B02.
Abstract B08: Correlations between weight gain and physical health among African American breast cancer survivors
Authors: Smith Selina A. , Claridy Mechelle D. , Whitehead Mary S. , Sheats Joyce Q. , Baban Bakak , Yoo Wonsuk , Gonzalez-Perez Ruben R. , Alema-Mensah Ernest 
Published: October 2015

Abstract
Purpose: Weight gain after diagnosis is common among women with breast cancer and may affect physical functioning and recurrence; yet few studies have addressed this problem among African American breast cancer survivors. The purpose of our study was to examine associations between weight gain and physical functioning in a population with disparities in overweight/obesity, health-related quality of life (HR-QoL) and breast cancer recurrence.
Procedures: We examined the effects of weight gain in a cohort of 220 African-American women diagnosed with breast cancer. Participants completed a 45-minute assessment tool recording weight and breast cancer history, physical health and general well being. Factorial analysis of variance (ANOVA) was used to assess the association between weight gain (pounds) and HR-QoL. We also determined the moderating effects of demographic variables on post-breast cancer diagnosis weight gain.
Results: More than half of the study sample (n=113) gained 10 pounds or more after breast cancer diagnosis. Predictors for weight gain included: 1) breast cancer recurrence-78% (p=0.0067); 2) annual income- from $25,000 to $49,999 55% (p=0.0167); 3) some college education-51% (0.0205), and 4) unmarried 46% (p=0.0007). Participants reporting poorer overall quality of life (p=0.0109), poorer physical health quality of life (p=0.0002), and poorer physical functioning (p=0.0263) were more likely to report weight gain after breast cancer diagnosis than those who reported a better quality of life.
Conclusions: These results highlight the importance of weight control for African American women after breast cancer diagnosis.
Citation Format: Selina A. Smith, Mechelle D. Claridy, Mary S. Whitehead, Joyce Q. Sheats, Bakak Baban, Wonsuk Yoo, Ruben R. Gonzalez-Perez, Ernest Alema-Mensah. Correlations between weight gain and physical health among African American breast cancer survivors. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr B08.
Abstract B15: Motivation for cancer control changes among African Americans
Authors: Jefferson Melanie S. , Briggs Vanessa , Delmoor Ernestine , Rice LaShanta , Johnson Jerry , Hughes-Halbert Chanita 
Published: October 2015

Abstract
Background: Healthy dietary behaviors are critical strategies for cancer control. Despite this, many African Americans do not meet the recommended guidelines for fruit and vegetable intake. To develop effective cancer control interventions for African Americans, it is first necessary to understand within group variation in motivations for making dietary behavior changes and identify socioeconomic, social, and clinical factors that have significant independent associations with these motivations.
Objectives: To characterize motivations for making dietary changes among African Americans and to identify socioeconomic, social, and clinical factors having significant independent associations with these intrinsic and extrinsic motivations among African American adults (n=530).
Results: The mean (SD) level for intrinsic motivation was 26.5 (3.5) whereas the mean (SD) level for extrinsic motivation was 16.1 (4.8). Increasing age (Beta=0.03, p=0.03) and membership in at least one community organization (Beta=1.20, p=0.0003) had significant independent associations in the regression model for intrinsic motivation (n=479, F=5.97, p=0.0001). Lower incomes (Beta=-1.10, p=0.02) and age (Beta=0.06, p=0.006) had significant independent associations with extrinsic motivation. None of the clinical factors were associated significantly with intrinsic and extrinsic motivation.
Conclusions: African Americans may be motivated to make dietary changes for cancer control because of intrinsic motivations. Different variables had significant independent associations with intrinsic and extrinsic motivations to make dietary changes among African Americans. It may be important to use alternative strategies to enhance these motivations as part of cancer control interventions that are developed for these individuals.
Citation Format: Melanie S. Jefferson, Vanessa Briggs, Ernestine Delmoor, LaShanta Rice, Jerry Johnson, Chanita Hughes-Halbert. Motivation for cancer control changes among African Americans. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr B15.
Abstract B28: Racial/ethnic differences in the association of obesity with hepatocellular carcinoma risk
Authors: Setiawan Veronica Wendy , Lipworth Loren , Wilkens Lynne R. , Marchand Loic Le , Blot William J. , Henderson Brian E. 
Published: October 2015

Abstract
The increasing trend of obesity is suggested to have contributed to the increasing hepatocellular carcinoma (HCC) incidence rates in the United States. However, no studies have examined whether the association between obesity and HCC differs across racial/ethnic groups. We examined body mass index (BMI) in relation to HCC risk in two large prospective cohort studies: the Multiethnic Cohort (MEC) and the Southern Community Cohort Study (SCCS). Between the two cohorts, a total of 637 incident HCC cases (86 Whites, 165 Blacks, 36 Native Hawaiians, 177 Japanese Americans, and 173 Latinos) were identified. BMI and other known HCC risk factor information were assessed from the baseline questionnaire (MEC: 1993-1996; SCCS: 2002-2009). The association between BMI and HCC incidence was examined using a nested case-control approach with four matched controls per case (MEC: 536 cases/2,131 controls; SCCS: 101 cases/404 controls). Conditional logistic regression, accounting for the matching factors was used to calculate multivariable odds ratios (ORs) and 95% confidence intervals (CI) for incident HCC in relation to BMI (&lt;25, 25-&lt;30, and 30 kg/m2, or per 5 kg/m2) in each racial/ethnic group. Additional covariates such as smoking status, diabetes, and alcohol intake were included in the models. Increasing BMI was associated with an elevated HCC risk in Japanese Americans (OR per 5 kg/m2 increase in BMI=1.69; 95% CI: 1.31, 2.16), Whites (OR=1.34; 95% CI: 0.98, 1.82), Native Hawaiians, (OR=1.23; 95% CI: 0.80, 1.89), and Latinos (OR=1.15; 95% CI: 0.95, 1.40), but not in Blacks in the MEC (OR=0.92; 95% CI: 0.70, 1.22) or in the SCCS (OR =0.93; 95% CI: 0.75, 1.15). The combined OR for Blacks across the two cohorts was 0.93 (95% CI: 0.78, 1.10; P heterogeneity=0.95). The association of BMI with HCC differed significantly across racial/ethnic groups (P heterogeneity=0.003). Our results suggest that the association of obesity, as measured by BMI, with HCC incidence varies across racial/ethnic groups. The null association in Blacks is particularly interesting and warrants further investigation.
Citation Format: Veronica Wendy Setiawan, Loren Lipworth, Lynne R. Wilkens, Loic Le Marchand, William J. Blot, Brian E. Henderson. Racial/ethnic differences in the association of obesity with hepatocellular carcinoma risk. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr B28.
Abstract B36: Helicobacter pylori exposure among Hispanic and non-Hispanic white men in San Antonio, Texas: Implications for gastric cancer risk disparities
Authors: Parma Dorothy Long , Munoz Edgar , Ogden Susan M. , Leach Robin J. , Thompson Ian M. , Ramirez Amelie G. 
Published: October 2015

Abstract
Background: Chronic Helicobacter pylori (H. pylori) infection is the most common gastric adenocarcinoma (GCA) risk factor. GCA more commonly affects U.S. Hispanics compared to non-Hispanic whites (NHWs). No study has examined this infection in South Texas Hispanics, a population facing multiple health disparities. This pilot project aimed to determine H. pylori exposure rates in Hispanic and NHW men residing in Bexar County, and examine relationships with ethnicity, residence, socioeconomic status, smoking history and cancer family history.
Methods: Age- and zip-code-matched subjects from a large community-dwelling cohort were randomly selected. Sera from 286 (143 Hispanic, 143 NHW) men were analyzed by enzyme immunoassay for H. pylori antibodies.
Results: Almost 20% of samples were H. pylori-positive; exposure was significantly higher among Hispanics (30.1%) compared to NHWs (9.1%). Unconditional logistic regression analyses of the seropositive-matched subsample showed strong associations between H. pylori seropositivity and Hispanic ethnicity (odds ratio [O.R.]=17.5; p&lt;0.001) and BMI category (O.R.=6.5; p=0.01 overweight and 4.0; p=0.02 obese). Ethnicity remained the strongest predictor of seropositivity after adjusting for all other factors (adjusted O.R.=16.9; p&lt;0.001). Adjusted O.R.s for overweight/obesity were high but non-significant.
Conclusions: H. pylori exposure rates are higher in South Texas Hispanic men and parallel the disproportionately-higher rates of GCA. Obesity is a contributing factor. This is the first study to explore the relationship between H. pylori exposure and Hispanic ethnicity and other GCA risk factors in South Texas. Results have implications for future studies on preventive measures targeted at reducing infectious burden and GCA risk in this vulnerable population.
Citation Format: Dorothy Long Parma, Edgar Munoz, Susan M. Ogden, Robin J. Leach, Ian M. Thompson, Jr., Amelie G. Ramirez. Helicobacter pylori exposure among Hispanic and non-Hispanic white men in San Antonio, Texas: Implications for gastric cancer risk disparities. [abstract]. In: Proceedings of the Seventh AACR Conference on The Science of Health Disparities in Racial/Ethnic Minorities and the Medically Underserved; Nov 9-12, 2014; San Antonio, TX. Philadelphia (PA): AACR; Cancer Epidemiol Biomarkers Prev 2015;24(10 Suppl):Abstract nr B36.