bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract 1767: Racial/ethnic disparities of obesity in a breast clinic population: Consideration for weight loss program in improving clinical outcomes
Authors: Puyana Barcha Carolina , Lee Eunkyung , Takita Cristiane , Wright Jean L. , Zhao Wei , Reis Isildinha M. , Hu Jennifer J. 
Published: July 2016

Abstract
Introduction: Accumulating evidence suggest that obesity is associated with breast cancer diagnosis, recurrence, and mortality. Obese subjects with genetic predisposition may need more aggressive weight loss management, such as bariatric surgery. Therefore, the primary aim of this study was to assess the racial/ethnic disparities in obesity and the prevalence of breast cancer study participants who may be eligible for bariatric surgery.
Methods: In three clinic-based studies conducted at University of Miami during 2008 to 2015, we evaluated 462 healthy controls and 975 breast cancer patients. Genotyping data of two obesity-related genes (FTO and MC4R) were also evaluated. Race/ethnicity and obesity-related comorbidities were self- reported. Body Mass Index (BMI) was calculated as kg/m2. The classification of BMI was: (1) &lt; 18.5, underweight; (2) 18.5-24.9, normal weight; (3) 25.0-29.9, overweight; (4) 30.0-34.9, class I obesity; (5) 35.0-39.9, class II obesity; and (6) ≥ 40.0, class III obesity. The NIH eligibility for bariatric surgery was for class II obese subjects with obesity-related comorbidities and class III obese subjects.
Results: The study consists of 70.0% Hispanic whites (HW), 21.7% black or African American (AA), and 6.4% non-Hispanic whites (NHW). Mean and SD of age was 54.1± 9.9 years and mean BMI was 29.0±6.1 kg/m2. Overall, about 11.1% of study participants met criteria for bariatric surgery and there were significant racial/ethnic disparities (19.7% AA, 8.5% HW, 8.8% NHW, and 17.2% others; p&lt;0.0001). Subgroup analysis observed increased BMI at follow up (29.60 vs. 29.16 kg/m2, p = 0.00229). Women with the AA risk genotype of rs1121980 (FTO gene) had 3.6-fold higher risk of obesity class II or III compared to those with the GG genotype (p = 0.00393).
Conclusion: In addition to cancer risk, obesity is a major risk factor for cancer treatment-related side effects and worse survival. Our results suggest that at least 11% of breast cancer patients may be eligible for bariatric surgery. Considering some other beneficial effects of bariatric surgery on physical quality of life, metabolic syndrome, diabetes, and microbiome, future studies will consider weight loss and bariatric surgery programs in breast cancer patients, particularly in underserved minorities with higher obesity rate and worse survival.
Citation Format: Carolina Puyana Barcha, Eunkyung Lee, Cristiane Takita, Jean L. Wright, Wei Zhao, Isildinha M. Reis, Jennifer J. Hu. Racial/ethnic disparities of obesity in a breast clinic population: Consideration for weight loss program in improving clinical outcomes. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1767.
Abstract 1768: Racial/ethnic differences in endometrioid endometrial cancer survival among cases identified through the National Cancer Database
Authors: Beckmeyer-Borowko Anna B. , Peterson Caryn E. , Brewer Katherine C. , Otoo Mary O. , Davis Faith G. , Hoskins Kent F. , Joslin Charlotte E. 
Published: July 2016

Abstract
OBJECTIVES: Past research suggests that at the local level, Non-Hispanic whites (NHW) have better survival when diagnosed with endometrioid endometrial cancer (EEC) than non-Hispanic blacks (NHB), Hispanics, and American Indians; however, little is known about survival differences at a national level and among other minorities. This study examined whether racial and ethnic differences in 5-year survival are present in U.S. women (NHW, NHB, Hispanics, non-Hispanic Asians (NHA), non-Hispanic Pacific Islanders/Hawaiians (NHPI), non-Hispanic American Indians/Aleutians or Eskimos (NHAI/AN) and non-Hispanics Others (NHO).
METHODS: EEC cases from the National Cancer Database were analyzed to evaluate racial/ethnic differences in 5-year survival among women diagnosed with EEC between 1998 and 2007. Chi-Square test was used to examine whether differences in demographic, clinical, institutional, and treatment variables varied by race/ethnicity. Multivariable Cox proportional hazard regression models were fit to estimate the adjusted hazard ratio (HR) and 95% confidence interval (95% CI) between race/ethnicity and survival.
RESULTS: A total of 178,310 women were diagnosed with EEC between 1998 and 2007. Of these; 74.8% were NHW, 8.3% were NHB, 13.9% were Hispanic, 1.8% were NHA, 0.2% were NHPI, 0.2% were NHAI/AN and 0.8% were NHO. Adjusting for covariates, NHB (HR = 1.29; 95%CI 1.24-1.34) and NHPI (HR = 1.59; 95%CI 1.50-1.67) had poorer survival than NHW. Yet results show that NHA (HR = 0.83; 95%CI 0.74-0.92) and NHO (HR = 0.81; 95%CI 0.69-0.94) had a better survival when compared to NHW. No survival differences were detected between Hispanics, NHAI/AN and NHW.
CONCLUSIONS: Results identify racial/ethnic differences in 5-year survival among women diagnosed with EEC cancer in the U.S. between 1998 and 2007. NHA and NHO had a better and NHB and NHPI had a poorer survival when compared to NHW.
Citation Format: Anna B. Beckmeyer-Borowko, Caryn E. Peterson, Katherine C. Brewer, Mary O. Otoo, Faith G. Davis, Kent F. Hoskins, Charlotte E. Joslin. Racial/ethnic differences in endometrioid endometrial cancer survival among cases identified through the National Cancer Database. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1768.
Abstract 177: Src family kinase Fyn promotes the neuroendocrine phenotype and visceral metastasis in advanced prostate cancer
Authors: Cavassani Karen , Gururajan Murali , Sievert Margarit , Duan Peng , Freeman Michael , Chu Gina Chia-Yi , Bhowmick Neil , Chung Leland , Posadas Edward 
Published: July 2016

Abstract
FYN is a SRC family kinase (SFK) that has been shown to be up-regulated in human prostate cancer (PCa) tissues and cell lines. In this study, we observed that FYN is strongly up-regulated in human neuroendocrine PCa (NEPC) tissues and xenografts, as well as cells derived from a NEPC transgenic mouse model. In silico analysis of FYN expression in prostate cancer cell line databases revealed an association with the expression of neuroendocrine (NE) markers such as CHGA, CD44, CD56, and SYP. The loss of FYN abrogated the invasion of PC3 and ARCaPM cells in response to MET receptor ligand HGF. FYN also contributed to the metastatic potential of NEPC cells in two mouse models of visceral metastasis with two different cell lines (PC3 and TRAMPC2-RANKL). The activation of MET appeared to regulate neuroendocrine (NE) features as evidenced by increased expression of NE markers in PCa cells lines treated with HGF. Importantly, the overexpression of FYN protein in DU145 cells was directly correlated with the increase of CHGA. Thus, our data demonstrated that the neuroendocrine differentiation that occurs in PCa cells is, at least in part, regulated by FYN kinase. Understanding the role of FYN in the regulation of NE markers will provide further support for ongoing clinical trials of SFK and MET inhibitors in castration-resistant PCa patients.
Citation Format: Karen Cavassani, Murali Gururajan, Margarit Sievert, Peng Duan, Michael Freeman, Gina Chia-Yi Chu, Neil Bhowmick, Leland Chung, Edward Posadas. Src family kinase Fyn promotes the neuroendocrine phenotype and visceral metastasis in advanced prostate cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 177.
Abstract 1785: Sociodemographic correlates of knowledge and risk perception of HPV and HPV-associated oropharyngeal cancer
Authors: Chen Betty Y. , Osazuwa-Peters Nosayaba , Adjei Boakeye Eric , Clancy Jennifer , Su Jonathan , Vallot Patrice , Beck Geoffrey , Walker Ronald J. , Varvares Mark A. 
Published: July 2016

Abstract
Purpose
To analyze how key sociodemographic variables correlate with risk perception and knowledge of HPV-associated oropharyngeal cancer in the community.
Methods
A cross-sectional study was conducted at a drag racing event on September 12-13, 2015 in Madison, Illinois. The independent variables were sociodemographic factors including age, gender, race, income level, education level, drinking history, smoking history, and number of sexual partners. The outcome variables were HPV risk perception and knowledge of HPV-associated oropharyngeal cancer, both derived from combining questionnaire items to form knowledge and perception scores. Multivariable linear regression analysis assessed the predictors of risk perception and knowledge of HPV-associated oropharyngeal cancer.
Results
Final sample population was 301. Mean risk perception score was 2.16 ± 1.37 out of 6, and mean knowledge score was 5.65 ± 4.63 out of 15. In multivariable linear regression, race and education were significant predictors of HPV risk perception. Compared to Caucasians, African Americans had a lower perceived risk of developing oropharyngeal cancer (β = -0.35; 95% CI: -0.69 - -0.02). Participants with ≤ high school diploma had a lower perceived risk of developing oropharyngeal cancer compared to those with ≥ college degree (β = -0.60; 95% CI: -1.05 - -0.15). Age, gender, race and education were significant predictors of HPV-associated oropharyngeal cancer knowledge in multivariable analysis. For every one year increase in age, HPV-associated oropharyngeal cancer knowledge decreased by 5%. Men had lower HPV-associated oropharyngeal cancer knowledge (β = -1.30; 95% CI: -2.35 - -0.26) as were African Americans compared to Caucasians (β = -1.30; 95% CI: -2.36 - -0.25). Participants with ≤ high school diploma had lower HPV-associated oropharyngeal cancer knowledge compared to those with ≥ college degree (β = -3.33; 95% CI: -4.75 - -1.91).
Conclusions
Age and gender were independent predictors of knowledge of HPV-associated oropharyngeal cancer, while race and education predict both knowledge and risk perception of HPV-associated oropharyngeal cancer. The sociodemographic correlates demonstrated in our study should inform future interventions targeted at increasing knowledge of HPV-associated oropharyngeal cancer in the community.
Citation Format: Betty Y. Chen, Nosayaba Osazuwa-Peters, Eric Adjei Boakeye, Jennifer Clancy, Jonathan Su, Patrice Vallot, Geoffrey Beck, Ronald J. Walker, Mark A. Varvares. Sociodemographic correlates of knowledge and risk perception of HPV and HPV-associated oropharyngeal cancer. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1785.
Abstract 1786: One in four Hispanic women with early onset breast cancer carry BRCA1, BRCA2, or PALB2 mutations: Results from a population-based study in South America
Authors: Tuazon Anna Marie , Bohorquez Mabel , Ramirez Carolina , Lott Paul , Estrada Ana , Criollo Angel , Wang Cathy , Echeverry Magdalena , Suarez John ,   COLUMBUS Consortium,   LaFamilia Consortium, Carvajal Carmona Luis G. 
Published: July 2016

Abstract
Breast cancer is the leading cause of cancer incidence and mortality among Hispanic women, who are often diagnosed with late stage tumors and are more likely to die after diagnosis when compared to non-Hispanic whites. While strides have been made in understanding Hispanic breast cancer genetics, most studies have been limited to investigating cases from high-risk clinics. In this study, we aimed to assess the prevalence of pathogenic mutations in three most important breast cancer genes (BRCA1, BRCA2 and PALB2) in an unselected Hispanic breast cancer cohort. Initially, six hundred and forty-six unselected Colombian breast cancer cases were screened for four known Hispanic BRCA1/2 mutations by genotyping. Subsequently, cases that remained mutation negative, as well as 186 cancer-free controls, were screened for BRCA1, BRCA2 and PALB2 mutations using targeted next generation sequencing. We identified 67 cases with pathogenic mutations, one case with a likely-pathogenic variant, and 16 carriers of variants of unknown significance. Among the pathogenic mutation carriers, 88.1% harbored a founder mutation (n = 59), which includes the known BRCA1 3450del4 mutation, strikingly found in 32 unrelated cases. Remarkably, we found that 1 in 4 of the cases diagnosed with breast cancer by age 40 years, regardless of family history of cancer, carried a pathogenic mutation. The high frequency of pathogenic mutations in this unselected cohort (10.4%), in particular those with an early age of onset (25.3%), suggests that population-based genetic testing among Hispanic communities can identify most carriers who would otherwise ineligible for testing. Identifying mutation carriers of these genes has implications in clinical management and surveillance for Hispanic women, a population that is vulnerable to breast cancer disparities in the U.S. and Latin America.
Citation Format: Anna Marie Tuazon, Mabel Bohorquez, Carolina Ramirez, Paul Lott, Ana Estrada, Angel Criollo, Cathy Wang, Magdalena Echeverry, John Suarez, COLUMBUS Consortium, LaFamilia Consortium, Luis G. Carvajal Carmona. One in four Hispanic women with early onset breast cancer carry BRCA1, BRCA2, or PALB2 mutations: Results from a population-based study in South America. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1786.
Abstract 1797: Loss of FoxO1 expression is associated with decreased IGF-1R levels and alters IGFBP-1 induction in tamoxifen-resistant breast cancer cells
Authors: Vaziri-Gohar Ali , Houston Kevin D. 
Published: July 2016

Abstract
Breast cancer is one of the leading causes of cancer-related deaths in the world. The majority of breast cancers express estrogen receptor alpha (ERα) and tamoxifen, a selective estrogen receptor modulator, is commonly prescribed as adjuvant therapy for ERα-positive breast cancer patients. The development of chemoresistance is a common occurrence in treated patients, however, the molecular mechanisms associated with acquired tamoxifen resistance are not well defined. Previous work from our lab identified a novel mechanism of tamoxifen action that involved the accumulation of extracellular Insulin-like growth factor binding protein-1 (IGFBP-1) and modulates IGF-1-dependent signaling transduction. Tamoxifen-induced IGFBP-1 induction in this model was mediated by G protein-coupled estrogen receptor (GPER)-dependent CREB activation as shown by phosphorylation on serine 133. To determine IGFBP-1 induction is altered during the development of chemoresistance, this mechanism of action was studied in tamoxifen resistant MCF-7 (TamR) cells. Whereas CREB was constitutively phosphorylated in TamR cells, IGFBP-1 levels were not elevated when compared to parental cells and IGFBP-1 was not induced by tamoxifen treatment in TamR cells. These data suggest that another transcription factor(s) are also necessary for the induction of IGFBP-1 in breast cancer cells. FoxO1 is a known regulator of IGFBP-1 transcription and we tested whether FoxO1 contributes to tamoxifen-induced IGFBP-1 transcription. Our results indicate that FoxO1 expression levels were significantly reduced in TamR cells compared with parental cells. Furthermore, FoxO1 knockdown experiments demonstrated this transcription factor mediates tamoxifen-induced IGFBP-1 induction in MCF-7 cells. Consistent with previously published observations, IGF-1R expression was reduced in TamR cells compared to parental MCF-7 cells. To determine if loss of IGF-1R expression in involved in the loss of FoxO1 expression in TamR cells, IGF-1R was exogenously expressed and FoxO1 expression was measured. IGF-1R expression increases FoxO1 levels and partially restores tamoxifen-induced IGFBP-1 induction in TamR cells. These results suggest that FoxO1-mediated IGFBP-1 accumulation is altered during the development of tamoxifen resistance and is associated with decreased IGF-1R expression.
Citation Format: Ali Vaziri-Gohar, Kevin D. Houston. Loss of FoxO1 expression is associated with decreased IGF-1R levels and alters IGFBP-1 induction in tamoxifen-resistant breast cancer cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1797.
Abstract 1811: ERβ sensitizes NSCLC cells to chemotherapeutic agents by regulating DNA damage response
Authors: Bado Igor , Nikolos Fotis , Gustafsson Jan-Åke , Thomas Christoforos 
Published: July 2016

Abstract
The expression of wild-type estrogen receptor β (ERβ1) correlates with increased survival in patients with Non-Small Cell Lung Cancer (NSCLC). However, the molecular mechanism that accounts for this association is unknown. ERβ1 was previously shown to sensitize breast cancer cells to chemotherapeutic agents. The role of the receptor in regulating sensitivity of NSCLC cells to chemotherapy, a common treatment option for advanced disease, has not been studied. Here we show that upregulation of ERβ1 decreases the survival of NSCLC cells in response to treatment with doxorubicin. This effect was observed in p53-defective but not wild-type p53-expressing cells. ERβ1 enhanced G2/M cell cycle arrest in NSCLC cells by activating the checkpoint kinase 1 (Chk1) and altering downstream signaling. The expression of the p63 target gene cyclin G2 that regulates the G2/M checkpoint was induced by ERβ1 proposing an ERβ1-p63 transcriptional cooperation. Our findings suggest the involvement of ERβ1 in the regulation of DNA damage response in NSCLC cells and support the potential predictive value of the receptor in clinical management of the disease.
Citation Format: Igor Bado, Fotis Nikolos, Jan-Åke Gustafsson, Christoforos Thomas. ERβ sensitizes NSCLC cells to chemotherapeutic agents by regulating DNA damage response. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1811.
Abstract 182: Dual inhibition of the MEK5 and PI3K pathways most effectively reduces proliferation and migration in triple negative breast cancer cells
Authors: Wright Thomas , Raybuck Christopher , Wendekier Katheryn , Cavanaugh Jane E. 
Published: July 2016

Abstract
Aberrations in the MAPK/extracellular signal-regulated kinase (MEK/ERK) and phosphoinositide-3-kinase (PI3K) pathways have been linked to increased proliferation and survival in triple negative breast cancer (TNBC) cells. It has been proposed that these survival characteristics are enhanced through compensatory signaling and crosstalk mechanisms. Promising combinations of MEK and PI3K inhibition have been evaluated in phase I clinical trials for various cancer types. However, these clinical trials have had limited efficacy and have yet to encompass the MEK5/ERK5 pathway, which has been shown to promote cell survival. The goal of this study was to examine the crosstalk between the MEK1/2, MEK5, and PI3K pathways and determine the most promising combination of the MEK1/2, ERK5, and PI3K inhibitors, U0126, XMD8-92, and LY294002, respectively, in a diverse panel of triple negative breast cancer cell lines: BT549, MDA-MB-231, and MDA-MB-468. Our results indicate that dual inhibition of the MEK5 and PI3K pathways significantly reduced both proliferation (45.53%) and migration (39.37%) in MDA-MB-231 TNBC cells. In contrast, inhibition of ERK1/2 alone or in combination with PI3K or ERK5 inhibition yielded mixed responses. Interestingly, dual inhibition of the MEK5 and PI3K pathways increased the activity of the MEK1/2 pathway. These data suggest that crosstalk between these kinases occurs and dual inhibition of PI3K and ERK5 may be a novel therapeutic approach for treating TNBC.
Citation Format: Thomas Wright, Christopher Raybuck, Katheryn Wendekier, Jane E. Cavanaugh. Dual inhibition of the MEK5 and PI3K pathways most effectively reduces proliferation and migration in triple negative breast cancer cells. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 182.
Abstract 1823: Mechanism of the anterograde transport of the androgen receptor
Authors: Li Jianzhuo , Zhang Guanyi , Park Hee-Won , Zhang Haitao 
Published: July 2016

Abstract
Androgen receptor (AR) is a ligand-activated nuclear receptor that plays a critical role in normal prostate physiology, as well as in the development and progression of prostate cancer. In addition to the classical paradigm in which AR exerts its biological effects by activating the transcription of its target genes, there is considerable evidence to support a rapid, non-genomic action mediated by membrane-associated AR, which facilitates the activation of kinase signaling cascades, leading to cell proliferation. While the nuclear translocation of AR is well studied, the molecular events controlling the recruitment of AR to the plasma membrane remain poorly understood. In this study, we set out to elucidate the mechanism underlying AR transport to the membrane. We found that a subpopulation of AR was localized to the membrane fraction shortly after androgen stimulation. Treatment with microtubule-targeting agents, but not actin inhibitors, blocked androgen-induced AR membrane localization, suggesting that AR transport to the membrane is mediated by the microtubule cytoskeleton. By utilizing dominant negative mutants, we identified the KIF5B, a member of the kinesin 1 family of motor proteins, is involved in the anterograde transport of AR. We further demonstrated that AR interacts directly with KIF5B, and such interaction is enhanced by androgens. Through a series of deletion constructs, a region includes the N-terminal and DNA binding domains of AR was determined to be involved in the association with KIF5B. Disruption of AR membrane transport decreased AKT phosphorylation. Together, our data suggest that KIF5B mediates AR membrane transport and regulates the non-genomic function of AR. Disruption of AR membrane translocation may represent a novel strategy to target AR signaling in prostate cancer.
Citation Format: Jianzhuo Li, Guanyi Zhang, Hee-Won Park, Haitao Zhang. Mechanism of the anterograde transport of the androgen receptor. [abstract]. In: Proceedings of the 107th Annual Meeting of the American Association for Cancer Research; 2016 Apr 16-20; New Orleans, LA. Philadelphia (PA): AACR; Cancer Res 2016;76(14 Suppl):Abstract nr 1823.