bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract IA27: Tumor suppressor and tumor maintenance genes
Authors: Lowe Scott W. 
Published: May 2019

Abstract
Cancer arises through an evolutionary process whereby normal cells acquire mutations that erode growth controls, leading to the expansion of aberrantly proliferating cells. Such mutations activate oncogenes or inactivate tumor suppressors, each bestowing new capabilities to emerging tumors. Still, cancer is not an inevitable consequence of mutation but is instead kept in check by intrinsic tumor-suppressor programs activated in damaged cells. Accordingly, our laboratory studies such mechanisms in order to reveal key regulatory nodes controlling basic cellular processes and to identify the strategies nature uses to combat cancer. More recently, our interests have expanded to explore the action of tumor maintenance genes---those genes needed to sustain the proliferation and survival of malignant cancer cells---with the goal of identifying cancer vulnerabilities and therapeutic targets. Our approach combines powerful mouse models, genetics, and genomics in a coordinated manner that allows us to study tumor suppressor and tumor maintenance networks in a comprehensive way. Recent efforts to combine these tools towards the production of flexible and accurate mouse models and their subsequent use to identify and characterize tumor suppressor and tumor maintenance genes will be discussed.
Citation Format: Scott W. Lowe. Tumor suppressor and tumor maintenance genes [abstract]. In: Proceedings of the AACR International Conference held in cooperation with the Latin American Cooperative Oncology Group (LACOG) on Translational Cancer Medicine; May 4-6, 2017; São Paulo, Brazil. Philadelphia (PA): AACR; Clin Cancer Res 2018;24(1_Suppl):Abstract nr IA27.
Abstract A03: Tumorigenesis involving expansion of CD24 high CD61 cells is abrogated by tamoxifen in mouse models of luminal breast cancer
Authors: Zhdankin Olga , Bomier Melanie , Parke Donna , Holy Jon , Rose-Hellekant Teresa 
Published: May 2019

Abstract
The cells within the mammary gland that are altered by tamoxifen chemoprevention and correlate with abrogation of tumorigenesis are unknown. We have documented that a 60 day tamoxifen chemopreventive regimen reduces tumor incidence in NRL-TGFalpha and MMTV-c-neu mouse models of luminal breast cancer. For this study our goal was to identify the aberrant and/or altered mammary cell subpopulations typically found in the mammary gland of TGFalpha and c-neu mice and determine the effect of tamoxifen on their relative quantity. Mammary cell subpopulations were evaluated using flow cytometric analysis by labeling lineage negative cells with CD24, CD61 and CD49f fluorescently tagged antibodies. TGFalpha mice developed an expanded CD24high CD61positive fraction of cells coinciding with hyperplasia and tumor presence. Prior to tumor development c-neu mice had an expanded CD24medium CD49f high cell fraction and by the time tumors developed, both nontumorous glands and tumors also displayed an expanded CD24high CD61positive cell fraction. Mammary glands from mice that received a 60 day tamoxifen chemopreventive regimen did not display expanded cell fractions compared to placebo treated mice in both models. Our data indicate that tamoxifen chemoprevention abrogates tumorigenesis that involves expansion of CD24high CD61positive cells. Further investigations into tamoxifen effects on mammary cell subpopulations is critical for a clearer understanding of the utility of tamoxifen and other estrogen receptor modulators as chemopreventives.
Citation Format: Olga Zhdankin, Melanie Bomier, Donna Parke, Jon Holy, Teresa Rose-Hellekant. Tumorigenesis involving expansion of CD24 high CD61 cells is abrogated by tamoxifen in mouse models of luminal breast cancer. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A03.
Abstract A22: Development and characterization of an oral cancer cell line resist to the cytotoxic effects of the green tea catechin, (-)-Epigallocatechin-3-gallate
Authors: Tao Ling , Chen Jennifer W. , Park Jong-Yung , Sae-tan Sudathip , Lambert Joshua D. 
Published: May 2019

Abstract
(-)-Epigallocatechin-3-gallate (EGCG) is the most abundant polyphenol in green tea (Camellia sinensis). Although many studies have demonstrated its cancer chemopreventive and chemotherapeutic effects, the potential for development of EGCG resistance in cancer cells has not been well-studied. The purpose of this study was to develop and characterize an EGCG-resistant oral squamous carcinoma cell line to understand potential mechanisms of resistance to the cytotoxic effects of EGCG. Exposure of oral squamous carcinoma (SCC-25) cells to gradually increasing concentrations of EGCG (10 – 75 μM) resulted in emergence of an EGCG-resistant phenotype (SCC-25E75R). SCC-25E75R cells were significantly resistant to EGCG-induced growth inhibition compared to SCC-25 cells (IC50=157 μM vs 70 μM). Treatment of SCC-25E75R cells with 75 μM EGCG caused a 34% increase in apoptosis compared to a 200% increase in SCC-25 parental cells treated with the same concentration. Microarray analysis showed that under untreated conditions, 73 genes were differentially expressed (≥4 fold change, p&lt;0.05) between SCC-25 and SCC-25E75R cells. The resistant cells have lower expression levels of tumor suppressor genes including absent in melanoma 2 (AIM) and inhibitor of DNA binding 4 (ID4) suggesting the resistance to tumor inhibition. EGCG treatment (75 μM) induced significant changes (≥1.75 fold change, p&lt;0.05) in 52 genes in SCC-25 and 164 genes in SCC-25E75R cells. Among these, 42 genes were found to be differentially regulated by EGCG between the two cell lines. For example, EGCG induced the DNA-damage-inducible transcript 3 (DDIT3) and heat shock 70kDa protein 5 (HSPA5) in resistant cells more significantly than in sensitive cells. This may result in a greater anti-apoptotic protein in SCC-25E75R cells and thereby confirm resistance to the effects of EGCG. In conclusion, this work represents a preliminary investigation into potential mechanisms of resistance to EGCG, and may be useful in understanding responsiveness of oral cancer, as well as other cancer types, to the treatment effects of EGCG.
Citation Format: Ling Tao, Jennifer W. Chen, Jong-Yung Park, Sudathip Sae-tan, Joshua D. Lambert. Development and characterization of an oral cancer cell line resist to the cytotoxic effects of the green tea catechin, (-)-Epigallocatechin-3-gallate. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr A22.
Abstract B12: The co-location of academia with the community in addressing cancer health disparities: A new model of partnerships for environmental public health
Authors: Wallington Sherrie Flynt , Dash Chiranjeev , Hamilton Rhonda , Dodson Everett , Adams-Campbell Lucile L. 
Published: May 2019

Abstract
Environmental factors play an important and explanatory role in health disparities. Research suggests that a community should be an integral part of the process of solving community problems. Consequently, there has been a shift from traditional academic research to more community participatory approaches. To our knowledge none of these approaches have examined the role of academic co-locations (multiple site locations) as part of a community-level cancer prevention and disparities approach. Our co-location strategy involves exporting faculty and staff, clinical trials, interventions, outreach, education, and research from Georgetown University's main campus to a newly established office site located in Southeast, DC, a medically underserved area. Using the environmental focus group study as a case example of the impact of our co-location strategy, we seek to put forward an academic co-location definition and framework for implementation. Our findings show that co-location is a viable strategy that should be considered as part of a multifaceted approach in building and sustaining collaborative partnerships and research capacity, particularly within minority underserved communities. Focus group themes emerged around six topical areas: (1) the concept of environment, (2) perception of pollution, (3) perceptions of water quality, 4) perceptions of air quality, 5) health issues related environmental pollutants, (6) personal and community environment, and 7) environmental information received. Our co-location strategy was also associated with the following outcomes: beneficial in establishing trust, respect, accessibility, and success in study accrual and retention. Co-location benefits, challenges, and lessons learned are also discussed.
Citation Format: Sherrie Flynt Wallington, Chiranjeev Dash, Rhonda Hamilton, Everett Dodson, Lucile L. Adams-Campbell. The co-location of academia with the community in addressing cancer health disparities: A new model of partnerships for environmental public health. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr B12.
Abstract B17: The evaluation of breast cancer chemoprevention uptake in a high-risk cohort
Authors: Nimmons Scott , Bambhroliya Arvind , Teresa Bevers , Ying Jun , Brown Powel , Cook Elise , Newman Lonzetta , Brewster Abenaa 
Published: May 2019

Abstract
Background: Population-based estimates in the United States indicate that uptake of breast cancer chemoprevention has remained low despite more than a decade of scientific evidence demonstrating clinical benefit. The objective of our study was to evaluate the uptake of breast cancer chemoprevention in a high-risk clinical setting. Methods: We evaluated the uptake of chemoprevention (tamoxifen, raloxifene or exemestane) 2007 to 2011 among 1,151 healthy women at high risk of breast cancer who were seen at the MD Anderson Cancer Center and enrolled in a high-risk breast cancer cohort. We used stepwise multivariable logistic regression to determine patient-related factors associated with use of chemoprevention. Results: Mean age of the cohort was 60 years; 85% of the women were white, 6% black and 9% of other ethnicities. Chemoprevention use was reported among 29% of women (n=340) (22% tamoxifen, 7% raloxifene). Among women with a history of lobular carcinoma in situ (LCIS), a proliferative breast lesion or Gail 5-year risk ≥1.66%, the uptake of chemoprevention was 52%, 42% and 14%, respectively. In multivariable analysis, history of osteoporosis (p=0.0034), prior use of hormone replacement therapy (p=0.0002) and elevated Gail model 5 year risk &gt;3.0% (p=0.003) were positively associated with uptake of chemoprevention. Conclusion: Women seen in a high-risk clinical setting may be more motivated to use chemoprevention and uptake was highest among women with a history of LCIS or a proliferative breast lesion. Individualized strategies are needed to improve breast cancer chemoprevention uptake among different subsets of high-risk patients.
Citation Format: Scott Nimmons, Arvind Bambhroliya, Bevers Teresa, Jun Ying, Powel Brown, Elise Cook, Lonzetta Newman, Abenaa Brewster. The evaluation of breast cancer chemoprevention uptake in a high-risk cohort. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr B17.
Abstract B19: Improving initiation of adjuvant hormonal therapy in black women under 50 may contribute towards narrowing racial gaps in breast cancer
Authors: Sheppard Vanessa B. , Isaacs Claudine , Tadesse Mahlet G. , Butler Melissa , Harper Felicity , Hirpa Fikru 
Published: May 2019

Abstract
Background: The advent of adjuvant hormonal therapy has greatly improved breast cancer survival in women with hormonal receptor (HR) positive breast cancer. Unfortunately, racial disparities have been noted in both the uptake of adjuvant hormonal therapy and in women with HR positive breast cancer.
Purpose: In a prospective study, we examined the influence of race, socio-cultural factors, and process of care factors on initiation of adjuvant hormonal therapy.
Methods: Eligible women were newly diagnosed with invasive, non-metastatic hormonal receptor positive (HR) breast cancer. Socio-cultural and healthcare factors were collected via telephone surveys; clinical data were abstracted from charts. Stepwise logistic regression models examined associations between hormonal initiation and study factors.
Results: The sample was 56% Black (n=150) and 44% White (n=120). Overall 70% initiated therapy with Black women &lt;50 having the lowest rate of initiation (51%) among all Black and White age groups. A significant interaction (p= .002) was found between race and age so a stratified race – age composite variable was created. In multivariate models, Black women &lt; 50 years were less likely to initiate therapy compared to Whites ≥50 (OR: .28; 95% CI: .10 to .82), whites &lt;50 (OR: 0.19; 95% CI: 0.05 to 0.68), or compared to blacks ≥50 (OR: .34; 95% CI: 0.12 to 0.96). Women reporting having higher ratings of financial access were more likely to initiate therapy as were those with higher ratings of communication with their providers.
Conclusion: Attention to financial aspects of cancer care and patient-provider communication may be useful points of intervention to improve initiation in patients, particularly Black patients &lt;50 years of age.
Citation Format: Vanessa B. Sheppard, Claudine Isaacs, Mahlet G. Tadesse, Melissa Butler, Felicity Harper, Fikru Hirpa. Improving initiation of adjuvant hormonal therapy in black women under 50 may contribute towards narrowing racial gaps in breast cancer. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr B19.
Abstract B22: The synergistic effect of a sulforaphane and maitake mushroom extract combination on the expression of the detoxifying enzymes NQO1 and UGT1A1
Authors: Cornblatt Grace A. , Ownby Stacy , Cornblatt Brian S. 
Published: May 2019

Abstract
Excess estrogen exposure, whether from endogenous estrogen, harmful estrogen metabolites, or exogenous xenoestrogens (e.g. BPA, parabenes, etc.) can be detrimental to overall breast health. Here we describe a novel blend of natural ingredients including sulforaphane and maitake-derived glucans and their effect on detoxifying enzymes capable of diminishing excess estrogens. Sulforaphane, an isothiocyanate found in broccoli seeds and sprouts, results from the hydrolization of a glucosinolate called glucoraphanin by the enzyme myrosinase. In vitro and in vivo studies reveal the ability of sulforaphane to induce Phase 2 detoxifying enzymes (e.g. NAD(P)H:Quinone Oxidoreductase (NQO1) which functions to rid the body of harmful quinone estrogen metabolites and UDP-Glucuronosyltransferase 1-1 (UGT1A1) which has been shown to play a role in the metabolism of Bisphenol-A, an estrogen mimic, via glucoronidation). Previous research involving maitake extracts has largely focused on their immune-boosting properties. We examined the effect of the combination of sulforaphane and maitake-derived glucans on NQO1 and UGT1A1. RAW 246.7 mouse monocyte/macrophages were treated with sulforaphane and maitake mushroom extract alone or in combination. mRNA levels of NQO1 and UGT1A1 were assessed via quantitative RT-PCR revealing a synergistic effect on the induction of both NQO1 and UGT1A1 gene expression. Further, we carried out an in vivo study in rats during which the animals were dosed with sulforaphane, maitake mushroom extract, or the combination for 14 days. The upregulation of UGT1A1 gene expression was greater in the mammary glands of the rats given the combination of sulforaphane and maitake extract compared to those receiving either agent alone. This study demonstrates the synergistic effect of the combination of sulforaphane and a maitake extract on the gene expression of Phase 2 detoxifying enzymes NQO1 and UGT1A1 suggesting the agents together may be effective at detoxifying the body of excess estrogens and promoting breast health.
Citation Format: Grace A. Cornblatt, Stacy Ownby, Brian S. Cornblatt. The synergistic effect of a sulforaphane and maitake mushroom extract combination on the expression of the detoxifying enzymes NQO1 and UGT1A1. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr B22.
Abstract B39: The Health of Women (HOW) Study: A novel approach to the cohort study
Authors: Love Susan , Fischetti Christine , Sullivan-Halley Jane , Clague Jessica , Bernstein Leslie 
Published: May 2019

Abstract
Purpose: The purpose of the Health of Women (HOW) Study is to examine risk factors for breast cancer and factors that may contribute to long-term survivorship through an innovative online system that allows for participant engagement and data sharing with the research community.
Methods: The HOW Study is conducted through online and mobile phone platforms. Questionnaires are developed in our custom built survey tool and are available for completion on the study's website. The system allows for automated skip patterns within questionnaires and collection of data directly into a SQL database. The cohort is open to anyone 18 years or older; recruitment sources include the Love Army of Women and the general public. Participants will be given the opportunity to pose questions they would like to see answered. The HOW Study is also a novel resource allowing outside researchers to submit questions to be incorporated into HOW questionnaires and creating a data sharing platform that facilitates researcher access to HOW data after an application process.
Results: The HOW Study launched October 2012 and currently has 42,600 participants from across the nation and the globe. We have released 1 baseline questionnaire and 4 breast cancer-specific questionnaires to capture diagnosis and treatment with greater than 90% completion rate for each.
Conclusion: We have shown that we can recruit and engage participants in an online cohort study. We believe that this study has the potential to transform epidemiologic research by engaging both participants and the research community. Our second baseline questionnaire will launch in the summer of 2013, which will give us the opportunity to increase enrollment and assess retention.
Citation Format: Susan Love, Christine Fischetti, Jane Sullivan-Halley, Jessica Clague, Leslie Bernstein. The Health of Women (HOW) Study: A novel approach to the cohort study. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr B39.
Abstract B53: Time to first cigarette and lung cancer risk in Japan
Authors: Ito Hidemi , Gallus Silvano , Hosono Satoyo , Oze Isao , Fukumoto Koichi , Yatabe Yasushi , Hida Toyoaki , Mitsudomi Tetsuya , Negri Eva , Vecchia Calro La , Tanaka Hideo , Matsuo Keitaro 
Published: May 2019

Abstract
Background: Cigarette smoking is the major cause of lung cancer. Although the time to first cigarette (TTFC) of the day is a distinct indicator of nicotine dependence, little information is available on its possible relation to LC.
Methods: This case-control study includes a total of 1,572 incident lung cancer cases and 1,572 non-cancer controls visiting for the first time the Aichi Cancer Center Hospital between 2001 and 2005. We estimated odds ratio (OR) and 95% confidence interval (CI) for TTFC using logistic regression model after adjustment for several potential confounders.
Results: TTFC was inversely associated with the risk of lung cancer. This association was consistent across histological subtypes of lung cancer. For all lung cancers considered among ever smokers and after accurate allowance for smoking quantity and duration, besides other relevant covariates, compared with TTFC more than 60 min, the adjusted ORs were 1.08 (95% CI, 0.73-1.61) for TTFC of 31-60 min, 1.40 (0.98-2.01) for 6-30 min and 1.86 (1.28-2.71) for within 5 min (ptrend, &lt;0.001). Statistically significant heterogeneity by histological subtype was observed (pheterogeneity, 0.002 for former smokers and 0.033 for current smokers).
Conclusions: Nicotine dependence, as indicated by the TTFC, is associated with increased risk of lung cancer and is therefore an independent marker of exposure to tobacco smoking.
Citation Format: Hidemi Ito, Silvano Gallus, Satoyo Hosono, Isao Oze, Koichi Fukumoto, Yasushi Yatabe, Toyoaki Hida, Tetsuya Mitsudomi, Eva Negri, Calro La Vecchia, Hideo Tanaka, Keitaro Matsuo. Time to first cigarette and lung cancer risk in Japan. [abstract]. In: Proceedings of the Twelfth Annual AACR International Conference on Frontiers in Cancer Prevention Research; 2013 Oct 27-30; National Harbor, MD. Philadelphia (PA): AACR; Can Prev Res 2013;6(11 Suppl): Abstract nr B53.