bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract ADV02: Black voices on health: Exploring possibilities for community-based research on cancer and co-morbidities amongst rural California Central Coast African Americans.
Authors: Austin-Schreher Carmelita 
Published: August 2014

Abstract
Carmelita Austin-Schreher, a breast cancer survivor who wanted to connect African-Americans to early detection education, support and services formed the African-American Community Health Group of the Central Coast with-in 4 months of her diagnosis. Beginning in 1998, we responded as a self-help group to the disproportionately high breast cancer mortality rates of African-American women, and the need for ethnically sensitive services. Carmelita and community members envisioned a group that would not only educate the African-American community about cancer, but one that would provide one-to-one and group support, a safe and comfortable environment for discussion, and would respect the cultural needs of our community. In order to provide its participants with the highest level of care and education, African-American Community Health Group is committed to staying on top of the latest news in health and cancer screening, treatment and research. African-American Community Health Group is proud of being a “grassroots” organization and is therefore dedicated to providing comprehensive screening outreach, health education, and long-term advocacy to empower all African-Americans in the central coast community.
We continue to provide crucial cancer education and prevention services as well as peer support for people with cancer through targeted projects. However, in addition to these activities we expanded health promotion and disease prevention activities of our organization to providing broad-based health education to the larger African-American and underserved communities including men and families, through office hours, library, support groups, seminars, peer and leadership training, and health fairs.
The mission of the African-American Community Health Group is to empower the African-American community of the central coast to be active and informed health consumers and survivors through self-help activities, advocacy training, and health education. Additionally, we work to create a dialogue with the community at large about racial disparities in health and the need for increased cultural and racial sensitivity.
Citation Format: Carmelita Austin-Schreher. Black voices on health: Exploring possibilities for community-based research on cancer and co-morbidities amongst rural California Central Coast African Americans. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr ADV02. doi:10.1158/1538-7445.AM2013-ADV02
Abstract ADV12: Banner Good Samaritan Medical Center's Oncology Program.
Authors: Jones Bonita 
Published: August 2014

Abstract
Banner Good Samaritan Medical Center in Phoenix, Arizona is the flagship medical center within Banner Health with over 650 beds. Our medical center has been consistently ranked as one of America's "Best Hospitals" by U.S. News & World Report.
Banner Good Samaritan Medical Center's mission statement: We exist to make a difference in the lives of the people we serve through excellent patient care.
Banner Good Samaritan's cancer program offer's state-of-the-art inpatient and outpatient services, advanced detection and treatments along with a wide range of support services for all types of cancer including breast cancer, lung cancer, head and neck cancers, leukemia and colorectal/pancreas/liver cancers.
Citation Format: Bonita Jones. Banner Good Samaritan Medical Center's Oncology Program. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr ADV12. doi:10.1158/1538-7445.AM2013-ADV12
Abstract ADV18: American indian screening initiatives: Gaining trust- reducing disparities.
Authors: Powell Kim 
Published: August 2014

Abstract
The Montana Affiliate of Susan G. Komen for the Cure® is dedicated to combating breast cancer at every front. Up to 75 percent of the Affiliate's net income goes toward funding grants to local hospitals and community organizations that provide breast health education and breast cancer screening and treatment programs for medically underserved women. The remaining income supports the national Komen Grants Programs, which funds groundbreaking breast cancer research, meritorious awards and educational and scientific programs around the world.
The Montana Affiliate of Susan G. Komen for the Cure serves the 4th largest geographic area in the country. American Indians living throughout Montana as members of seven distinct and independent tribal reservations, most in rural or “frontier” regions of the state. American Indian women in MT are more likely to live in poverty, be uninsured and face a higher risk of death from breast cancer due to late diagnosis.
To address this, Komen Montana has embarked on a comprehensive approach to address disparities and barriers that American Indian Women face in breast cancer screening. Since 2002, Komen Montana has funded screening mammography programs including funding mobile mammography clinics at PowWow events. Komen MT has partners with state as private agencies to identify traditional beliefs and Native cultural beliefs that serve as a deterrent to quality breast health programs. Most recently, a Komen Montana Community Grant, “Going Pink on the Red Road: has facilitated formation of a seven-tribe advisory council to draw upon the strengths of tribal representatives in the development of culturally specific resources and methods.
Komen Montana seeks to provide a significantly positive impact for American Indian women in the area of breast health by decreasing barriers, increasing culture-specific access and intervention, and decreasing the morbidity and mortality among Native women.
Citation Format: Kim Powell. American indian screening initiatives: Gaining trust- reducing disparities. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr ADV18. doi:10.1158/1538-7445.AM2013-ADV18
Abstract ADV20: For constructing an open society to cancer recognition.
Authors: Sakurai Naomi 
Published: August 2014

Abstract
Our mission: Getting a better understanding of cancer survivorship in Japan.
Our vision: Constructing an open society to cancer recognition.
HOPE Project started as a campaign of survivorship in Japan. We target cancer survivors including child cancer their and families. We have approximately 100 members.
Cancer patients face three kinds of problems; physical, emotional and social situations. In Japan, cancer survivors have to go through many misunderstandings and prejudices.
HOPE Project focuses on these issues and problems cancer survivors face that are difficult to solve in Japan.
Citation Format: Naomi Sakurai. For constructing an open society to cancer recognition. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr ADV20. doi:10.1158/1538-7445.AM2013-ADV20
Abstract LB-112: Increase in glutaminase (GLS1) levels through SLUG-induced repression of hsa-miR-23a in triple negative breast cancer cells.
Authors: Mittal Mukul K. , Chaudhuri Gautam 
Published: August 2014

Abstract
Aggressive breast cancers of the triple negative type (TNBC) are often characterized by their high rate of proliferation and dissemination to other organs. One hallmark of this type of cancer cells is their adaptation to rely upon an altered metabolic scheme that includes changes in the glycolytic pathway, known as the Warburg effect, and elevated glutamine metabolism. Glutamine is taken up in a high rate by the proliferating cells and metabolized to provide a major source of energy and nitrogen for biosynthesis of nucleic acids. It is also used as a carbon substrate for anabolic processes in the cancer cells but the regulation of glutamine metabolism in the TNBC cells is not studied in details. Glutamine metabolism is thus implicated as a viable target for anticancer chemotherapy. Here we report that the transcriptional repressor protein SLUG, which is highly expressed in the most of the subtypes of the TNBC cells, indirectly up regulates the level of the glutaminase GLS1 through the repression of hsa-miR-23a gene. Knockdown of SLUG in the SLUG-high TNBC cells increases the hsa-miR-23a levels with subsequent decrease in the GLS1 levels. SLUG binds to the E2-box sequences at the hsa-miR-23a gene promoter and heterochromatinizes the promoter DNA through chromatin remodeling. A specific double-stranded DNA decoy against SLUG also alleviates the SLUG repression of the hsa-miR-23a gene promoter and thus decreases the glutaminase levels in the TNBC cells inhibiting the tumor cell growth. We postulate that maintenance of normal levels of GLS1 in the TNBC cells through the inhibition of the functions of SLUG will control aggressiveness and multiplication of breast tumors. Supported in parts by the DOD-CDMRP grants BC050641, BC086542 and BC103645 to GC.
Citation Format: Mukul K. Mittal, Gautam Chaudhuri. Increase in glutaminase (GLS1) levels through SLUG-induced repression of hsa-miR-23a in triple negative breast cancer cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-112. doi:10.1158/1538-7445.AM2013-LB-112
Abstract LB-120: Large-scale cancer cell line screening with a novel and selective HDAC-6 inhibitor (ACY-1215) identifies candidate predictive biomarkers for breast cancer.
Authors: Yang Min , Tamang David , Jones Simon S. , Di Lie 
Published: August 2014

Abstract
ACY-1215 is a novel and selective inhibitor of HDAC6 currently in Phase 1 clinical trials in combination with bortezomib (Velcade) or lenalidomide (Revlimid) in relapsed/refractory multiple myeloma. Inhibitors of HDACs have demonstrated potent anti-cancer activity mediated by increased levels of acetylation of both histone and non-histone proteins, resulting in growth arrest, cell differentiation and apoptosis. In the present work, the broader anti-tumor activity of ACY-1215 was investigated with a panel of 65 human tumor cell lines derived from the major cancer types, to define additional oncology indications for clinical development and to identify candidate biomarkers of tumor sensitivity and drug resistance.
A group of 14 breast cancer cell lines was used to identify potential predictive biomarkers based on the wide range of sensitivity to ACY-1215 allowing robust correlation analysis. A panel of 42 genes was identified based on cellular sensitivity to ACY-1215 (IC50 values) correlating to gene expression levels and underlying genetic mutations in the individual cell lines as reported in the Cancer Cell Line Encyclopedia (CCLE). The Reactome “Functional Interaction Cytoscape Plugin” was used to partition these signatures genes into cancer-associated networks, which included the PIK3R2, ERBB2/STAT3, and TGFB3 signaling pathways. Association with these pathways and potential mechanism of action is consistent with observed synergistic anti-tumor activity between ACY-1215 and PI3K inhibitors. Also Gene Set Enrichment Analysis (GSEA), correlating ACY-1215 sensitivity with gene expression levels, revealed significant over-representation of genes in the p53 pathway, and pathways regulating cytoskeletal structure, cell adhesion, cell cycle and proliferation. A subset of these results support the proposed cytotoxic activity of selective HDAC6 inhibition through blocking of cell motility and misfolded protein clearance, while other findings suggest further novel pathways affected by inhibition of HDAC6.
Confirmation of predicted sensitive and resistant cell lines using the gene signatures will lead to the development of predictive biomarkers and selection of tumor type(s) for in vitro and in vivo validation with ACY-1215 in combination with novel and approved standard of care therapeutics.
Citation Format: Min Yang, David Tamang, Simon S. Jones, Lie Di. Large-scale cancer cell line screening with a novel and selective HDAC-6 inhibitor (ACY-1215) identifies candidate predictive biomarkers for breast cancer. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-120. doi:10.1158/1538-7445.AM2013-LB-120
Abstract LB-125: A novel telomerase inhibitor.
Authors: Mender Ilgen , Gryaznov Sergei , Dikmen Zeliha Gunnur , Wright Woodring , Shay Jerry 
Published: August 2014

Abstract
Telomeres are highly specialized structures that are found at the very ends of linear chromosomes. Normal human somatic cells progressively lose their telomeres with each cell division due to the end replication problem. Unlike most normal somatic cells, the vast majority of advanced cancers have telomerase activity, which overcomes the end replication problem by adding multiple TTAGGG sequences to the end of linear chromosomes. Because of the selective expression of this enzyme in cancer cells, it is an almost universal target for antitumor drug development. However, there are surprisingly few telomerase inhibitors in clinical trials. We have modified a chemotherapeutic antimetabolite agent, 6-thioguanine (6-thio-G) so that this newly synthesized compound targets telomeres while retaining its antimetabolite activity. 6-thio-dG is a nucleoside analogue that is recognized by telomerase and is incorporated into telomeres. Telomeric incorporation results in structurally modified telomeres, functionally uncapping the shelterin protective complex, resulting in telomere associated DNA damage foci. Here, we report that 6-thio-dG causes progressive telomere shortening independent from inhibition of telomerase activity and induces telomere dysfunction in HCT116 human colon cancer cell line. Combination of the telomerase inhibitor GRN163L, which is in advanced clinical trials, and 6-thio-dG have additive effects on telomere shortening in HCT116 cells. 6-thio-dG treatment altered HCT116 cellular morphology and killed most of these cells within 1 week. Normal BJ fibroblast cells, which are telomerase silent, were not affected by 6-thio-dG in either cell morphology after 1 week or in enhanced telomere shortening after long-term treatment. These results show that 6-thio-dG is a novel anti-cancer inhibitor and a potential therapeutic agent targeting both telomeres and general DNA damage.
Citation Format: Ilgen Mender, Sergei Gryaznov, Zeliha Gunnur Dikmen, Woodring Wright, Jerry Shay. A novel telomerase inhibitor. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-125. doi:10.1158/1538-7445.AM2013-LB-125
Abstract LB-136: Creation of androgen independent prostate cancer cell lines using targeting nucleases.
Authors: Nyquist Michael D. , Li Yingming , Dehm Scott M. 
Published: August 2014

Abstract
Understanding mechanisms by which advanced prostate cancer (PCa) progresses to a castration resistant PCa (CRPC) phenotype is crucial for tailoring targeted therapies for individual patients. Constitutively active androgen receptor (AR) splice variants that lack the ligand binding domain drive androgen independent growth in cell lines and xenograft models of PCa and their overexpression in CRPC metastases is associated with poor prognosis. However, the mechanism of AR splice variant overexpression in CRPC is not completely understood. We have shown that diverse genomic rearrangements within the AR gene are linked to AR splicing alterations in PCa cell lines, xenografts, and CRPC metastases. To test whether these AR gene rearrangements drive AR splice variant synthesis and a CRPC phenotype, we developed transcription activator-like effector nucleases (TALENs) for precision genome engineering in androgen-sensitive PCa cells. Engineering of specific AR gene rearrangements induced splicing alterations and efficient expression of AR splice variants. Functionally, these genome-engineered cells displayed constitutive, ligand-independent AR transcriptional activity and an androgen-independent growth profile. These fundamental properties of CRPC were blocked following siRNA-mediated knock-down of truncated AR variants. Overall, these data demonstrate that AR gene rearrangements induce fundamental aspects of the CRPC phenotype including constitutive, ligand-independent, AR splice variant activity. Overall, these data advance the concept of AR splice variants as key drivers of advanced disease, and provide new genome-engineered models that could be used to develop agents targeted to these AR-derived species.
Citation Format: Michael D. Nyquist, Yingming Li, Scott M. Dehm. Creation of androgen independent prostate cancer cell lines using targeting nucleases. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-136. doi:10.1158/1538-7445.AM2013-LB-136
Abstract LB-15: Frequency of aspirin use and prostate cancer mortality among prostate cancer cases in the control arm of the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial.
Authors: Daugherty Sarah E. , Pfeiffer Ruth , Ghazarian Armen , Izmirlian Grant , Prorok Phil , McGlynn Katherine 
Published: August 2014

Abstract
Background: Aspirin may slow progression of cancer through the inhibition of platelet aggregation as experimental research has shown that platelets play a role in cancer cell dissemination and metastatic growth. While a 10% reduction in prostate cancer risk has been associated with regular aspirin use, only a few epidemiological studies have evaluated the association between aspirin use and prostate cancer mortality among prostate cancer cases.
Methods: Participants included 3857 men, age 55-74, who were diagnosed with prostate cancer in the control arm of the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial between 1993-2009. The frequency of aspirin use one year prior to baseline (1993-2001) was ascertained through a self-administered questionnaire. Death due to prostate cancer was ascertained by annual questionnaire and linkage to the National Death Index. Hazard ratios (HRs) and 95% confidence intervals (CIs) were estimated using COX proportional hazards models using age as the time metric and adjusting for clinical stage, Gleason score, primary treatment, smoking status, body mass index, race, history of heart attack, and history of stroke.
Results: After a median of 5 years of follow-up, 136 cases died of prostate cancer. No significant association with prostate cancer mortality was observed between cases who reported pre-diagnostic daily or more than daily aspirin use compared to cases who reported no aspirin use (HR=0.77; 95% CI 0.48-1.25). Among those diagnosed with clinically advanced stage (III, IV) disease, an inverse association with prostate cancer mortality was observed for cases who reported daily or more than daily aspirin use (HR=0.37; 95% CI 0.15-0.92), while no association for daily or more than daily users was seen among those with clinically localized prostate cancer (HR=0.86; 95% CI 0.47-1.58).
Conclusion: Pre-diagnostic use of aspirin was not significantly associated with prostate cancer mortality based on cases diagnosed in the PLCO control arm, although a reduction in risk of prostate cancer mortality was observed among those with advanced stage disease in a subgroup analysis.
Citation Format: Sarah E. Daugherty, Ruth Pfeiffer, Armen Ghazarian, Grant Izmirlian, Phil Prorok, Katherine McGlynn. Frequency of aspirin use and prostate cancer mortality among prostate cancer cases in the control arm of the Prostate, Lung, Colorectal, and Ovarian (PLCO) Cancer Screening Trial. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-15. doi:10.1158/1538-7445.AM2013-LB-15
Abstract LB-150: Carcinogenic Helicobacter pylori infection induces base excision repair intermediates to trigger homologous-dependent repair in human gastric epithelial cells.
Authors: Kidane Dawit , Murphy Drew L , Sweasy Joann.B 
Published: August 2014

Abstract
Helicobacter pylori infection of the human stomach is associated with disease-causing inflammation that elicits DNA damage in both bacterial and host cells. To investigate base excision repair (BER) as the first line of defense against bacterial infection to maintain host cell genomic stability, we examined H. pylori induced BER intermediates that could be responsible for double strand break (DSB) and homologous dependent repair (HDR). Here, we show that H. pylori infection significantly increases abasic sites (AP) that are not repaired by BER. As a result, unrepaired BER intermediates lead to slow replication fork speed and replication fork collapse that eventually is converted to double strand breaks. To determine if H. pylori infection enhances recombinational repair to process DSBs, we have analyzed the cells for homologous directed repair pathways. Direct measurement of HDR using a GFP-based assay demonstrates significantly increased HDR in cells infected with H. pylori. Our data suggest that H. pylori induced BER intermediates are required to activate homologous directed repair pathways. Therefore, our finding suggests that BER is the first line of defense against H. pylori induced DNA damage followed by HDR, to maintain genomic integrity of gastric cells.
Citation Format: Dawit Kidane, Drew L Murphy, Joann.B Sweasy. Carcinogenic Helicobacter pylori infection induces base excision repair intermediates to trigger homologous-dependent repair in human gastric epithelial cells. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr LB-150. doi:10.1158/1538-7445.AM2013-LB-150