bluuebunny/crossref_metadata_2025_split huggingface dataset:
Abstract LB-58: Advocacy within the PS-OC: Evolution of the program
Authors: Baas Carole L. , Samson Susan 
Published: August 2012

Abstract
The National Cancer Institute (NCI) has emphasized the importance of innovation and creativity in exploring strategies to control and eradicate cancer. This effort resulted in the formation of the Physical Sciences in Oncology program (PS-OC), which utilizes the fields of mathematics, physics, chemistry and engineering to address cancer. The NCI has sponsored a network of twelve PS-OC centers across the U.S. in an effort to have a cross-sectional evaluation of the physical principles used to study cancer. The PS-OC program aims to advance cancer research and move the research closer to practical application. A key instrument to move the research into clinical practice is the voice of patient advocates on the PS-OC research team. Patient advocacy has traditionally been focused on providing support and education for patients and stimulating research for better understanding of diseases and their treatment. The inclusion of patient advocates in the physical sciences is rare as the majority of advocates work in clinically-focused research and researchers in these fields seldom interact with advocates and patients. The PS-OC program has expanded the role of patient advocates to include involvement in basic and translational research in the physical sciences. The PS-OC advocacy program is a cooperative effort between the Centers and advocate advisors, who serve as liaisons between the patient and scientific communities. Each Center is developing an advocacy program unique to its research focus and the skills and interests of the advocate community. Advocates are an integral part of the scientific team, providing insight into clinical aspects of cancer; communicating research findings to the public through public lectures, lay articles and social media; presenting the patient perspective in university courses as guest speakers; and participating in legislative advocacy. However, the most important role of advocates is to provide the human element and perspective to the research.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-58. doi:1538-7445.AM2012-LB-58
Abstract LB-59: Progressing Forward in Timely Fashion
Authors: Ford Peg 
Published: August 2012

Abstract
Peg Ford, Chair, and Kathy Hagan, Co-Chair, caregiver who lost her mother to ovarian cancer, formalized Peg's advocacy efforts in launching the Ovarian Cancer Advocacy Alliance (OCAA) of San Diego in May 2011. OCAA's Mission was formulated in three aspects of Advocacy: 1) Affect change in the way medical doctors approach diagnosis and treatment of ovarian cancer by education of the medical community, patient organizations, and the community at large to achieve early diagnosis and improved treatment options; 2) advance ovarian cancer research toward early diagnosis and improved quality of care; and 3) Address legislative issues that affect ovarian cancer care and research. From becoming a proud partner of the Ovarian Cancer National Alliance (OCNA); successfully expanding OCNA's “Survivors Teaching Students: Saving Women's Lives®” Program to Schools of Nursing; publishing articles; and actively participation in legislative actions, 2011 was a banner year. The poster reflects the continued outstanding success of the STS Program, and Peg Ford, OCAA Chair's, commitment to pursue her initiative to blossom into a voice as a Research Advocate for the ovarian cancer community on a local, state, national and international level, as a guest speaker, facilitator, or writer for community outreach efforts. Progressing forward in a timely fashion will continue to set the initiatives to strengthen Ovarian Cancer Advocacy Alliance's (OCAA) vision of patient advocates as the bridge between the patient community and the scientific/medical world, working hand-in-hand to advance research and impact changes to better serve both communities.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-59. doi:1538-7445.AM2012-LB-59
Abstract LB-64: Selective estrogen receptor modulators (SERMs) act as breast cancer chemopreventive agents by attenuating oxidative estrogen metabolism
Authors: Hemachandra L P Madhubhani P. , Choi Jaewoo , Bolotn Judy , Thatcher Gregory 
Published: August 2012

Abstract
Possibility of developing hormone dependent cancer in women will increase with long term exposure to endogenous estrogens. Estrogen induced, estrogen receptor (ER) mediated cell proliferation (hormonal pathway) and formation of reactive estrogen metabolites (chemical pathway) are believed to contribute to estrogen carcinogenesis. Estrogens are oxidized to the catechols, 2-hydroxyestradiol (2-OHE2) and 4-hydroxyestradiol (4-OHE2) by P450 1A1/1A2 and P450 1B1 respectively. Both catechols are further oxidized to form electrophilic o-quinones which can react with DNA and proteins, while 4 hydroxyestradiol O-quinone (4-OHE2-Q) is considered as the ultimate carcinogen. Selective Estrogen Receptor Modulators (SERMs) are used in cancer chemoprevention and in the treatment of post menopausal osteoporosis. The current study focuses on elucidating the influence of clinical and pre clinical benzothiophene SERMs on oxidative estrogen metabolism in ER negative non tumerigenic human breast epithelial cells (MCF-10A). Upon exposure to 17β-estradiol (E2), MCF-10A cells transformed into a malignant phenotype and showed anchorage independent colony growth in soft agar. After treatment of MCF-10A cells with E2 and SERMs, estrogen metabolites were analyzed using a sensitive LC-MS/MS method. Among the SERMs tested, raloxifene and desmethylarzoxifen (DMA) showed a significant reduction in catechol estrogen formation whereas 4′F-DMA had little effect. Furthermore, raloxifene and DMA significantly inhibited E2 induced malignant transformation and reactive oxygen species formation in MCF-10A cells. These data suggest that raloxifene and DMA possess chemopreventive activity through inhibition of genotoxic estrogen quinone formation, in addition to their action via estrogen receptors.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-64. doi:1538-7445.AM2012-LB-64
Abstract LB-65: Protein kinase Cε, which is linked to development of squamous cell carcinomas, potentiates ultraviolet radiation-induced expression of novel transcription factors GATA and PAX, which regulates expression of cell survival genes
Authors: Jamal Mohammad S. , Hafeez Bilal B. , Verma Ajit K. 
Published: August 2012

Abstract
Protein kinase C epsilon (PKCε) is among the six PKC isoforms (α, δ, ε, η, μ, ξ) expressed in both mouse and human skin. We have reported that epidermal PKCε levels dictate the susceptibility of PKCε transgenic mice (TG) to the development of squamous cell carcinomas (SCC) elicited by repeated exposures to ultraviolet radiation (UVR). Histologically, SCC in TG mice, like human SCC, is poorly differentiated and metastatic. To find clues about the mechanism by which PKCε may impart susceptibility to UVR-induced development of SCC, we compared the effects of UVR treatment of TG mice with their wildtype (WT) littermates on global transcription factors (TFs) activation profile. In this experiment, mice were exposed to UVR (2kj/m2) four times (Monday, Wednesday, Friday and Monday). At 1hr and 3hrs post last UVR exposure, these mice were sacrificed. Nuclear lysates were prepared from the scraped epidermis of these mice. To screen for unknown TFs, we employed the Panomics Combo Protein array, which contains consensus complimentary sequences of 345 TFs binding sites. Array results from samples of UVR exposed mice were directly compared to the unexposed mice. TFs that had increased over 2-fold in the UVR exposure experiments were scored as positive for activation. We observed (&gt;2-fold) activation of 70 TFs as early as 1hr post UVR exposure. Among all seventy TFs, highly activated TFs were GATA-1, GATA-2, PAX-4, PAX-6, PAX-8, Thy-1BP, HFH-2, HFH-3, HIF-1, CEA, HOXD8/9/10, AhR/Amt, and MUSF. We performed the validation of various activated TFs and among them we found that GATA and PAX families of transcription factors were found activated. UVR-induced expression level of GATA-1, GATA-2, PAX-4 was enhanced in PKCε over-expressing transgenic mice as compared to wild-type littermates. We employed the Genego program and found that VEGFR-2, CyclinD1, Bcl-2, c-Myc, BMP-4, WT1 and survivin are the downstream target genes of GATA1 and GATA-2. All of these genes are known to play role in the cell survival pathway. We have previously shown that PKCε overexpressing transgenic mice also exhibit constitutive activation of Stat3. Taken together, we conclude that PKCε-mediated activation of Stat-3, GATA-1, GATA-2 and PAX-4 may contribute to the susceptibility of PKCε transgenic mice to UVR-induced development of SCC. (Support: NIH Grant CA 35368)
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr LB-65. doi:1538-7445.AM2012-LB-65
Abstract SY09-02: Molecular mechanisms in prostate cancer in African Americans
Authors: Li Yirong , Zhang David , Ren Qinghu , Ye Fei , Daniels Garrett , Wu Xinyu , Osman Iman , Melamed Jonathan , Dynlacht Brian , Lee Peng 
Published: August 2012

Abstract
African American men have long been known to have the highest rates of prostate cancer (PCa) in the world. In addition, age adjusted mortality rates from PCa patients are two times worse among African Americans (AA) than Caucasians (CA). The reasons for the disparity in PCa risk, incidence, clinical progression, and disease-specific death are still controversial. In addition to socioeconomic and environmental factors, such as diet, access to care, and screenings, a biologically more aggressive cancer is proposed as one important explanation for the racial disparity observed in AA men. Androgens and the androgen receptor pathway are well established key regulators of aggressive PCa behavior.
Using a novel proteomic pathway analysis comparing the distinct signal pathway and network proteins different between AA and CA PCa, we identified a number of markers including stem/progenitor cell and EMT related proteins that are overexpressed in PCa among AA. Our ongoing study indicates a novel link among Notch, WNT and androgen receptor (AR) pathways.
In contrast to increase in epithelial AR, our data revealed a decrease in the expression of the stromal AR in AA PCa compared to CA PCa. Androgen and its receptor inhibit proliferation of prostate stromal cells through transcriptional suppression of cyclin B1. Mechanistically, the negative regulation of cyclin B1 by AR is mediated through switching between E2F1 and E2F4 on the promoter of cyclin B1. E2F1 binds to cyclin B1 promoter and maintains its expression and subsequent cell cycle progression in AR negative stromal cells or AR positive stromal cells under androgen depleted condition. Upon stimulation with androgen in AR positive stromal cells, E2F1 is displaced from the binding site by AR and replaced with E2F4, leading to recruitment of the SMRT/HDAC3 co-repressor complex and repression of cyclin B1. Furthermore, the switch between E2F1 and E2F4 at the E2F binding site of the cyclin B1 promoter coincides with an androgen-dependent interaction between AR and E2F1 as well as cytoplasm to nucleus translocation of E2F4.
In summary, our study revealed an association between distinct epithelial and stromal AR expression and PCa racial disparity as well as the molecular mechanism involved in regulating AR expression in epithelial and stromal prostate cells.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr SY09-02. doi:1538-7445.AM2012-SY09-02
Abstract SY10-03: Cell of origin in pediatric medulloblastomas
Authors: Kawauchi Daisuke , Robinson Giles , Uziel Tamar , Elisson David W. , Gilbertson Richard J. , Roussel Martine F. 
Published: August 2012

Abstract
Medulloblastoma is the most common malignant brain tumor in children with a median age of 3 to 7 years old. Human medulloblastomas are molecularly classified into four major subgroups including two with constitutive activation of developmental signaling pathways Sonic Hedgehog/Patched defining the SHH-subgroup and Wnt for the WNT-subgroup, subgroup 3 with amplification or overexpression of c-MYC and subgroup 4 with as yet undefined genetic anomalies. To date, all medulloblastomas regardless of their subgroup are treated with the same therapeutic regimen with different outcome. If children with WNT-subgroup tumors fair well, those with subgroup 3 medulloblastoma, the most aggressive form of the disease have a dismal prognosis.
Most mouse models of medulloblastoma developed to date mimic the human SHH-subgroup. However, we recently developed two new mouse models that faithfully recapitulate the human WNT-subgroup and subgroup 3 (MYC). The SHH-subgroup and subgroup 3 medulloblastomas were derived from cerebellar granule progenitors in the external granule layer which sustain mutations in the SHH pathway associated with MYCN overexpression, or C-MYC amplification, respectively. In contrast, the WNT-subgroup medulloblastoma with mutations in β-Catenin originate from the lower rhombic lip, the germinal neuroepithelium surrounding the floor of the 4th ventricle, suggesting that each subgroup may originate from specific neuronal precursors within the developing cerebellum.
Mouse subgroup 3 medulloblastomas, but not SHH- or WNT-subgroup tumors can be passaged indefinitely as neurospheres that express markers characterizing stem cells, including Lgr5, Oct4, Nanog, and Sox2 and induce secondary medulloblastomas with similar characteristics as the primary tumors, after orthotopic transplant into the cortices of recipient mice.
These novel medulloblastoma mouse models should significantly advance our efforts to develop new therapeutic modalities for this deadly childhood cancer.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr SY10-03. doi:1538-7445.AM2012-SY10-03
Abstract SY12-02: Epstein-Barr virus (EBV) and cancer: Opportunities for etiologic research and prevention
Authors: Hildesheim Allan 
Published: August 2012

Abstract
Infections are known to cause approximately one in every five cancers. Helicobacter pylori (H. pylori), human papillomavirus (HPV), and hepatitis (B & C) infections each account for approximately 5% of cancers each year. Understanding the role of these infections in cancer etiology has led to numerous promising approaches to primary and secondary prevention, including prophylactic vaccination (HPV & HBV), screening (HPV), and treatment (H. pylori & HCV). EBV is a ubiquitous infection that establishes lifelong latency. Infection with EBV has been shown to be linked to the development of a subset of various forms of lymphoma, nasopharyngeal carcinomas, salivary gland cancers, and gastric cancers, totaling approximately 200,000 new cases each year worldwide. In addition, in countries where first infection with EBV tends to occur in late childhood or early adulthood, EBV is responsible for infectious mononucleosis (150,000 cases per year in the US alone), a condition that is typically benign but associated with prolonged morbidity. Despite our knowledge that EBV is associated with the development of various cancers, little attention has been placed to date on potential measures to prevent diseases associated with this common infection. In this presentation, our understanding of the link between EBV infection and cancer is summarized, and the potential for applying our knowledge to cancer prevention efforts discussed.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr SY12-02. doi:1538-7445.AM2012-SY12-02
Abstract SY13-02: In vivo cancer theranostics
Authors: Pomper Martin G. 
Published: August 2012

Abstract
A theranostic agent enables diagnosis and treatment concurrently. Although a relatively new concept to pharmaceutics, theranostics have been used in nuclear medicine for over 50 years - dating back to the iodine-131 thyroid scan. Today we most frequently associate theranostics with nanotechnology since nanomedicines tend to present an appropriate platform for complex, multifunctional capability such as simultaneous or sequential imaging and therapy. Unlike low molecular weight agents, nanomedicines can carry sufficient information to enable local control of imaging and therapeutic species. But not all theranostics are nanomedicines - they may also be multifunctional genes or suitably functionalized small molecules or serve as biomarkers themselves. Introduction to theranostics with examples of existing and emerging theranostic agents as well as their clinical potential and application will be discussed.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr SY13-02. doi:1538-7445.AM2012-SY13-02
Abstract SY13-03: Molecular imaging for advanced practice in oncology
Authors: Larson Steven M. 
Published: August 2012

Abstract
Positron Emission Tomography (PET) with 2-flouro-2-D-oxyglucose (FDG) has been the poster child for MI and several million studies are performed for oncology indications in the US alone. FDG takes advantage of the Warburg effect, which is the aerobic glycolysis that is a common feature of many malignant tumors. The incorporation of high resolution CT into the same gantry with a high resolution PET scanner, has given a further boost to PET imaging of tumors and in fact, PET CT is the most rapidly growing clinical imaging modality in the US today. Tumors for which staging, monitoring treatment response are common place include, Lung, Lymphoma, Thyroid, head and neck, melanoma, colorectal cancers.
But MI with PET/CT is potentially much more than FDG PET imaging, and several 100 tracers for specific molecular imaging have been developed in the last decade. Examples include amino acid tracers, like F-18 FACBC, nucleoside analogs, like F-18 FLT, and Na 124I to imaging iodide metabolism, Androgen receptor imaging (AR) with F-18 FDHT, and Estrogen receptor imaging with F-18 FES. In addition to small molecules, positron emitting tracers like 124I-, 68 Ga and 89 Zr are widely used for radiolabeling of antibodies and peptides, opening the entire universe of ligand receptor binding for human tumors. Radiolabeled drugs are being developed and examples include F-18 desatinib, a src family tyrosine kinase inhibitor and 124I-PUH71, a heat-shock protein 90 inhibitor. These radiolabeled drugs should facilitate the study of intratumoral pharmacology of human cancers. In addition radiolabeled nanoparticles are being developed and promise specialized targeting properties, and to serve as carriers for drugs to improve therapeutic index. In summary, MI with PET is rapidly evolving as a major frontier for development of the knowledge of tumor biology and pharmacology needed to optimize treatment of the individual oncology patient.
References
Schoder H, Grimm J and Larson SM: Molecular Imaging Section 6 in DeVita VT Lawrence TS and Rosenberg SA: Cancer Principles and Practice of Oncology 8th Edition Volume 1 p 746
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr SY13-03. doi:1538-7445.AM2012-SY13-03
Abstract SY14-02: p53-mediated senescence impairs the apoptotic response to chemotherapy in breast cancer
Authors: Lozano Guillermina , Jackson James G. 
Published: August 2012

Abstract
Studies on the role of p53 mutation in human breast cancer response to chemotherapy are controversial. Using MMTV-Wnt1 murine breast tumor model, we show that tumors with mutant p53 exhibited a superior clinical response compared to tumors with wild-type p53. Doxorubicin treated p53-mutant tumors failed to arrest proliferation leading to abnormal mitoses and cell death, while p53 wild-type tumors underwent arrest and senescence with expression of senescence-associated cytokines that led to autocrine/paracrine activity and mitogenic potential. Wild-type p53 could still mediate arrest and inhibit drug response even in the context of a heterozygous p53 point mutation or absence of p21. Thus, we show wild-type p53 activity hinders chemotherapy response and demonstrate the need to reassess the paradigm for p53 in cancer therapy.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr SY14-02. doi:1538-7445.AM2012-SY14-02
Abstract SY17-01: Intratumor diversity in breast cancer
Authors: Polyak Kornelia 
Published: August 2012

Abstract
Tumor heterogeneity is a major challenge toward understanding and clinical management of cancers. Intratumor diversity for hereditary traits is the diver of tumor evolution including disease progression and therapeutic resistance. We have been investigating intratumor genetic and phenotypic heterogeneity during breast tumor progression and treatment. We found high degree of genetic and phenotypic heterogeneity within and between distant metastases of the same patient. The degree of intratumor heterogeneity was influenced by treatment and it was associated with clinical characteristics. We also characterized the dependency of distinct cell populations in human breast tumors on specific genes and signaling pathways by performing a large-scale loss-of-function screen. Using this approach, we identified genes required for cell growth or proliferation in specific subsets of breast cancer cells. Our results highlight the differences between distinct breast cancer cell types and identify cell type-specific targets that may lead to more effective breast cancer therapies.
Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr SY17-01. doi:1538-7445.AM2012-SY17-01