tbuckley/cabot-search huggingface dataset:
A phase III randomized trial of metformin versus placebo on recurrence and survival in early-stage breast cancer (BC) (NCIC Clinical Trials Group MA.32).
Authors: W. Parulekar, B. E. Chen, C. Elliott, L. E. Shepherd, K. A. Gelmon, K. I. Pritchard, T. J. Whelan, J. A. Ligibel, D. L. Hershman, I. A. Mayer, T. J. Hobday, P. Rastogi, J. Lemieux, P. A. Ganz, V. Stambolic, P. J. Goodwin
Journal: Journal of Clinical Oncology (2011)

TPS103 Background: There has been a recent convergence of epidemiologic, clinical and preclinical evidence suggesting metformin (a biguanide used to treat type 2 diabetes) may lower BC risk and improve BC outcomes. This evidence raises the intriguing possibility that metformin may act (i) indirectly by lowering circulating insulin levels (secondary to reduced hepatic gluconeogenesis) leading to reduced insulin/IGF-I receptor mediated PI3K signaling in BC cells or (ii) directly on tumor cells, largely via an AMPK mediated mechanism, leading to mTOR inhibition. Methods: NCIC CTG led, CTEP sponsored, randomized, phase III trial of metformin 850 mg po bid vs placebo bid for 5 years. Eligibility criteria: pTIcNO (and > one: grade 3, ER/PR-, HER2Neu+, lymphovascular invasion, Oncotype DX recurrence score>25, Ki67>14%) or pT2/T3 N0 or pT1-3 N1-3. Standard adjuvant therapy (chemotherapy, hormone, biologics) Adequate organ function and PS Age 18-75 Endpoints: Primary: invasive disease free survival (IDFS). Secondary: overall survival, distant disease free survival, BC free survival, adverse events, new diabetes, cardiovascular hospitalizations, BMI, insulin resistance syndrome attributes (ATP III criteria), Quality of Life, diet and physical activity. Correlative studies: Embedded correlative research examines prognostic factors and targets and predictors of metformin benefit.Variables include: Fasting Insulin, glucose, Homeostasis Model Assessment (HOMA) (baseline, 6 months, end of treatment): genomic/gene expression analysis of blood and tumour, tumor insulin receptor (IR), IGF-IR, tumor molecular markers of target pathways (LKBI, PI3K (STMN1), PKB/Akt (P-PKB/Akt,) mTOR (P-4E-BP1) and IRS-1 (P-IRS-1); Fatigue sub-study with biological correlates (NSABP led). Statistical design: Planned accrual is 3,582 subjects over 3 years with 3 more years follow-up. Target hazard ratio is 0.76 (5 year IDFS of 88.4% vs 85%, power 0.80, 2-tail type 1 error of 0.05). Two interim analyses are planned. Conduct to Date: Study activation: June 2010. Enrollment: 145 subjects. In Nov 2010 a DSMC review supported trial continuation.
SNP-Arrays: a Routine Cytogenetic Tool In Chronic Lymphocytic Leukemia ?.
Authors: Alban Godon, Franck Genevieve, Malgorzata Truchan-Graczyk, Laurence Baranger, Virginie Eclache, Anne Coutolleau, Norbert Ifrah, Marc Zandecki, Philippe Guardiola
Journal: Blood (2010)
Fecal microbiota transplant in severe and severe-complicated<i>Clostridium difficile</i>: A promising treatment approach
Authors: Monika Fischer, Brian Sipe, Yao-Wen Cheng, Emmalee Phelps, Nicholas Rogers, Sashidhar Sagi, Matthew Bohm, Huiping Xu, Zain Kassam
Journal: Gut Microbes (2016)

Severe and severe-complicated Clostridium difficile infection (CDI) is associated with high morbidity and mortality. Colectomy is standard of care; however, post-surgical mortality rates approach 50%. Case reports suggest fecal microbiota transplant (FMT) is a promising treatment of severe and severe-complicated disease but there is a paucity of data. Here, we present a single center experience with a novel sequential FMT protocol for patients refractory to maximal medical therapy. This approach consists of at least one FMT delivered via colonoscopy with criteria for repeat FMT and continued vancomycin therapy based on clinical response and pseudomembranes. Our cohort included 57 consecutive inpatients diagnosed with severe or severe-complicated CDI and treated with FMT. Overall, 91% (52/57) experienced clinical cure at 1 month with a 100% cure rate among severe CDI (n = 19) patients and an 87% cure rate for severe-complicated CDI (n = 33) patients. For the cohort, the survival rate was 94.7% at 1 month and 78.6% at 3 months. There were no serious adverse events related to FMT including no procedure-related complications or perforation. There was no difference in outcome between fresh or frozen fecal material. Sequential FMT for inpatients with severe or severe-complicated CDI is promising and may be preferred over colectomy in certain patients.
Abstract 1517: G0-like cells support an oral cancer stem cell pool by transitioning to a JARID1B-high state
Authors: Nicole Facompre, Zachary Belden, Phyllis Gimotty, Anil Rustgi, Meenhard Herlyn, Hiroshi Nakagawa, Devraj Basu
Journal: Cancer Research (2015)

Abstract Oral squamous cell carcinomas (OSCCs) likely contain a subset of tumor cells whose stem cell-like molecular and functional properties help sustain tumor growth. There is growing evidence that this cancer stem cell (CSC) pool exists in dynamic equilibrium with other subpopulations with tumorigenic potential. To characterize this plasticity in OSCC, we examined the developmental potential of tumor cells in a “G0-like” cell state previously shown to have high growth capacity and innate drug resistance in other tumor types. G0-like cells in OSCC exhibited hallmark molecular traits of low reactive oxygen species (ROS), high Hes1, and low total Akt levels. However, despite lacking high levels of CD44 and other stem cell markers, they prominently displayed stem cell-like functional properties of in vitro sphere formation and in vivo tumorigenicity. To evaluate the contribution of G0-like cells to the oral CSC pool, a GFP reporter system was used to isolate CSCs based on high expression of JARID1B, an H3K4me3 demethylase associated with multiple normal and malignant stem cell phenotypes. JARID1B-high OSCC cells were distinct from the G0-like subset, highly expressed CD44 and ALDH1, and possessed both molecular and functional CSC traits. Silencing JARID1B expanded the G0-like subset but abrogated its functional CSC properties, suggesting these cells mediate such functions by returning to a JARID1B-high CSC state. The G0-like and JARID1B-high subsets were further distinguished by widely disparate levels of PI3-kinase pathway activation, which corresponded to distinct responses to cytotoxic and targeted therapies. These findings reveal a JARID1B-mediated mechanism underlying a contribution of G0-like cells to a CSC pool. Further they may provide a novel basis for OSCC therapy by simultaneously targeting the CSCs and a subset G0-like cells that appear uniquely primed to return to a CSC state. Citation Format: Nicole Facompre, Zachary Belden, Phyllis Gimotty, Anil Rustgi, Meenhard Herlyn, Hiroshi Nakagawa, Devraj Basu. G0-like cells support an oral cancer stem cell pool by transitioning to a JARID1B-high state. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1517. doi:10.1158/1538-7445.AM2015-1517
Abstract 350: HER3 mediates acquired resistance to HER2-targeted therapy in esophageal adenocarcinoma
Authors: Eva A. Ebbing, Jan Paul Medema, Sybren L. Meijer, Kausilia K. Krishnadath, Mark I. van Berge Henegouwen, Maarten F. Bijlsma, Hanneke W. M. van Laarhoven
Journal: Cancer Research (2015)

Abstract Esophageal adenocarcinoma is an aggressive malignancy and its incidence is rapidly increasing. Despite multimodality treatment, patients face a poor 5-year survival of 15-25%, underscoring the urgency to improve treatment strategies. Receptor tyrosine kinases of the HER-family are involved in the development and progression of multiple epithelial tumors, and have consequently become widely used targets for the development of new anti-cancer therapies. Trastuzumab, an antibody against HER2, has shown potent growth inhibitory effects on HER2 overexpressing tumors, including gastro-esophageal cancer, however, resistance to this therapy is inevitable. Unfortunately, a paucity of data on cellular mechanisms of resistance to targeted therapeutic agents exist in esophageal adenocarcinoma. In order to study the effect of HER2 inhibition in vitro and in vivo, we established unique primary cultures of esophageal adenocarcinoma and patient-derived xenograft models. Using these novel tools, we demonstrate a conserved, hard-wired mechanism in which HER3 is upregulated upon trastuzumab-induced resistance in esophageal adenocarcinoma. Furthermore, blocking upregulated HER3 effectively resulted in a strong decrease in cell viability and induced cell death. Taken together, our data provide preclinical insight that strategies targeting HER3 in combination with trastuzumab could possibly prevent acquired resistance. Citation Format: Eva A. Ebbing, Jan Paul Medema, Sybren L. Meijer, Kausilia K. Krishnadath, Mark I. van Berge Henegouwen, Maarten F. Bijlsma, Hanneke W. M. van Laarhoven. HER3 mediates acquired resistance to HER2-targeted therapy in esophageal adenocarcinoma. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 350. doi:10.1158/1538-7445.AM2015-350
Preferential Hypermethylation of the DKK-1 Promoter in Core-Binding Factor Leukaemia.
Authors: Rikio Suzuki, Makoto Onizuka, Minoru Kojima, Masako Shimada, Satomi Fukagawa, Kosuke Tsuboi, Hiroyuki Kobayashi, Ayumi Shintani, Yoshiaki Ogawa, Hiroshi Kawada, Tomomitsu Hotta, Kiyoshi Ando
Journal: Blood (2007)
Abstract 5678: Fast-Fast Form of Atypical AV Nodal Reentrant Tachycardia: Incidence, Electrophysiological Characteristics and Results of Catheter Ablation
Authors: Kiyoshi Otomo, Yasutoshi Nagata, Hiroshi Tachiguchi, Kikuya Uno, Hideomi Fujiwara, Yoshito Iesaka
Journal: Circulation (2008)

Both the typical (slow-fast (S/F)) and atypical (slow-slow (S/S) and fast-slow (F/S)) forms of the AV nodal reentrant tachycardias (AVNRT) are usually amenable to the classical slow pathway (SP) ablation at the inferoseptal atrial region. However, rare cases of unusual forms AVNRT do not involve an SP in the tachycardia circuits (TC), and they are resistant to the classical SP ablation. The characteristics of the atypical AVNRTs not involving an SP in the TCs remain to be elucidated. A total of 1252 AVNRTs induced during the electrophysiological study in 950 cases were analyzed. Both the anterograde and retrograde limbs of the TC were classified into the fast pathway (FP) or SP according to the A-H (AHI) and H-A intervals (HAI) during the tachycardia; the anterograde FP: AHI of &lt;220 ms, anterograde SP: AHI of ≥220 ms, retrograde FP: HAI of &lt;120 ms, and retrograde SP: HAI of ≥120 ms. Accordingly, each tachycardia was classified into one of the S/F, S/S, F/S and fast-fast (F / F) forms . There were 998 S/F forms (79.7%), 119 S/S forms (9.5%), 129 F/S forms (10.3%) and 6 F / F forms (0.5%). The F / F forms were induced by atrial or ventricular extrastimulation without an associated jump-up in the AHI and HAI, and they were characterized by a shorter tachycardia cycle length (260±55 ms), short AHI (153±39 ms) and HAI (107±19 ms) during the tachycardia, earliest retrograde atrial activation (ERAA) at the right superoseptum (n=2) or midseptum (n=4), and 2nd degree AV block without a tachycardia interruption. The retrograde atrial activation sequence during the F / F forms was identical to that during ventricular pacing. The tachycardias could be entrained from the RV, and they resumed with a V-A-V sequence after the cessation of the entrainment pacing. The classical SP ablation at the right inferoseptal region was unsuccessful in all 6 cases with the F / F forms . The successful ablation was achieved at the right superoseptum (n=2) or midseptum (n=4) without creating AV block in all 6 cases. The F / F forms of atypical AVNRT not involving a classical SP in the TC were observed in 0.5% of all AVNRT cases. The results of this study suggested that the TC was smaller and confined to the superior part of the AV nodal area in this extremely rare form of AVNRT.
PO27IDH1 MUTATIONS COMPROMISE THE ADAPTIVE RESPONSE TO HYPOXIA
Authors: Kate E.R. Hollinshead, Christian Ludwig, Seth J. Parker, Christian M. Metallo, Susan E. Critchlow, Garth S. Cruickshank, Daniel A. Tennant
Journal: Neuro-Oncology (2015)

INTRODUCTION: The recent identification of recurrent heterozygous somatic mutations in the isocitrate dehydrogenase (IDH1) gene in low-grade gliomas and secondary glioblastoma, provides a much-needed advance in our understanding of the drivers of these tumours. Patients with this mutation are generally younger and have improved prognosis. Mutations in IDH1 occur at an arginine residue at codon 132 (R132) and result in production of the putative oncometabolite - (R)-2-hydroxyglutarate (2HG). (R)-2HG production has subsequently been shown to induce changes in DNA and histone methylation. However, there are conflicting reports regarding the metabolic role of IDH1 mutations and subsequent production of (R)-2HG in hypoxia, which are yet to be reconciled. METHOD: To define the hypoxic metabolic phenotype of IDH1 mutations, we applied complementary techniques - gas chromatography mass spectrometry (GC-MS), and nuclear magnetic resonance (NMR) spectroscopy to probe differences in the metabolic adaptation to hypoxia using [13C6]-glucose and [13C5]-glutamine tracers. RESULTS: Employing a human oligodendroglioma (HOG) cell line model, infected with mutant IDH1 by lentivirus, we show that IDH1 mutations metabolically compromise the adaptation to hypoxia, despite observable HIF1alpha stabilisation. CONCLUSION: We hypothesise that the adaptive transcriptional responses of hypoxia is blunted in IDH1 mutants resulting in the inability ofHIF1alpha to fully regulate downstream targets and ultimately cell metabolism. These results may account for the improved prognosis associated with this subset of glial tumours. Increasing our understanding of metabolic redundancies in tumour cells will aid the development of more effective treatments.
17-allylaminogeldanamycin in advanced medullary and differentiated thyroid carcinoma.
Authors: J. F. Moley, D. Adkins, K. C. Bible, A. M. Traynor, J. R. Molina, G. Colon-Otero, T. J. Pluard, M. H. Shah, R. Suresh, C. Erlichman, S. P. Ivy, V. Suman, S. M. Geyer, P. M. Fracasso, M. S. Cohen, H. Tang, E. Fialkowski, A. Traugott, R. C. Smallridge
Journal: Journal of Clinical Oncology (2011)

5582 Background: 17-allylaminogeldanamycin (17-AAG) is a benzoquinone ansamycin antibiotic that destabilizes heat shock protein 90 (HSP-90) complexes, including RET and multiple cancer-involved proteins. 17-AAG promotes apoptosis and down-regulates RET in thyroid cancer cell lines. Methods: Two one-stage phase II clinical trials were conducted to assess whether the 1 year (yr) treatment failure-free (TFF) rate with 17-AAG was at least 20% in patients (pts) with locoregionally advanced/metastatic MTC or in pts with DTC. Eligibility criteria included: measurable disease by RECIST criteria; ECOG status 0-2; adequate laboratory values, no significant cardiac disease, and no active CNS metastases. 17-AAG dosing was 220 mg/m2 IV over 2 hours (days 1, 4, 8, and 11 of a 21-day cycle). Treatment was discontinued for disease progression, unacceptable toxicity or refusal. If 4 or more of 33 pts in a given cohort remained on treatment at 1 yr, 17-AAG would be considered promising in that cohort. Both trials were discontinued due to slow accrual. Results: 41 pts were enrolled (Table). All pts were followed until death or a minimum of 13 months. The median number of cycles administered was 7 for MTC and 4 for DTC. Severe (≥grade 3) toxicities possibly related to treatment occurred in 4 MTC pts and 9 DTC pts, the most common being grade 3 AST/ALT elevations. Reasons for discontinuation were: disease progression (MTC:10; DTC:8); refusal (MTC:4; DTC:2); toxicity (MTC:2; DTC:3); desire for surgery (DTC:1); or death (MTC:1). 1 MTC and 3 DTC completed one year of treatment. 1 MTC pt had a partial response. 15 pts (10 DTC) died within one year of entry. Conclusions: 17-AAG appears to have only modest single agent activity in advanced MTC and DTC. Supported by NCI N01-CM62205. Patient characteristics MTC (n=17) DTC (n=24) Median age (range) 56 (33-70) 61 (34-80) Male 70.6% 54.2% Prior radiation therapy 47.1% 95.8% Prior systemic therapy 41.2% 41.7% Stage at study entry: < IV IV Not specified 11.8% 88.2% 0% 12.5% 75.0% 12.5% Dominant disease sites: Nodes Lungs Liver 88.2% 64.7% 52.9% 70.8% 62.5% 0% Median survival (months): Progression free Overall 6.4 25.1 4.2 17.8 1-year TFF rate (90% CI) 5.9% (0.3-25.0%) 12.5% (3.5-29.2%)
First-in-human study with ARQ 621, a novel inhibitor of Eg5: Final results from the solid tumors cohort.
Authors: L. C. Chen, L. S. Rosen, T. Iyengar, J. W. Goldman, R. Savage, J. Kazakin, T. C. K. Chan, B. E. Schwartz, G. Abbadessa, D. D. Von Hoff
Journal: Journal of Clinical Oncology (2011)

3076 Background: ARQ 621 is an allosteric, potent and selective inhibitor of Eg5, a microtubule-based ATPase motor protein involved in cell division. Over-expression of Eg5 causes genomic instability and tumor formation in mice; therefore, Eg5 is a potential anti-cancer target. Preclinical data shows anti-tumor activity of ARQ 621 across a wide range of cell lines from human solid and hematological malignancies. We present here safety, pharmacokinetics (PK), and preliminary activity of ARQ 621 in patients with solid tumors. Methods: Patients (pts) were enrolled into this multi-cohort phase I trial at the initial intravenous dose of 10 mg/m2/week. Drug was administered over 1-2 hours weekly. Cohorts of 3 or 6 patients were based on a 3+3 dose escalation schedule. Dose was increased according to a modified Fibonacci scheme. Treatment continued until disease progression or unacceptable toxicity. Results: The bone marrow toxicity and DNA damage seen with other Eg5 inhibitors were not evident with ARQ 621. As of January 20, 2011, 48 pts (22 male; median age 60.5 yrs, ECOG PS 0 [N=11], PS 1 [N=36], PS 2 [N=1]) with solid tumors were enrolled. The most common tumors in enrolled pts were colorectal (N=11), pancreatic (N=5) and breast (N=4). Treatment-emergent adverse events (TEAEs) were reported in 47 (95.9%) pts. The most common (> 10%) include fatigue 17 (34.7%), nausea 12 (24.5%), anemia 11 (22.4%), and vomiting 10 (20.4 %). Sixteen pts experienced 27 serious AEs (including anemia, sepsis, pneumonia, pleural effusion, DVT). SAEs considered at least possibly drug related were fatigue, acute intravascular hemolysis, abdominal pain (at 400 mg/m2/wk) and DVT (at 140 mg/m2/wk). Two cases of transient neutropenia were reported at 400mg/m2/wk. The next lower dose of 280mg/m2/wk was deemed to be the recommended phase 2 dose. Six pts (cholangiosarcoma, liposarcoma, leiomyosarcoma, cervical, carcinoid, colorectal carcinoma) remained stable for > 4 months. Conclusions: ARQ 621 appears well tolerated at the weekly dose of 280mg/m2. The dose and frequency are higher than those reported with other Eg5 inhibitors.
Comparative Analysis of Aberrant Autophagy in HAX1-Mutated and ELANE/ELA2-Mutated Neutrophil Granulocytes.
Authors: Giridharan Appaswamy, Kaan Boztug, Rebecca Elisabeth Rittner, Gudrun Brandes, Karl Welte, Cornelia Zeidler, Christoph Klein
Journal: Blood (2009)
Phase I Trial Results Testing Adoptively Transferred T Cells Expressing CD20-Specific Chimeric Antigen Receptors Containing CD28 and CD137 Costimulatory Domains In Patients with Mantle Cell Lymphoma and Indolent Lymphoma
Authors: Brian G. Till, Michael C. Jensen, Xiaojun Qian, Jinjuan Wang, Ajay K Gopal, David G. Maloney, Catherine G. Lindgren, Yukang Lin, John M. Pagel, Lihua E Budde, Andrew Raubitschek, Stephen Forman, Philip Greenberg, Stanley R. Riddell, Oliver W. Press
Journal: Blood (2010)
The DART Study: Results from the Dose-Escalation and Expansion Cohorts Evaluating the Combination of Dalantercept plus Axitinib in Advanced Renal Cell Carcinoma
Authors: Martin H. Voss, Rupal S. Bhatt, Elizabeth R. Plimack, Brian I. Rini, Robert S. Alter, J. Thaddeus Beck, Dawn Wilson, Xiaosha Zhang, Musa Mutyaba, Chad Glasser, Kenneth M. Attie, Matthew L. Sherman, Shuchi S. Pandya, Michael B. Atkins
Journal: Clinical Cancer Research (2016)

Purpose: Activin receptor-like kinase 1 (ALK1) is a novel target in angiogenesis. Concurrent targeting of ALK1 and VEGF signaling results in augmented inhibition of tumor growth in renal cell carcinoma (RCC) xenograft models. Dalantercept is an ALK1-receptor fusion protein that acts as a ligand trap for bone morphogenetic proteins 9 and 10. The DART Study evaluated the safety, tolerability, pharmacokinetics, pharmacodynamics, and antitumor activity of dalantercept plus axitinib in patients with advanced RCC and determined the optimal dose for further testing.Experimental Design: Patients received dalantercept 0.6, 0.9, or 1.2 mg/kg subcutaneously every 3 weeks plus axitinib 5 mg by mouth twice daily until disease progression or intolerance.Results: Twenty-nine patients were enrolled in the dose escalation (n = 15) and expansion (n = 14) cohorts. There were no dose-limiting toxicities or grade 4/5 treatment-related adverse events. In addition to common VEGFR tyrosine kinase inhibitor effects, such as fatigue and diarrhea, commonly seen treatment-related adverse events were peripheral edema, epistaxis, pericardial effusion, and telangiectasia. The objective response rate by RECIST v1.1 was 25% with responses seen at all dose levels. The overall median progression-free survival was 8.3 months.Conclusions: The combination of dalantercept plus axitinib is well tolerated and associated with clinical activity. On the basis of safety and efficacy results, the 0.9 mg/kg dose level was chosen for further study in a randomized phase II trial of dalantercept plus axitinib versus placebo plus axitinib. Clin Cancer Res; 23(14); 3557-65. ©2016 AACR.
Abstract 1578: Identification of type X collagen as a pan-cancer serum biomarker
Authors: Maria J. Prendes, Karen B. Chapman, Orlena Tam, Joseph Wagner
Journal: Cancer Research (2015)

Abstract We previously reported elevated expression of Type X Collagen (COL10A1) in solid tumors of diverse origin (Future Oncology 2012 Aug;8(8): 1031-40). This elevated expression in tumors was primarily localized to vasculature, while COL10A1 expression in most adult tissues was negligible. Given this pattern of expression, we hypothesized that COL10A1 might demonstrate utility as a blood-born tumor biomarker. Serum samples from healthy volunteers and from patients with active cancers of the breast, lung, pancreas, colon, kidney, and bladder were obtained from multiple existing bio-banks. COL10A1 serum levels were assessed in over 400 total patient samples using a polyclonal COL10A1 sandwich ELISA. The overall utility of COL10A1 levels in determining presence of cancer was judged by calculating ROC-AUC scores for each individual cancer type. In general, COL10A1 levels were increased in cancer patients, although this increase varied as a function of cancer type as well as by the bio-bank the sera was obtained from. Given the sensitivity and specificity limitations of polyclonal ELISA technology, even greater performance of COL10A1 as a tumor biomarker could be attainable using high-specificity monoclonal antibodies. We are currently characterizing such tests in prospectively collected sera samples from breast cancer patients. These data suggest that COL10A1 is a potential blood-born pan-cancer biomarker that could prove useful in non-invasive cancer screening as well as in monitoring tumor progression and treatment response. Citation Format: Maria J. Prendes, Karen B. Chapman, Orlena Tam, Joseph Wagner. Identification of type X collagen as a pan-cancer serum biomarker. [abstract]. In: Proceedings of the 106th Annual Meeting of the American Association for Cancer Research; 2015 Apr 18-22; Philadelphia, PA. Philadelphia (PA): AACR; Cancer Res 2015;75(15 Suppl):Abstract nr 1578. doi:10.1158/1538-7445.AM2015-1578