tbuckley/cabot-search huggingface dataset:
Exonic expression variations of EGFR and KRAS in small bronchoscopic biopsies from patients with advanced non-small cell lung cancer treated by combined bevacizumab/erlotinib therapy followed by platinum-based chemotherapy at disease progression: A multicenter phase II trial SAKK19/05.
Authors: M. H. Brutsche, M. Frueh, S. Crowe, K. J. Na, C. Droege, D. C. Betticher, R. von Moos, F. Zappa, M. Pless, L. Bubendorf, F. Baty
Journal: Journal of Clinical Oncology (2011)

10570 Background: The Swiss Group for Clinical Cancer Research (SAKK) investigated the activity of bevacizumab/erlotinib (BE) in 101 treatment-naïve non-squamous stage IIIB and IV non-small cell lung cancer (NSCLC) patients in a single arm phase II trial (SAKK 19/05). We explored the effect of BE focusing on the exon intensity levels of EGFR and KRAS, a target and a prognostic gene, in these patients. Methods: The genome-wide exon expression level of 42 bronchoscopic biopsies was investigated using Affymetrix exon arrays. Unsupervised multivariate approaches, including principal component analysis (PCA) and hierarchical clustering were used to describe the exonic variations within EGFR and KRAS among patients having various EGFR/KRAS mutational status. All analyses were blinded for the mutational status and clinical outcome. Results: All probe sets measured within EGFR (n=451) and KRAS (n=261) were extracted for the purpose of the analysis. Fifty-one and 11 exonic probe sets were available within EGFR and KRAS respectively. PCA revealed a gradient of expression among patients which was homogeneous among different EGFR exons (average within-patient coefficient of variation=0.28), whereas more complex exonic variations were found within KRAS (average within-patient coefficient of variation=0.43). In contrast to KRAS, there was a trend showing an association between gender and the expression of EGFR (p=0.06). Conclusions: Using exon arrays, it was possible to assess the exonic expression level of 2 key genes involved in non-squamous NSCLC growth pathways. EGFR expression level was homogeneous among exons, advocating independence between the exon intensity level and the patient mutational status. Conversely, KRAS showed a significantly larger within-patient variation in the exonic expression level. We hypothesize that the exonic heterogeneity within KRAS provides additional prognostic information complementary to the patients’ mutational status. These results will be provided after the unblinding of the trial.
Clinical Impact of WT1 Mutations in the Context of Other Molecular Markers in Cytogenetically Normal Acute Myeloid Leukemia (AML): A Study of the German-Austrian AML Study Group (AMLSG).
Authors: Verena I. Gaidzik, Marianne Habdank, Simone Moschny, Silja Groner, Daniela Spath, Jurgen Krauter, Brigitte Schlegelberger, Arnold Ganser, Hartmut Dohner, Richard F. Schlenk, Konstanze Dohner
Journal: Blood (2007)
Antibiotics and Obesity—A Burgeoning or Thinning Argument?
Authors: Frank I. Scott, Ronac Mamtani
Journal: JAMA Pediatrics (2016)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA Pediatrics HomeNew OnlineCurrent IssueFor Authors Podcast Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA Pediatrics journal
Reduced Relapse and Similar Progression-Free Survival After Double Umbilical Cord Blood Transplantation (DUCBT): Comparison of Outcomes Between Sibling, Unrelated Adult and Unrelated DUCB Hematopoietic Stem Cell (HSC) Donors.
Authors: Claudio G. Brunstein, Jonathan A Gutman, Todd E. DeFor, Ted Gooley, Michael R Verneris, Ann Woolfrey, Daniel J. Weisdorf, Frederick R Appelbaum, John E. Wagner, Colleen Delaney
Journal: Blood (2009)
202. pMNTC Is a Cone-Specific Regulatory Cassette Designed To Treat Cone-Associated Disorders
Authors: Maureen Neitz, Jay Neitz, Adam C. Crain, Christopher L. Chavez, Elizabeth Alcamo, Sharmila Vijay, Trevor Kniffin, Elham Moradi, Ming Ni, Kathryn W. Woodburn, Thomas W. Chalberg
Journal: Molecular Therapy (2015)

New therapies are needed for the treatment of many cone photoreceptor associated disorders, including macular dystrophies such as cone-rod dystrophy, progressive cone dystrophy, Stargardt macular dystrophy, and achromatopsia. As these vision disorders are associated with a loss of function and/or viability of the cone photoreceptors, it is hypothesized that these disorders may be treatable by delivering a therapeutic gene to cone photoreceptors to rescue cone viability and function. To optimize efficient expression in cone cells, the regulatory cassette "pMNTC" was designed in which enhancer, promoter, 5'UTR, intron, Kozak, and polyadenylation sequences were optimized for cone-specific expression. pMNTC-directed transgene expression was evaluated in a number of species with varying numbers of retinal cones cells among total photoreceptors, including mouse (3% cones), rat (1% cones), gerbil (13% cones), and nonhuman primate (5% cones). pR2.1, a well-characterized cone-specific promoter, was used as a control. AAV vectors carrying a reporter gene under control of the pMNTC regulatory cassette were injected intravitreally. Robust reporter gene expression was seen in the rat, gerbil, and nonhuman primate retina, with expression levels and anatomic location correlating with cone abundance and location in these species. Analysis of transduced mouse retina by immunohistochemistry demonstrated that this expression is highly cone-specific. Abundant expression was seen in nonhuman primate around the fovea. Reporter expression was detected sooner and in more cones in nonhuman primate transduced with the pMNTC expression cassette as compared to the pR2.1 expression cassette. In conclusion, the pMNTC regulatory cassette is an improved regulatory element that may facilitate the development of therapeutic agents for cone-associated disorders.
PYRAMID and LYM2034: Targeted randomized phase II studies of bortezomib with or without immunochemotherapy in newly diagnosed nongerminal center B-cell-like (GCB) diffuse large B-cell lymphoma (DLBCL), including rapid prospective non-GCB subtype identification.
Authors: J. Leonard, J. Reeves, B. Ferhanoglu, K. T. Doner, H. Eom, I. W. Flinn, J. Raposo, N. M. Chowhan, C. Suh, S. Noga, G. Tumyan, S. Aung, J. Hajdenberg, B. K. Ulrich, K. B. Pendergrass, G. Mulligan, A. Rizo, S. Kussick, F. Offner
Journal: Journal of Clinical Oncology (2011)

TPS226 Background: The recognition of prognostically distinct subtypes of DLBCL by gene expression profiling has, until now, not led to improved outcomes. Conducting targeted studies in prospectively identified, molecularly distinct entities is challenging. PYRAMID and LYM2034 are prospectively identifying and enrolling non-GCB patients (pts). This subtype has inferior outcomes vs GCB following (R-)CHOP alone (Lenz, NEJM 2008; Fu, JCO 2008). The rationale for these studies is provided by data suggesting bortezomib shows benefit specifically in non-GCB DLBCL resulting from inhibition of the critical NF-κB survival pathway, which is activated in the non-GCB subtype. Bortezomib + dose-adjusted EPOCH showed superior response rates and survival in non-GCB vs GCB relapsed DLBCL (Dunleavy, Blood 2009), and in newly diagnosed DLBCL, bortezomib + R-CHOP showed similar outcomes in GCB and non-GCB pts (Ruan, JCO 2010). Methods: PYRAMID is enrolling pts at 55 centers in the US; LYM2034 is enrolling pts at 86 sites in Canada, Australia, and countries in Central and South America, Europe, and Asia. Pts aged ≥18 yrs with previously untreated non-GCB DLBCL (PYRAMID: all stages; LYM2034: stages II–IV), ECOG PS 0–2, and ≥1 measurable tumor mass are eligible. Non-GCB tumor subtyping for both studies is done at a single central laboratory via the Hans immunohistochemical assay (Hans, Blood 2004). Non-GCB pts are then randomized to receive six 3-week cycles of R-CHOP alone (rituximab 375 mg/m2, cyclophosphamide 750 mg/m2, doxorubicin 50 mg/m2, vincristine 1.4 mg/m2, all on day 1, plus prednisone 100 mg, days 1–5), or bortezomib 1.3 mg/m2 on days 1 and 4 plus R-CHOP (PYRAMID) or bortezomib 1.3 mg/m2 on days 1, 4, 8, and 11 plus R-CAP (R-CHOP minus vincristine; LYM2034). The primary endpoint is PFS at 2 yrs in PYRAMID and CR rate in LYM2034. To date in PYRAMID and LYM2034, respectively, 100 and 167 DLBCL pts have been screened, and 34 of the planned 190 and 62 of the planned 164 non-GCB pts have been randomized. PYRAMID (NCT00931918) and LYM2034 (NCT01040871) are registered with ClinicalTrials.gov.
Protein Expression in Acute Myelogenous Leukemia Stem Cells Compared to Bulk AML Cells Using Reverse Phase Proteins Arrays (RPPA)
Authors: Steven M. Kornblau, YiHua Qiu, David Graber, Wenjing Chen, Jose Melendez, Marina Konopleva, Stefan Faderl, Michael Andreeff, Gautam Borthakur, Hui Yao, Kevin R. Coombes
Journal: Blood (2008)
Addition of Rituximab to CHOP Regimen Improves Clinical Outcome in Non-Germinal Center Type Diffuse Large B-Cell Lymphoma.
Authors: Masahiro Yokoyama, Daisuke Ennishi, Kyoko Ueda, Makoto Kodaira, Shuhei Yamada, Tomohiro Myojo, Sakura Sakajiri, Yuko Mishima, Kengo Takeuchi, Takashi Saotome, Yasuhito Terui, Shunji Takahashi, Yoshinori Ito, Kiyohiko Hatake
Journal: Blood (2006)
Phase I/II Trial of Fludarabine in Combination with Intravenous Busulfan and Allogeneic Progenitor Cell Support for Patients with High Risk Hematologic Malignancies; Dose Matters in Reduced Intensity Regimens
Authors: Simrit Parmar, Gabriela Rondon, Peter F Thall, Roland Bassett, Marcos De Lima, Chitra M Hosing, Paolo Anderlini, Partow Kebriaei, Issa Khouri, Prasanth Ganesan, Yvonne A Efebera, Richard Champlin, Sergio A Giralt
Journal: Blood (2011)
Randomized, double-blind, placebo-controlled phase II trial of low-dose metronomic cyclophosphamide alone or in combination with veliparib (ABT-888) in chemotherapy-resistant ER and/or PR-positive, HER2/neu-negative metastatic breast cancer: New York Cancer Consortium trial P8853.
Authors: E. Andreopoulou, A. P. Chen, J. Zujewski, M. Kim, D. L. Hershman, K. Kalinsky, T. Cigler, L. T. Vahdat, G. Raptis, B. Ramaswamy, Y. Novik, F. Muggia, J. A. Sparano
Journal: Journal of Clinical Oncology (2011)

TPS114 Background: Veliparib is an orally available, small molecule inhibitor of poly(ADP-ribose) polymerase (PARP). PARP is an essential nuclear enzyme that plays a role in recognition of DNA damage and facilitation of DNA repair. PARP inhibitors potentiate the cytotoxicity of DNA-damaging agents, including cyclophosphamide (C). The rationale for the proposed trial is as follows: (1) low-dose, continuous metronomic cyclophosphamide (50 mp PO daily) has activity in refractory metastatic breast cancer (MBC), (2) PARP is induced by DNA damaging agents, (3) PARP expression is comparable in ER-positive compared with ER-negative disease, (4) some ER-positive breast cancers exhibit defective homologous recombination pathway repair genes (eg, RAD51 and XRCC3), (5) the PARP inhibitor iniparib appears to be more effective when used chemotherapy resistant disease. Taken together, these findings suggest that veliparib-C combination may be more effective than metronomic C alone in chemotherapy resistant MBC. Methods: Major eligibility criteria include: (1) ER- and or PR-positive, HER2-negative MBC, (2) ECOG PS 0-1, (3) at least 2 prior chemotherapy regimens for MBC, including a taxane and capecitabine. Patients are randomized to oral C (50mg PO daily) plus either veliparib (60mg PO daily) or matching placebo.The primary endpoint is progression-free survival (PFS), and is powered to detect an increase in median PFS from 3 to 6 months (alpha=0.10, beta=0.10), which will require enrollment of 62 eligible patients over 12 months. Exploratory analyses will evaluate whether the macroH2A1.1 and PARP1 expression status in archival paraffin, or veliparib-induced PAR downregulation in peripheral blood mononuclear cells, is predictive of benefit from veliparib.
90yttrium Ibritumomab Tiuxetan-BEAM Followed by Autologous Stem Cell Transplantation Significantly Improves Overall Survival After Rituximab Containing Induction Therapy in Patients with High-Risk Aggressive B Cell Non-Hodgkin's Lymphoma
Authors: Marielle Wondergem, Madelon de Rooij, Josee Zijlstra, Otto J Visser, Gert Ossenkoppele, Peter C. Huijgens
Journal: Blood (2011)
514. Targeting the Negative Immune Regulatory Molecule B7-H4 on Both Tumor and Normal Tissue With Anti-B7-H4 CAR T Cells
Authors: Jenessa B. Smith, Evripidis Lanitis, Denarda Dangaj, Mathilde Poussin, Michael McLane, Nathalie Scholler, Daniel J. Powell
Journal: Molecular Therapy (2015)

B7-H4 is a negative immune regulatory molecule frequently overexpressed on the surface of cancer cells and immunosuppressive tumor-associated macrophages (TAMs). Ligation of B7-H4 with an unknown receptor on activated T cells results in inhibited effector function via cell cycle arrest, decreased proliferation and reduced IL-2 production. B7-H4 expression levels in ovarian cancer inversely correlate with patient survival, making B7-H4 an attractive candidate for therapeutic intervention. However, trials of B7-H4 targeted therapy have not been conducted and the biodistribution of B7-H4 protein in mice or humans is not well understood. Here, we tested the hypothesis that safe and effective B7-H4 targeting can be achieved using T cells genetically redirected with chimeric antigen receptors (CARs) against B7-H4 in a preclinical model of human ovarian cancer. Four independent anti-B7-H4 CAR lentivirus constructs were generated using anti-B7H4 single chain variable fragments (scFv) with affinities ranging from low to high, which were transduced into primary human T cells. Transduced T cells efficiently expressed CARs on their cell surface, and each CAR was capable of binding both human and mouse recombinant B7-H4 protein with distinct binding patterns; two CARs (3#68 and 3#54) had high capacity for rhB7-H4 protein binding, another had low binding capacity (56), and the last had virtually none (26). In co-culture assays, high binding B7-H4 CAR T cells secreted Th1 cytokines and specifically lysed human B7-H4+ ovarian cancer cells. In an immunodeficient mouse model, transferred B7-H4 CAR T cells persisted after infusion and exerted efficient anti-tumor activity against subcutaneous B7-H4+ human ovarian tumor xenografts. Unexpectedly, B7-H4 CAR T cell treated mice reproducibly showed signs of delayed onset, lethal toxicity emerging 6-8 weeks after therapy. Postmortem analysis revealed widespread immunopathology in nearly all tissue analyzed, with marked infiltration and destruction of peripheral nerve bundles and perivasculature regions that was inconsistent with non-specific graft versus host disease (GVHD). Immunopathology was evident in both tumor-bearing and healthy mice administered B7-H-4 CAR T cells, and mice administered control CAR T cells experienced tumor regression but without concomitant toxicity, ruling out a generalizable GVHD effect. Our results indicate that CAR T cell-based targeting of B7-H4 can mediate control of B7-H4+ cancer outgrowth in vivo, however, long-term engraftment of B7-H4 CAR T cells mediates lethal on-target, off-tumor toxicity that is likely due to wide expression of B7-H4 in healthy mouse organs. Accordingly, B7-H4 CAR T cells represent an important preclinical model system for the evaluation of safety approaches that limit CAR-mediated toxicity whilst maintaining potent anti-tumor activity in vivo.
Targeting RANKL for Immunotherapy of Multiple Myeloma
Authors: Benjamin J Schmiedel, Ludger Grosse-Hovest, Stefanie Bugl, Hans-Georg Kopp, Stefan Wirths, Bernd J Pichler, Miyuki Azuma, Pascal Schneider, Lothar Kanz, Gundram Jung, Helmut R. Salih
Journal: Blood (2011)
Rapamycin-insensitive companion of mTOR (RICTOR) amplification defines a subset of advanced gastric cancer and is sensitive to AZD2014-mediated mTORC1/2 inhibition
Authors: S.T. Kim, S.Y. Kim, S.J. Klempner, J. Yoon, N. Kim, S. Ahn, H. Bang, K.-M. Kim, W. Park, S.H. Park, J.O. Park, Y.S. Park, H.Y. Lim, S.H. Lee, K. Park, W.K. Kang, J. Lee
Journal: Annals of Oncology (2016)
SAMHD1 is a biomarker for cytarabine response and a therapeutic target in acute myeloid leukemia
Authors: Constanze Schneider, Thomas Oellerich, Hanna-Mari Baldauf, Sarah-Marie Schwarz, Dominique Thomas, Robert Flick, Hanibal Bohnenberger, Lars Kaderali, Lena Stegmann, Anjali Cremer, Margarethe Martin, Julian Lohmeyer, Martin Michaelis, Veit Hornung, Christoph Schliemann, Wolfgang E Berdel, Wolfgang Hartmann, Eva Wardelmann, Federico Comoglio, Martin-Leo Hansmann, Alexander F Yakunin, Gerd Geisslinger, Philipp Ströbel, Nerea Ferreirós, Hubert Serve, Oliver T Keppler, Jindrich Cinatl
Journal: Nature Medicine (2016)
Recommendations for the Implementation of Telehealth in Cardiovascular and Stroke Care: A Policy Statement From the American Heart Association
Authors: Lee H. Schwamm, Neale Chumbler, Ed Brown, Gregg C. Fonarow, David Berube, Karin Nystrom, Robert Suter, Mirian Zavala, Daniel Polsky, Kavita Radhakrishnan, Nathaniel Lacktman, Katherine Horton, Mary-Beth Malcarney, John Halamka, A. Colby Tiner
Journal: Circulation (2016)

The aim of this policy statement is to provide a comprehensive review of the scientific evidence evaluating the use of telemedicine in cardiovascular and stroke care and to provide consensus policy suggestions. We evaluate the effectiveness of telehealth in advancing healthcare quality, identify legal and regulatory barriers that impede telehealth adoption or delivery, propose steps to overcome these barriers, and identify areas for future research to ensure that telehealth continues to enhance the quality of cardiovascular and stroke care. The result of these efforts is designed to promote telehealth models that ensure better patient access to high-quality cardiovascular and stroke care while striving for optimal protection of patient safety and privacy.
Limited Tumor Tissue Drug Penetration Contributes to Primary Resistance against Angiogenesis Inhibitors
Authors: Szilvia Torok, Melinda Rezeli, Olga Kelemen, Akos Vegvari, Kenichi Watanabe, Yutaka Sugihara, Anna Tisza, Timea Marton, Ildiko Kovacs, Jozsef Tovari, Viktoria Laszlo, Thomas H. Helbich, Balazs Hegedus, Thomas Klikovits, Mir Alireza Hoda, Walter Klepetko, Sandor Paku, Gyorgy Marko-Varga, Balazs Dome
Journal: Theranostics (2016)

Resistance mechanisms against antiangiogenic drugs are unclear. Here, we correlated the antitumor and antivascular properties of five different antiangiogenic receptor tyrosine kinase inhibitors (RTKIs) (motesanib, pazopanib, sorafenib, sunitinib, vatalanib) with their intratumoral distribution data obtained by matrix-assisted laser desorption ionization mass spectrometry imaging (MALDI-MSI). In the first mouse model, only sunitinib exhibited broad-spectrum antivascular and antitumor activities by simultaneously suppressing vascular endothelial growth factor receptor-2 (VEGFR2) and desmin expression, and by increasing intratumoral hypoxia and inhibiting both tumor growth and vascularisation significantly. Importantly, the highest and most homogeneous intratumoral drug concentrations have been found in sunitinib-treated animals. In another animal model, where - in contrast to the first model - vatalanib was detectable at homogeneously high intratumoral concentrations, the drug significantly reduced tumor growth and angiogenesis. In conclusion, the tumor tissue penetration and thus the antiangiogenic and antitumor potential of antiangiogenic RTKIs vary among the tumor models and our study demonstrates the potential of MALDI-MSI to predict the efficacy of unlabelled small molecule antiangiogenic drugs in malignant tissue. Our approach is thus a major technical and preclinical advance demonstrating that primary resistance to angiogenesis inhibitors involves limited tumor tissue drug penetration. We also conclude that MALDI-MSI may significantly contribute to the improvement of antivascular cancer therapies.
Serum Soluble Transferrin Receptor in Heterozygous β-Thalassaemia: Application in the Diagnosis of Iron Deficiency and as Hematologic Marker of Erythroid Activity According to Thalassaemic Genotypes (β0 vs β+).
Authors: Jose Manuel Calvo-Villas, María Francisca Zapata, Ivan Alvarez, Silvia de la Iglesia, Jorge Cuesta, Elena Carreter, Francisco Sicilia
Journal: Blood (2006)
Abstract 3082: miR-155-5p expression is associated with response to neoadjuvant paclitaxel treatment of locally advanced breast cancer
Authors: Anne Hege Straume, Einar Birkeland, Stian Knappskog, Per Eystein Lønning
Journal: Cancer Research (2015)

Abstract Introduction Resistance to chemotherapy remains a prominent obstacle to cure in cancer. We have previously shown that genetic defects in key pathways involved in processes like apoptosis, cell-cycle arrest and senescence may be involved in resistance to chemotherapy in vivo. MicroRNAs (miRNAs) are known to be crucial regulators of gene expression, and to potentially affect the response to drugs, including chemotherapy. Here, we aimed to explore the potential role of miRNAs in mechanisms of breast cancer chemoresistance in-vivo, by analyzing miRNA expression in breast cancer patients with recorded responses to chemotherapy. Patient materials and Methods Breast tumour biopsies were collected before chemotherapy in a prospective clinical study, where patients were randomized to receive epirubicin or paclitaxel monotherapy (n = 223). Information about the response to therapy, as defined by the UICC criteria, in addition to long-term outcome, was available for all patients. The global miRNA expression levels were analyzed in 50 breast tumour biopsies by deep sequencing. The patients were selected based on their response to first-line chemotherapy. To verify the results obtained by miRNA sequencing, selected miRNAs were quantified in all patients by qPCR. Results No global miRNA patterns were observed when performing unsupervised clustering of miRNA sequencing data. Among samples from paclitaxel-treated patients, we identified three differentially expressed miRNAs between response groups; the expression of miR-155 was significantly lower (p = 0.005) in patients with poor response to paclitaxel, and the expression of both miR-181a and miR-181b were significantly higher (p = 0.003 and 0.012, respectively) in patients with poor response to paclitaxel. qPCR data validated the initial association identified between high miR-155-5p expression levels and response to paclitaxel treatment. Intriguingly though, high levels of miR-155 were also associated with a poor prognosis in the study population as a whole (p = 0.012), as well as with the presence of mutations in TP53 (p &amp;lt; 0.001). Conclusion Here, we show that breast cancer patients responding to paclitaxel treatment have higher expression levels of miR-155-5p. Also, patients with elevated levels of miR-155-5p expression have a poor prognosis and a higher frequency of TP53 mutations. Citation Format: Anne Hege Straume, Einar Birkeland, Stian Knappskog, Per Eystein Lønning. miR-155-5p expression is associated with response to neoadjuvant paclitaxel treatment of locally advanced breast cancer. [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 3082. doi:10.1158/1538-7445.AM2015-3082