tbuckley/cabot-search huggingface dataset:
The evaluation of the eighth edition of the AJCC/UICC staging system for intrahepatic cholangiocarcinoma: A proposal of a modified new staging system.
Authors: Yusuke Yamamoto, Teiichi Sugiura, Yukiyasu Okamura, Takaaki Ito, Ryo Ashida, Katsuhisa Ogi, Katsuhiko Uesaka
Journal: Journal of Clinical Oncology (2019)

206 Background: The objective was to clarify the prognostic impact of the 8 th edition of American Joint Committee on Cancer (AJCC)/International Union Against Cancer (UICC) of intrahepatic cholangiocarcinoma (ICC). Methods: ICC patients who underwent hepatectomy for ICC between 2002 and 2016 were enrolled. The survival impact of AJCC/UICC 8 th edition was examined. Results: A total of 103 resected patients were enrolled. The 5-year disease-specific survival (DSS) rate was 75.9% in T1a (n = 23), 88.9% in T1b (n = 10), 14.9% in T2 (n = 24), 52.5% in T3 (n = 11), and 15.2% in T4 (n = 35). The DSS was comparable among T2, T3, and T4 (p = 0.345, 0.295). The 5-year DSS was 87.5% in stage IA, 88.9% in IB, 18.1% in II, 66.7% in IIIA, and 15.0% in IIIB. The DSS rates of stage II and stage IIIB were comparable, and the DSS rate of stage II was worse than that of stage IIIB. A multivariate analysis identified multiple tumors (hazard ratio [HR]: 2.821), periductal infiltrating (HR: 2.439), perforation of the visceral peritoneum (HR: 1.850), and vascular invasion (HR: 1.872) as independent prognostic factors that were associated with the DSS. Lymph node metastasis (HR: 1.715) was not an independent prognostic factor. The optimum tumor size with the greatest difference in the DSS was 2 cm (p = 0.014). The new T classification was developed as follows: T1, size ≤ 2 cm without other factors; T2, size &gt; 2 cm without other factors; T3, vascular invasion or perforation of the visceral peritoneum; and T4, multiple tumors or periductal infiltrating. The HR of lymph node metastasis was similar to that of the low-HR factors, so lymph node metastasis was categorized as Stage IIIA. The 5-year DSS was 100% in T1 (n = 7), 76.6% in T2 (n = 28), 45.1% in T3 (n = 28), and 3.4% in T4 (n = 40). There were differences in the DSS between T2 and T3 (p = 0.035) and between T3 and T4 (p = 0.003). The 5-year DSS was 100% in stage I, 85.6% in II, 42.4% in IIIA, and 3.4% in IIIB (Fig. 2d). There were significant differences in the DSS between stage II and IIIA (p = 0.013) and between IIIA and IIIB (p = 0.026). Conclusions: T2, T3, and T4 of AJCC/UICC overlapped with regard to the DSS. The new staging can classify ICC patients with sufficient prognostic differences.
Circulating free tumor DNA copy number index (CNI) as a predictor of therapeutic response in pancreatic ductal adenocarcinomas (PDAC).
Authors: Madappa N. Kundranda, Julia Beck, Jana Bergelin, Tomislav Dragovich, Patricia Lucente, Marie Conn, Boris Naraev, John Chang, Howard Urnovitz, Ekkehard Schütz
Journal: Journal of Clinical Oncology (2019)

261 Background: Cell-free tumor DNA (cfDNA) has potential to provide minimally invasive patient specific biomarkers to monitor tumor burden. Tumor-specific copy number instability (CNI) are used to quantify tumor-derived cfDNA in the plasma. We prospectively computed CNI Scores of cfDNA to compare with radiological and Ca 19-9 responses. Methods: In a laboratory blinded, prospective single-institution study, 119 plasma samples from 33 patients (pts) with PDAC were analyzed. Time-points were at baseline (C1), 2 nd (C2) and 3 rd (C3) cycle of systemic therapy. Tumor cfDNA was measured with a CNI scoring assay that quantifies cfDNA with somatic macro-alterations. CNI Score (CNIs) of 31 was defined as ref. range (97.5 % - control group; N = 135), pts below this threshold were censored. Progression of disease (PD) defined as C3 CNIs &gt; 93 (3-fold threshold) and difference to the baseline &gt; 31 (dispersion of reference population). Mutant KRAS in plasma was measured using ddPCR in a subset 22 pts. Pts with an increase of &gt; 0.06% (critical difference) were classified PD. Radiologic imaging results were compared with CNIs and CA19-9 changes from baseline to C3, respectively. Results: By standard radiological imaging 33 pts were classified as: 14 PR/CR, 10 SD, 9 PD. 27/33 pts (81%) were evaluable by CNIs which ranged from decrease of 2017 - increase of 645. The C3 CNI classifier yielded a sensitivity of 86% for predicting PD and 95% for SD/PR/CR. KRAS classification yielded an accuracy of 72%, and only 3/9 PD were accurately predicted (33%). 26/33 pts were secretors evaluable by CA19-9. Only 2/8 PD pts showed increasing values in CA19-9 and 6/8 of evaluable by CNI; 5/6 showed increasing CNI scores. 3/20 deemed as SD on imaging with increasing values of CA19-9 were noted to have decreasing CNIs. CNI Score classification was significantly better than CA19-9 (P = 0.001 and 0.63, respectively). Conclusions: Our evaluation of a comparative study on cfDNA and CA19-9 versus imaging suggest that CNI quantification is potentially a more reliable blood-based marker for early assessment of efficacy to systemic therapy in PDAC. Furthermore, for patients not expressing CA19-9 it could serve as an alternative monitoring aid.
Hepatocellular carcinoma (HCC) survival by etiology: A SEER-Medicare database analysis.
Authors: Gagandeep Brar, Tim McNeel, Katherine McGlynn, Barry Graubard, Charalampos S. Floudas, M. Pia Morelli, Changqing Xie, Tim F. Greten, Sean Altekruse
Journal: Journal of Clinical Oncology (2019)

201 Background: HCC is the 6 th most common occurring cancer worldwide and the 4 th leading cause of cancer mortality, with a survival of 6-9 months. While survival varies by stage at diagnosis and treatment, the effect of HCC etiology on survival is unclear. We analyzed the SEER-Medicare database to evaluate whether HCC survival varied by etiology, after adjusting for stage, treatment, and survival. Methods: A total of 11,522 SEER-Medicare HCC cases (ICD-O-3 codes C22 for topography, 8170-8175 for morphology) met criteria for the Cox proportional hazard analyses to assess survival differences among the risk factors for hepatitis C virus (HCV) infection, hepatitis B virus (HBV) infection, alcohol disorders, and metabolic disorders. These analyses were adjusted for covariates for gender, age at diagnosis, race, ethnicity, tumor size and extent of disease, a modified Charlson Index of comorbidities, and treatments that included resection, transplantation, ablation, arterial directed therapy and radiotherapy. Cases with multiple and unknown etiologies were included in analyses, however genetic disorders and primary biliary cirrhosis were excluded due to their rarity. Results: HBV associated cases had the highest proportion of single nodules (40% vs 33% overall), localized stage disease (57% vs 49%), treatment (40% vs 27%), and greatest frequency of resection (18.6% vs 9%). Non-Hispanic Asians/Pacific Islanders accounted for 69% of HBV infection-related HCC cases but only 16% of all cases. HBV associated cases had better survival than did HCC cases with other etiologies. Specifically, after adjusting for demographic and clinical attributes, compared to cases with HBV infection, the risk of death was highest for alcohol-related HCC (HR=1.69; 95%CI:1.42-2.01) followed by multiple etiologies (HR = 1.40; 95% CI: 1.20-1.64), metabolic disorders (HR = 1.32; 95% CI: 1.13-1.55), HCV infection (HR = 1.30; 95% CI: 1.10-1.53), and HCC of unknown etiology (HR = 1.22; 95% CI: 1.04-1.43). Conclusions: Persons with HBV associated HCC had better survival than persons with HCC of other etiologies. Efforts to identify people with any etiologic risk factors for HCC, treat their conditions, and screen for HCC may improve overall survival.
Summaries of Key Journal Articles
Authors: Kim A. Eagle, Christopher P. Cannon, William F. Armstrong, David S. Bach, Ragavendra R. Baliga, Timothy B. Cotts, Daniel T. Eitzman, James B. Froehlich, Caren S. Goldberg, Hitinder S. Gurm, Jennifer C. Hirsch, Elizabeth Anne Jackson, Fred Morady, Debabrata Mukherjee, Himanshu J. Patel, Melvyn Rubenfire, Gilbert R. Upchurch
Journal: Journal of the American College of Cardiology (2009)
Abstract P008: Repeatability of Ectopic Beats From 48-hour Ambulatory Electrocardiography: The Atherosclerosis Risk in Communities (ARIC) Study
Authors: Michelle L Meyer, Elsayed Z Soliman, Lisa Wruck, Thomas H Mosley, Anna Poon, Eric A Whitsel, Alonso Alvaro, Gerardo Heiss, Laura R Loehr
Journal: Circulation (2016)

Background: Ectopic beats, defined by premature atrial contractions (PACs) and premature ventricular contractions (PVCs), are one of the most common findings on the electrocardiogram (ECG). Excess ectopic beats on ambulatory ECG monitoring are associated with atrial fibrillation (AF), stroke and death in symptomatic patients and in population-based studies. However, the repeatability of ECG-enumerated ectopic beats has not been sufficiently examined in a general population. Objectives: Characterize the repeatability of PACs and PVCs in a community-based population of older adults. Methods: Ambulatory, 48-hour ECG was measured in a subsample of the Atherosclerosis Risk in Communities Study (ARIC; 2011-2013) at two locales. Participants were randomly invited to participate in the repeatability study (n=92). Following an identical, standardized protocol, the participants wore a Holter monitor for two, 48-hour periods separated by a mean of 38 days (range: 11, 130 days) and completed a symptom questionnaire during each period. Each visit included new electrodes and Holter placement. All participants wore monitors for 48 hours and had recordings with &lt;1% noise. Participants with AF (n=4) or paced rhythm (n=2) were excluded (total n=86; mean age 74.6 years; 56 females, 55 black). Visit-specific quartiles and 80th percentile cut-points for the total counts of PACs and PVCs over the 48 hour monitoring period were used. Between-visit agreement was quantified using the weighted kappa for quartiles and kappa for 80th percentile cut-points. Results: About 17% of the participants reported symptoms of dizziness, palpitations, or chest pain while wearing the monitor. During the 48-hour recordings, all participants had ≥1 PAC count and 2 participants had a 0 PVC count. The overall median (interquartile range (IQR)) was 266 counts (IQR: 80, 1,692.5) for PACs and 223 counts (IQR: 17.5, 1,085.5) for PVCs. The median between-visit difference (visit 2 - visit 1) was -12.5 counts for PACs (IQR: -154, 65) and 0 counts for PVCs (IQR: -78, 320). The between-visit, weighted kappa for count quartiles was 0.70 (95% confidence interval (CI): 0.61, 0.80) for PACs and 0.68 (95% CI: 0.58, 0.78) for PVCs. The kappa for counts &gt;80th percentile was 0.56 (95% CI: 0.34, 0.78) for PACs and 0.71 (95% CI: 0.52, 0.90) for PVCs. Conclusion: Between-visit agreement is high to moderate for 48-hour, Holter-based PACs and PVCs quantiles, according to common interpretations for kappa coefficients. When paired with pending examination of how agreement varies over shorter duration recordings within the 48-hour monitoring period, the present results can facilitate epidemiologic and clinical applications in which knowledge of measurement error, variability and misclassification are needed to inform risk assessment.
Targeting the Glyco-Antigen CD75s with the Tetravalent, Fc-Engineered Antibody 'Ebu-141 Tetra' Induces Potent Killing of B Cell Lymphoma and Plasma Cell Tumors
Authors: Katja Klausz, Amir Karimzadeh-Tabrizi, Malena Buck, Steffen Krohn, Anna-Kathrin Otte, Christian Kellner, Giorgio Alberto Croci, Wolfram Klapper, Matthias Peipp, Martin Gramatzki
Journal: Blood (2018)
Frequency and feasibility of detecting FGFR mRNA expression in archival samples of patients with cholangiocarcinoma (CCA).
Authors: Abhijit Chougule, Jochen K Lennerz, Andrew X. Zhu, Nabeel Bardeesy, David Tsai Ting, Vikram Deshpande, Lipika Goyal
Journal: Journal of Clinical Oncology (2019)

281 Background: Fibroblast growth factor receptor (FGFR) inhibitors show promising activity in patients with intrahepatic CCA harboring FGFR2 fusions, but these alterations have a modest frequency of 15-20%. FGFR mRNA expression has shown preliminary potential as a predictive biomarker for FGFR inhibition in advanced urothelial cancer and is currently being used for patient selection in clinical trials. To assess if we can increase the number of patients with CCA eligible for FGFR inhibitor trials, we evaluated the frequency and feasibility of detecting FGFR mRNA overexpression in archival CCA tissue. Methods: Patients with intrahepatic and extrahepatic CCA who received treatment at the MGH between 1/2004 and 12/2013 were included. Tissue microarrays of archival specimens were stained using the FGFR1-3 pooled, FGFR1, and FGFR2 RNA in situ hybridization probes (RNAscope 2.5 assay). Clinicopathologic data were obtained from the medical record. CCA cell lines were assessed for sensitivity to the FGFR selective inhibitor BGJ398 and also for FGFR expression by qPCR. Results: 90/111 (81%) TMA specimens were evaluable: median age 62.6 years, female 63%, median tumor size 5.1cm, intrahepatic/extrahepatic 71%/29%%. Among the 90 samples, 14% samples stained negative for the pooled FGFR1-3 probe, and 23%, 32%, and 30% stained 1+, 2+, and 3+ positive, respectively. Of note, majority of the samples stained 3+ for FGFR2. Examination of 11 ICC cell lines lacking FGFR gene abnormalities revealed that the single line with marked overexpression of FGFR1 exhibited hypersensitivity to BGJ398. Conclusions: Selection of patients with CCA for treatment with FGFR inhibitors based on mRNA expression levels is feasible on archival tissue with the FGFR RNA ISH probes, and this technique may identify a subpopulation of patients without FGFR genetic abnormalities who may benefit from FGFR inhibitors. [Table: see text]
Association of Aspirin Use for Primary Prevention With Cardiovascular Events and Bleeding Events
Authors: Sean L. Zheng, Alistair J. Roddick
Journal: JAMA (2019)

<h3>Importance</h3> The role for aspirin in cardiovascular primary prevention remains controversial, with potential benefits limited by an increased bleeding risk. <h3>Objective</h3> To assess the association of aspirin use for primary prevention with cardiovascular events and bleeding. <h3>Data Sources</h3> PubMed and Embase were searched on Cochrane Library Central Register of Controlled Trials from the earliest available date through November 1, 2018. <h3>Study Selection</h3> Randomized clinical trials enrolling at least 1000 participants with no known cardiovascular disease and a follow-up of at least 12 months were included. Included studies compared aspirin use with no aspirin (placebo or no treatment). <h3>Data Extraction and Synthesis</h3> Data were screened and extracted independently by both investigators. Bayesian and frequentist meta-analyses were performed. <h3>Main Outcomes and Measures</h3> The primary cardiovascular outcome was a composite of cardiovascular mortality, nonfatal myocardial infarction, and nonfatal stroke. The primary bleeding outcome was any major bleeding (defined by the individual studies). <h3>Results</h3> A total of 13 trials randomizing 164 225 participants with 1 050 511 participant-years of follow-up were included. The median age of trial participants was 62 years (range, 53-74), 77 501 (47%) were men, 30 361 (19%) had diabetes, and the median baseline risk of the primary cardiovascular outcome was 10.2% (range, 2.6%-30.9%). Aspirin use was associated with significant reductions in the composite cardiovascular outcome compared with no aspirin (60.2 per 10 000 participant-years with aspirin and 65.2 per 10 000 participant-years with no aspirin) (hazard ratio [HR], 0.89 [95% credible interval, 0.84-0.94]; absolute risk reduction, 0.41% [95% CI, 0.23%-0.59%]; number needed to treat, 241). Aspirin use was associated with an increased risk of major bleeding events compared with no aspirin (23.1 per 10 000 participant-years with aspirin and 16.4 per 10 000 participant-years with no aspirin) (HR, 1.43 [95% credible interval, 1.30-1.56]; absolute risk increase, 0.47% [95% CI, 0.34%-0.62%]; number needed to harm, 210). <h3>Conclusions and Relevance</h3> The use of aspirin in individuals without cardiovascular disease was associated with a lower risk of cardiovascular events and an increased risk of major bleeding. This information may inform discussions with patients about aspirin for primary prevention of cardiovascular events and bleeding.
Landscape of circulating tumor DNA profiling of advanced pancreatic cancer (PDAC).
Authors: Kabir Mody, Pashtoon Murtaza Kasi, Phani Keerthi Surapaneni, Mitesh J. Borad, Daniel H. Ahn, Amit Mahipal, Jason Scott Starr, Ashton Ritter, Jessica McMillan, Natasha Wylie, Ali Roberts, Rebecca J Nagy, Tanios S. Bekaii-Saab
Journal: Journal of Clinical Oncology (2019)

289 Background: PDAC has limited treatment options. Genomic analyses have led to development of targeted therapies now in several clinical trials, and may enable the discovery of new treatment options. However, biopsy often yields limited tissue, thus hampering tissue-based profiling opportunities. Data regarding circulating tumor DNA (ctDNA) profiling in PDAC during real time clinical practice is limited. Methods: We performed ctDNA NGS analysis in pts with advanced PDAC (December 2014–August 2018). ctDNA analysis was performed using Guardant 360 (Guardant Health, CA), which detects single nucleotide variants, amplifications, fusions, and specific insertion/deletion mutations in up to 73 different genes. The mutant allele fraction (MAF) for detected alterations was calculated relative to wild type in ctDNA. Therapeutic relevance (TR) was defined as possible treatments within OncoKB levels 1-3B and R1. The study was conducted in accordance with Mayo Clinic Institutional Review Board requirements. Results: Among 171 pts and 206 total samples, ctDNA NGS revealed at least one genomic alteration in 150 pts (88%). Median number of alterations per patient was 3 [range, 1-15]. The total number of unique alterations was 450 with the most commonly altered genes being: TP53 (181 alterations, 40%), followed by KRAS (118 alterations, 26%), CDKN2A (23 alterations, 5%), SMAD4 (15 alterations, 3%), EGFR (11 alterations, 2.4%), PIK3CA (9 alterations, 2%), GNAS (8 alterations, 1.5%). Amplifications were noted in 16 genes, including BRAF, CCND2, CCNE1, CDK4, CDK6, EGFR, ERBB2, FGFR1, FGFR2, KIT, KRAS, MET, MYC, PDGFRA, PIK3CA and RAF1. Therapeutically relevant alterations were seen in 95 pts of the 150 pts (63%). Tissue based profiling (Results to be shown) was done in 56 (33%) pts of total 171 pts with a median of 130 days between ctDNA and tissue biopsy. KRAS and TP53 were the most common gene mutations found in patients with both liquid and tissue biopsy results. Conclusions: ctDNA plasma profiling of pts with advanced PDAC is a feasible alternative method to gather comprehensive genomic data.
Epidemiology of Invasive Group B Streptococcal Infections Among Nonpregnant Adults in the United States, 2008-2016
Authors: Louise K. Francois Watkins, Lesley McGee, Stephanie J. Schrag, Bernard Beall, Jennifer Hudson Jain, Tracy Pondo, Monica M. Farley, Lee H. Harrison, Shelley M. Zansky, Joan Baumbach, Ruth Lynfield, Paula Snippes Vagnone, Lisa A. Miller, William Schaffner, Ann R. Thomas, James P. Watt, Susan Petit, Gayle E. Langley
Journal: JAMA Internal Medicine (2019)

Group B Streptococcus (GBS) is an important cause of invasive bacterial disease. Previous studies have shown a substantial and increasing burden of GBS infections among nonpregnant adults, particularly older adults and those with underlying medical conditions.
Venous Thromboembolism in Blood or Marrow Transplant (BMT) Survivors: A Report from BMT Survivor Study (BMTSS)
Authors: Radhika Gangaraju, Yanjun Chen, Lindsey Hageman, Jessica Wu, Liton F. Francisco, Michelle Kung, Emily Ness, Mariel Parman, Daniel J. Weisdorf, Stephen J Forman, Mukta Arora, Saro H. Armenian, Smita Bhatia
Journal: Blood (2018)
Abstract 19037: Protection Against Venous Thrombogenesis by the Vascular Ectonucleotidase CD39
Authors: Yogendra Kanthi, Benjamin N Jacobs, Liguo Chi, Vinita Yadav, Raymond Zhao, Benjamin Tourdot, Scott H Visovatti, Michael A Holinstat, Jason S Knight, David J Pinsky
Journal: Circulation (2017)

Background: Deep vein thrombosis (DVT) is a major health burden, carrying significant morbidity, mortality and socioeconomic cost. The molecular determinants of venous thrombogenesis are beginning to be elucidated. CD39 is a circulating and membrane-spanning enzyme in the vasculature that is responsible for the phosphohydrolysis of the thromboinflammatory extracellular “danger” signals, ATP and ADP. We hypothesized that CD39 plays a protective role in venous thrombogenesis. Methods: Using a restricted-flow model of inferior vena cava (IVC) stenosis, DVT was induced in Cd39+/- and WT control mice. Thrombus frequency and size were assessed 48h following IVC stenosis. Neutrophil engagement with extracellular traps (NETs) was quantified with immunoblotting thrombus protein for citrullinated histone 3 (H3cit), and immunofluorescent staining. Whole blood aggregation (WBA) was performed with ADP-agonist. Results: Cd39+/- mice were twice as likely to develop venous thrombosis compared with WT mice (21/36 (58%) vs...
Invariant Natural Killer T Cells from Donor Lymphocyte Infusions (DLI-iNKTs) Contribute to Anti-Tumor Immunity after Allogeneic Hematopoietic Cell Transplantation
Authors: Simona Jahnke, Hannes Schmid, Kathy-Ann Secker, Silke Duerr-Stoerzer, Hildegard Keppeler, Rebecca Baur, Michael Schumm, Rupert Handgretinger, Wolfgang Bethge, Lothar Kanz, Corina Schneidawind, Dominik Schneidawind
Journal: Blood (2018)
Abstract P2-02-14: Metabolic regulation and drug resistance in c-Src activated triple negative breast cancer
Authors: KH Jung, JH Park, T Sirupangi, D Jia, N Gandhi, S Pudakalakatti, J Elswood, W Porter, N Putluri, XH-F Zhang, X Chen, PK Bhattacharya, CJ Creighton, MT Lewis, JM Rosen, L-JC Wong, GM Das, CK Osborne, MF Rimawi, BA Kaipparettu
Journal: Cancer Research (2019)

Abstract c-Src (Src) is a proto-oncogene involved in signaling that culminates in the control of multiple biological functions. Src is also one of the most frequently upregulated pathways in triple negative breast cancer (TNBC). Dysregulation of Src has been detected in TNBC and is strongly associated with tumor metastasis and poor prognosis. However, even after promising preclinical studies, Src inhibitors did not show major clinical advantage in unselected TNBC populations. We have previously published that metastatic TNBC has high energy-dependency to mitochondrial fatty acid beta-oxidation (FAO) and FAO activates Src by inducing autophosphorylation at Y419. However, our recent analysis suggests that as observed with the Src inhibitors, TNBC tumors treated with FAO inhibitors also develop drug-resistance and continue tumor growth. Evaluation of their drug resistance mechanism revealed that while short-term inhibition of FAO or Src induces autophagic and apoptotic cell deaths, long-term inhibition results in autophagy-mediated drug resistance and survival. Further analyses suggest that FAO and Src inhibitors activate mitogen-activated protein (MAP) kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) pathway via the induction of cellular reactive oxygen species (ROS) in TNBC. Activated MEK/ERK then induces survival pathways for drug resistance and tumor survival. Validation of in vitro findings using in vivo TNBC models confirmed that combination of FAO/Src inhibitors with MEK/ERK inhibitors can provide significant benefit to overcome the therapeutic resistance of TNBC. These findings open-up new therapeutic opportunities to manage TNBC patients with currently non-targetable metastatic tumors. Citation Format: Jung KH, Park JH, Sirupangi T, Jia D, Gandhi N, Pudakalakatti S, Elswood J, Porter W, Putluri N, Zhang XH-F, Chen X, Bhattacharya PK, Creighton CJ, Lewis MT, Rosen JM, Wong L-JC, Das GM, Osborne CK, Rimawi MF, Kaipparettu BA. Metabolic regulation and drug resistance in c-Src activated triple negative breast cancer [abstract]. In: Proceedings of the 2018 San Antonio Breast Cancer Symposium; 2018 Dec 4-8; San Antonio, TX. Philadelphia (PA): AACR; Cancer Res 2019;79(4 Suppl):Abstract nr P2-02-14.