tbuckley/cabot-search huggingface dataset:
A single-center survey of health-related quality of life among acute myeloid leukemia survivors in first complete remission.
Authors: Mok-Chung Jennifer Cheng, B. Douglas Smith, Christopher Simon Hourigan, Ivana Gojo, Keith William Pratz, Amanda Blackford, Thomas J. Smith
Journal: Journal of Clinical Oncology (2016)

223 Background: To better understand adult acute myeloid leukemia (AML) survivorship and health related quality of life, we piloted a survey exploring patient reported outcomes for patients in first complete remission (CR) to determine if patients feel the survey is relevant to their overall well-being. Methods: A cross-sectional survey measuring: quality of life, physical, role, emotional, cognitive, social functioning (EORTC QLQ-C30 v 3.0); physical, psychological, social, and spiritual well-being (Quality of Life-Cancer Survivor (QOL- CS) scale); fatigue (Functional Assessment of Chronic Illness Therapy – Fatigue Scale (FACIT-Fatigue)); anxiety and depression (Hospital Anxiety and Depression Scale (HADS)); sociodemographic and 5 open-ended questions. Results: 18 participants completed the survey; mean age was 57.2 years. Nine patients were in CR for &lt;2 years, and 9 were in CR for ≥2 years. Participants scored well on the EORTC QLQ-C30 and reported symptoms ranging from 11% (constipation) to 83% (fatigue). The FACIT-Fatigue (worst 0-best 52) mean score was 28.7 and median score was 33.5 (normal ≥30). On the HADS anxiety scale, 2 participants scored in the abnormal range. One scored in the abnormal range on the depression scale. On the QOL-CS, participants scored above 6 out of 10 in all domains, with exceptions of the psychological subscales of distress and fear (Table 1). Most participants felt the survey was completely or mostly relevant (88.8%) in understanding their quality of life. Most felt the length was optimal (77.8%). Conclusions: Most survivors scored well on quality of life and well-being, but with ongoing fatigue, distress, and fear of future tests and recurrence. Few consistently scored worse on the scales. There may be a population coping less well and it would be informative for survivorship programs to prospectively characterize their medical and psychosocial-spiritual needs. [Table: see text]
IGF-Binding Protein-1 Levels Are Related to Insulin-Mediated Glucose Disposal and Are a Potential Serum Marker of Insulin Resistance
Authors: Timon W. van Haeften, Maria L. Zonderland, Louise W.E. Sabelis, Jaap van Doorn
Journal: Diabetes Care (2007)

We were interested in the article of Maddux et al. (1) in which they found a correlation coefficient of 0.75 for the relationship of IGF-binding protein (IGFBP)-1 with insulin sensitivity. Often, the homeostasis model assessment of insulin resistance (HOMA-IR) or other assessments such as the Stumvoll Index (2) are used. Because hepatic production of IGFBP-1 is under direct inhibitory influence of insulin, plasma IGFBP-1 levels could potentially be of use …
Target and Agent Prioritization for the Children’s Oncology Group—National Cancer Institute Pediatric MATCH Trial
Authors: Carl E. Allen, Theodore W. Laetsch, Rajen Mody, Meredith S. Irwin, Megan S. Lim, Peter C. Adamson, Nita L. Seibel, D. Williams Parsons, Y. Jae Cho, Katherine Janeway
Journal: JNCI Journal of the National Cancer Institute (2016)

Over the past decades, outcomes for children with cancer have improved dramatically through serial clinical trials based in large measure on dose intensification of cytotoxic chemotherapy for children with high-risk malignancies. Progress made through such dose intensification, in general, is no longer yielding further improvements in outcome. With the revolution in sequencing technologies and rapid development of drugs that block specific proteins and pathways, there is now an opportunity to improve outcomes for pediatric cancer patients through mutation-based targeted therapeutic strategies. The Children's Oncology Group (COG), in partnership with the National Cancer Institute (NCI), is planning a trial entitled the COG-NCI Pediatric Molecular Analysis for Therapeutic Choice (Pediatric MATCH) protocol utilizing an umbrella design. This protocol will have centralized infrastructure and will consist of a biomarker profiling protocol and multiple single-arm phase II trials of targeted therapies. Pediatric patients with recurrent or refractory solid tumors, lymphomas, or histiocytoses with measurable disease will be eligible. The Pediatric MATCH Target and Agent Prioritization (TAP) committee includes membership representing COG disease committees, the Food and Drug Administration, and the NCI. The TAP Committee systematically reviewed target and agent pairs for inclusion in the Pediatric MATCH trial. Fifteen drug-target pairs were reviewed by the TAP Committee, with seven recommended for further development as initial arms of the Pediatric MATCH trial. The current evidence for availability, efficacy, and safety of targeted agents in children for each class of mutation considered for inclusion in the Pediatric MATCH trial is discussed in this review.
From Bench to Bedside: Hematopoietic Growth Factors (HGFs)- a Cause of Serious and Unanticipated Class Toxicities.
Authors: Charles L. Bennett, Ari Polish, Athena T Samaras, Mi Zheng, Dennis P West, Steven M Trifilio, Beatrice J Edwards, Simone N Boyle, Matthew J Fisher, June M McKoy
Journal: Blood (2009)
Hippocampus reidi, a Marine Natural Product Reduces TH2 Cytokine Levels and Attenuates NF-KB Expression
Authors: Hugo Bernardino Ferreira Silva, Raimon RIOS Silva, Norma Vilany Queiroz Carneiro, Anaque Oliveira Pires, Marta Santos Serafim Machado, Cíntia Rodrigues Marques, Ryan Santos Costa, Tamires Carneiro Brasil, Paulo Pessoa ALBUQUERQUE Filho, Eryvelton Souza Franco, Maria Bernadete Souza Maia, Rosana Beatriz Silveira, Neuza Maria Alcântara-Neves, Camila Alexandrina Figueiredo
Journal: Journal of Allergy and Clinical Immunology (2017)
Glucagon-like Peptide 1 Receptor (GLP-1R) Signaling Inhibits Aeroallergen-Induced IL-33 Release and Reduces Group 2 Innate Lymphoid Cell (ILC2) Activation In Vivo
Authors: Shinji Toki, Kasia Goleniewska, Sara Reiss, Jian Zhang, Melissa H. Bloodworth, Matt T. Stier, Weisong Zhou, Dawn C. Newcomb, Kelli L. Boyd, Kevin D. Niswender, Stokes Peebles
Journal: Journal of Allergy and Clinical Immunology (2017)
Sphingosine Kinase1 Inhibitor SK178 Preferentially Hinders Growth of KIT D816V Mast Cells In Vitro and In Vivo.
Authors: Bandara Geethani, Rosa Munoz-Cano, Avanti Desai, Araceli Tobio, Dean D. Metcalfe, Ana Olivera
Journal: Journal of Allergy and Clinical Immunology (2017)
Genetic Testing and Counseling Among Patients With Newly Diagnosed Breast Cancer
Authors: Allison W. Kurian, Kent A. Griffith, Ann S. Hamilton, Kevin C. Ward, Monica Morrow, Steven J. Katz, Reshma Jagsi
Journal: JAMA (2017)

Germline genetic testing of breast cancer patients is an important model of how increasingly widespread genomic sequencing can influence treatment decision-making. Testing of two breast cancer-associated genes, BRCA1/2, has been available for twenty years, but new massively parallel sequencing technology and less restrictive patent laws have made multiplex panel tests available at much lower costs.1 Yet little is known about recent patient experience with genetic testing and counseling. Genetic counselors are expert in risk assessment and communication, but because of workforce limitations, some physicians must counsel and test patients without their assistance.2 These challenges motivated this investigation of patients’ use of and perspectives on genetic counseling and testing.
Abstract A56: Identification of an ErbB2+ early disseminating cancer cell subpopulation with metastatic potential
Authors: Kathryn Harper, Maria Soledad Sosa, Hedayatollah Hosseini, Alvaro Avivar Valderas, Chandandaneep Nagi, Roger Davis, Christoph Klein, David Entenberg, John Condeelis, Eduardo Farias, Julio Aguirre-Ghiso
Journal: Cancer Research (2016)

Abstract Recent clinical evidence suggests that cells are capable of disseminating from pre-invasive breast cancer lesions. It has been proposed that these early disseminating cancer cells (eDCCs) lodge into secondary sites, enter a state of dormancy, escape conventional therapy, and potentially evolve through different pathways from the primary tumor to form metastases. However, the mechanisms that endow these early cancer cells to disseminate and their behavior in target organs remain unknown. Here we show that ErbB2+ early cancer cells, while non-tumorigenic are highly efficient in disseminating. While a majority of these eDCCs remain dormant in target organs they are still endowed with a metastatic capacity. We identified an ErbB2HIGH/p38LOW/E-cadherinLOW/PRHI population of early cancer cells, which undergo a Wnt-dependent EMT and disseminate. Based on this signature we propose that these early cancer cells tap into motility programs similar to what is seen during branching morphogenesis (PRHI/WntHI/p38LOW) in order to disseminate. Using intra-vital imaging of transgenic ErbB2-T-CFP pre-malignant lesions we imaged this process at high resolution revealing that ErbB2HIGH/p38LOW/E-cadherinLOW cells display activate cancer cell motility, invadopodia formation and intravasation capacity. This correlated with CK8/18+/HER2+ circulating cancer cells as well as eDCCs in the lung and bone marrow of mice, a process that was enhanced following 2 weeks of systemic p38α/β inhibition. We conclude that during stages previously considered non-invasive, some HER2+ cancer cells can aberrantly activate an invasive morphogenetic program causing early dissemination that is normally restricted by active p38 signaling. These eDCCs carry latent metastatic initiating capacity and may contribute to relapse, altering our understanding of metastasis onset and how it might be targeted effectively. Citation Format: Kathryn Harper, Maria Soledad Sosa, Hedayatollah Hosseini, Alvaro Avivar Valderas, Chandandaneep Nagi, Roger Davis, Christoph Klein, David Entenberg, John Condeelis, Eduardo Farias, Julio Aguirre-Ghiso. Identification of an ErbB2+ early disseminating cancer cell subpopulation with metastatic potential. [abstract]. In: Proceedings of the AACR Special Conference on Tumor Metastasis; 2015 Nov 30-Dec 3; Austin, TX. Philadelphia (PA): AACR; Cancer Res 2016;76(7 Suppl):Abstract nr A56.
Development of laser-driven proton beam therapy
Authors: L. Karsch, E. Beyreuther, W. Enghardt, M. Gotz, T. Hermannsdörfer, M. Krause, U. Masood, J. Pawelke, R. Sauerbrey, U. Schramm, M. Schürer, M. Baumann
Journal: Annals of Oncology (2016)
Immune Inflammatory Consequences of Mutations in the Autophagy Gene ATG9A
Authors: Pia J. Hauk, Michael J. Morgan, Courtney Banks, Tsz-Yin Chan, Jordan K. Abbott, Michaela Schedel, Robin R. Deterding, Bradford R. Miller, Joshua L. Andersen, Erwin W. Gelfand
Journal: Journal of Allergy and Clinical Immunology (2017)
Sleep apnoea and pulmonary hypertension in high-altitude dwellers: more than an association?
Authors: Urs Scherrer, Samuel Verges
Journal: European Respiratory Journal (2017)

Increased pulmonary arterial pressure (PAP) is a hallmark of high-altitude exposure and, if exaggerated, may be associated with morbidity and mortality. High altitude also alters nocturnal breathing and altered nocturnal respiration has recently been reported to be associated with altered pulmonary and systemic vascular function in Andean high-altitude dwellers [1], suggesting the possibility of a causal link. Consistent with this hypothesis, in this issue of the European Respiratory Journal , Latshang et al. [2] report an association between pulmonary hypertension and sleep apnoea in Kyrgyz highlanders which remains significant even when adjusting for several potentially confounding factors. The authors are to be commended for their interesting study, performed in a remote area in a so far little investigated high-altitude population; however, this study also leaves open some intriguing questions. Pulmonary hypertension and sleep apnoea in high-altitude dwellers: more than an association? <http://ow.ly/U9AH306HQrn>
153P Ramucirumab safety in East Asian (EA) compared to non-EA patients: A meta-analysis of adverse events (AEs) in 6 global, randomized, double-blind, phase 3 clinical trials
Authors: H.C. Chung, Y. Chao, K.-W. Lee, M. Kudo, C.-J. Yen, T.W. Kim, K. Yamazaki, J.-Y. Shih, S.-W. Kim, J.-H. Sohn, R. Cheng, Y. Zhang, P. Binder, G. Mi, M. Orlando, K. Muro
Journal: Annals of Oncology (2016)
A Temporary Gating of Actin Remodeling during Synaptic Plasticity Consists of the Interplay between the Kinase and Structural Functions of CaMKII
Authors: Karam Kim, Gurpreet Lakhanpal, Hsiangmin E. Lu, Mustafa Khan, Akio Suzuki, Mariko Kato Hayashi, Radhakrishnan Narayanan, Thomas T. Luyben, Tomoki Matsuda, Takeharu Nagai, Thomas A. Blanpied, Yasunori Hayashi, Kenichi Okamoto
Journal: Neuron (2015)
P08.13 Pattern of care and outcome in elderly glioblastoma patients: a multicenter retrospective study on 151 patientsi from 3 hospitals in Lombardia
Authors: A. Silvani, A. Rigamonti, F. Imbesi, F. Legnani, G. Grimod, V. Arienti, V. Prone, C. Soatti, L. Fariselli, A. Salmaggi
Journal: Neuro-Oncology (2016)
285TiP DANUBE: A Phase 3 randomised study of first-line durvalumab (MEDI4736) ± tremelimumab vs standard of care (SoC) chemotherapy (CT) in patients (pts) with Stage IV urothelial carcinoma (UC)
Authors: S.H. Park, D. Castellano, D.P. Petrylak, M.D. Galsky, M.S. van der Heijden, Y. Loriot, O. Ogawa, W-P. Su, W. Huang, W. Levin, S. Ferro, Y. Ben, J. Bellmunt, T. Powles
Journal: Annals of Oncology (2016)
IDH1 mutation status and outcome in clinical trials for recurrent glioblastoma.
Authors: Jacob Joseph Mandel, David Cachia, Diane D Liu, Kenneth D. Aldape, Greg Fuller, John Frederick De Groot
Journal: Journal of Clinical Oncology (2015)

2073 Background: IDH1 mutated glioblastoma (GB) has a better prognosis than IDH1 wildtype GB. Clinical trials for recurrent GB currently do not stratify patients (pts) based upon IDH status. It is not known if pts with IDH1 mutated GB on clinical trials are more likely to have a higher 6-month progression free survival (PFS6) or radiographic response (RR) rate. Methods: A retrospective review of GB pts treated at MD Anderson Cancer Center between 2006-2012 identified 330 pts enrolled in recurrent GB trials. 93 pts (28%) either had PFS6 or a complete or partial RR per RANO criteria. 49/93(53%) pts with PFS6 or a complete or partial RR were found to have tumor tissue available for IDH1 testing. A matched cohort of pts on the same recurrent GB clinical trials with tissue for IDH1 testing but no PFS6 or RR was identified based on the specific clinical trial, age and KPS. 49 pts were identified for comparison resulting in a total of 98 patients. Results: IDH1 status was obtained in 92 (94%) pts of which 17 (18%) had an IDH1 mutation. Recurrent GB trial was at 1st-4th recurrence with 62% at 1st, 26% at 2nd, 8% at 3rd and 4% at 4threcurrence. Median time from GB diagnosis to recurrent trial was 8.4 months (mo) for IDH1 wildtype GB vs. 10.9 mo for IDH1 mutated GB (p < 0.66). PFS6 was seen in 26/49 (53%) pts of which 2 pts IDH status was unknown. 5/24 (21%) pts with PFS6 had IDH1 mutations compared to 5/24 (21%) pts of their matched cohort without PFS6. RR was found in 46/49 (94%) pts of which 4 pts IDH status was unknown. IDH1 mutation was present in 7/42 (17%) pts with RR compared to 10/42 (24%) pts of their matched cohort without RR (p < 0.49). For all patients, median PFS on a recurrent trial was 3.68 mo for IDH1 wildtype GB vs. 3.52 mo for IDH1 mutated GB (p < 0.72). Median OS on recurrent trial was 8.64 mo for IDH1 wildtype GB vs. 9.59 mo for IDH1 mutated GB (p < 0.49). Conclusions: IDH1 mutation status does not appear to be predictive of PFS6 or RR in recurrent GB trials. However, further examination in larger randomized prospective studies is needed.
SURG-41. “JOURNAL BIAS” IN NEURO-ONCOLOGY: AN ANALYSIS OF THE SURGICAL HIGH GRADE GLIOMA LITERATURE
Authors: Brian Hirshman, Laurie Jones, Jessica Tang, Mir Amaan Ali, James Proudfoot, Kathleen Carley, Bob Carter, Clark Chen
Journal: Neuro-Oncology (2016)

The core premise of evidence-based medicine is that clinical decisions are informed by the peer-reviewed literature. To extract meaningful conclusions from this literature, it is important to first understand the various forms of biases inherent within the publication process. Here, we examine whether an author’s educational background -- as evidenced by his or her academic mentors or “medical academic genealogy” -- are associated with journal publications in the high grade glioma (HGG) resection literature. We performed an PUBMED literature search that identified articles from US institutions exploring whether there was a survival benefit associated with maximal HGG resection. We analyzed the 108 identified papers for patterns in journal choice. As part of this analysis we constructed medical academic genealogies using the training history of key authors as identified via publicly available information (e.g. web CVs). We found that the distribution of these 108 articles among the 26 journals to be non-random (p<0.01), with 75 of the 108 published articles (69%) appearing in just 6 of the 26 journals (25%). Moreover, certain journals were likely to publish a large number of articles from the same medical academic genealogy (p<0.01). These trends were found to be independent of other quantitative characteristics such as impact factor (p>0.05). We termed the tendency of certain types of articles to be published in select journals “journal bias” and discuss the implication of this form of bias as it pertains to evidence-based medicine.
Towards the Care of Hemophilia a Patients Using Induced Pluripotent Stem Cell (iPSC)-Derived Megakaryocytes (iMks) Expressing Coagulation Factor (F) VIII
Authors: Randolph B Lyde, Li Zhai, Karen Vo, Danuta Jadwiga Jarocha, Spencer Sullivan, Valder R Arruda, Rodney M. Camire, Deborah French, Mortimer Poncz
Journal: Blood (2015)
A Selective Inhibitor of c-Met Blocks an Autocrine HGF Growth Loop in ANBL-6 Cells and Prevents Migration and Adhesion of Myeloma Cells.
Authors: Magne Borset, Hakon Hov, Randi U. Holt, Torstein B. Ro, Unn-Merete Fagerli, Henrik Hjorth-Hansen, Vadim Baykov, James G. Christensen, Anders Waage, Anders Sundan
Journal: Blood (2004)
Increased Myelofibrosis in Thrombospondin-1-Null Mice Is Associated with Enhanced TGF-β1-Mediated Response by Bone Marrow Fibroblasts
Authors: Solène Evrard, Micheline Tulliez, Eva Zetterberg, Jan Palmblad, William Vainchenker, Jean-Luc Villeval, Stéphane Giraudier, Orianne Wagner-Ballon
Journal: Blood (2008)
CBIO-11. COMPREHENSIVE ANALYSIS OF miRNA-mRNA REGULATORY MODULES AND THEIR ASSOCIATION WITH SURVIVAL IN DIFFUSE LOWER GRADE GLIOMAS
Authors: Mehmet Gönen, Tarık Tihan, Güven Evren Keleş, İhsan Solaroğlu
Journal: Neuro-Oncology (2016)

MicroRNAs (miRNAs) are short non-coding RNAs and have emerged as key regulators of many biological processes. They can also function as oncogenes or tumor suppressors that play a crucial role in the pathogenesis of human neoplasms such as diffuse lower grade gliomas (LGGs). There is emerging evidence that miRNAs are promising biomarkers with diagnostic or prognostic implications in LGGs. In this study, we first analyzed the matched miRNA and messenger RNA (mRNA) expression profiles of 512 LGGs from the NCI Cancer Genome Atlas network to identify important miRNA-mRNA relationships and determined a series of regulatory modules. We then prioritized these regulatory modules that were associated with survival in LGG patients. Some of the regulatory modules stratified LGGs into well recognized groups based on histological type and grade as well as recognized mutations in ATRX, IDH1, IDH2, and TP53 genes. This finding confirmed the relevance of miRNA-mRNA relationship in well recognized molecular tumor groups. In addition, we have identified miRNA-mRNA regulatory modules without any correlation to histological type, grade, or well-known mutations, even though they were independently associated with survival. Regulatory modules containing hsa-mir-21, hsa-mir-99b, hsa-mir-125a, hsa-mir-142, and hsa-mir-223 emerged as important, which may be significant in diagnosis, prognostication, and may even be useful as potential targets. Exploration of miRNA-mRNA regulatory modules can also provide additional information in the biology of LGGs.
565O_PR Predictors of financial catastrophe following cancer in a high-middle-income Asian country
Authors: N. Bhoo Pathy, C.-W. Ng, R. Sullivan, G.C. Lim, M. Mellor, N.S. Ibrahim Tamim, M. Kimman, S. Subramaniam, P.-P. Goh, C.-H. Yip
Journal: Annals of Oncology (2016)
First evidence of significant clinical activity of PD-1 inhibitors in metastatic, castration resistant prostate cancer (mCRPC)
Authors: J.N. Graff, J.J. Alumkal, C.G. Drake, G.V. Thomas, W.L. Redmond, M. Farhad, R. Slottke, T.M. Beer
Journal: Annals of Oncology (2016)
Levels of endogenous anti-beta-glucan IgG antibodies (ABA) predict clinical outcomes for imprime PGG: Evidence from phase 3 PRIMUS study in patients (pts) with metastatic colorectal cancer (mCRC)
Authors: M. Shum, J.T. Beck, J. Meyerhardt, R. Patel, M. Kochenderfer, T. Crocenzi, M. Patchen, M.A. Gargano, B. Ma, J. Lowe, J.L. Iglesias
Journal: Annals of Oncology (2016)
Transcription factor NFAT5 promotes macrophage survival in rheumatoid arthritis
Authors: Susanna Choi, Sungyong You, Donghyun Kim, Soo Youn Choi, H. Moo Kwon, Hyun-Sook Kim, Daehee Hwang, Yune-Jung Park, Chul-Soo Cho, Wan-Uk Kim
Journal: Journal of Clinical Investigation (2017)

Defective apoptotic death of activated macrophages has been implicated in the pathogenesis of rheumatoid arthritis (RA). However, the molecular signatures defining apoptotic resistance of RA macrophages are not fully understood. Here, global transcriptome profiling of RA macrophages revealed that the osmoprotective transcription factor nuclear factor of activated T cells 5 (NFAT5) critically regulates diverse pathologic processes in synovial macrophages including the cell cycle, apoptosis, and proliferation. Transcriptomic analysis of NFAT5-deficient macrophages revealed the molecular networks defining cell survival and proliferation. Proinflammatory M1-polarizing stimuli and hypoxic conditions were responsible for enhanced NFAT5 expression in RA macrophages. An in vitro functional study demonstrated that NFAT5-deficient macrophages were more susceptible to apoptotic death. Specifically, CCL2 secretion in an NFAT5-dependent fashion bestowed apoptotic resistance to RA macrophages in vitro. Injection of recombinant CCL2 into one of the affected joints of Nfat5+/- mice increased joint destruction and macrophage infiltration, demonstrating the essential role of the NFAT5/CCL2 axis in arthritis progression in vivo. Moreover, after intra-articular injection, NFAT5-deficient macrophages were more susceptible to apoptosis and less efficient at promoting joint destruction than were NFAT5-sufficient macrophages. Thus, NFAT5 regulates macrophage survival by inducing CCL2 secretion. Our results provide evidence that NFAT5 expression in macrophages enhances chronic arthritis by conferring apoptotic resistance to activated macrophages.
Systemic Iron Overload in Patients Undergoing Allogeneic Stem Cell Transplantation – a Magnetic Resonance Imaging Based Study in 81 AML and MDS Patients
Authors: Martin Wermke, Anne Schmidt, Jan Moritz Middeke, Katja Sockel, Malte von Bonin, Verena Plodeck, Michael Laniado, Johannes Schetelig, Gerhard Ehninger, Martin Bornhauser, Uwe Platzbecker
Journal: Blood (2011)
Analysis of cancer outcomes after desensitization protocols in patients with metastatic disease
Authors: C. Pulido, J. Caiado, A.R. Ferreira, I. Vendrell, A.L. Costa, A. Mendes, M.E. Pedro, N. Fernandes, L. Pestana, P.L. Almeida, C. Pinto, A. Quintela, L. Ribeiro, I.C. Fernandes, P. Filipe, R. Sousa, C. Abreu, D. Macedo, M.P. Barbosa, L.A.M. Costa
Journal: Annals of Oncology (2016)