RT Journal Article
SR Electronic
T1 Toward a comprehensive view of cancer immune responsiveness: a synopsis from the SITC workshop
JF Journal for ImmunoTherapy of Cancer
JO J Immunother Cancer
FD BMJ Publishing Group Ltd
SP 131
DO 10.1186/s40425-019-0602-4
VO 7
IS 1
A1 Davide Bedognetti
A1 Michele Ceccarelli
A1 Lorenzo Galluzzi
A1 Rongze Lu
A1 Karolina Palucka
A1 Josue Samayoa
A1 Stefani Spranger
A1 Sarah Warren
A1 Kwok-Kin Wong
A1 Elad Ziv
A1 Diego Chowell
A1 Lisa M. Coussens
A1 Daniel D. De Carvalho
A1 David G. DeNardo
A1 Jérôme Galon
A1 Howard L. Kaufman
A1 Tomas Kirchhoff
A1 Michael T. Lotze
A1 Jason J. Luke
A1 Andy J. Minn
A1 Katerina Politi
A1 Leonard D. Shultz
A1 Richard Simon
A1 Vésteinn Thórsson
A1 Joanne B. Weidhaas
A1 Maria Libera Ascierto
A1 Paolo Antonio Ascierto
A1 James M. Barnes
A1 Valentin Barsan
A1 Praveen K. Bommareddy
A1 Adrian Bot
A1 Sarah E. Church
A1 Gennaro Ciliberto
A1 Andrea De Maria
A1 Dobrin Draganov
A1 Winson S. Ho
A1 Heather M. McGee
A1 Anne Monette
A1 Joseph F. Murphy
A1 Paola Nisticò
A1 Wungki Park
A1 Maulik Patel
A1 Michael Quigley
A1 Laszlo Radvanyi
A1 Harry Raftopoulos
A1 Nils-Petter Rudqvist
A1 Alexandra Snyder
A1 Randy F. Sweis
A1 Sara Valpione
A1 Roberta Zappasodi
A1 Lisa H. Butterfield
A1 Mary L. Disis
A1 Bernard A. Fox
A1 Alessandra Cesano
A1 Francesco M. Marincola
A1 Society for Immunotherapy of Cancer (SITC) Cancer Immune Responsiveness Task Force and Working Groups
YR 2019
UL http://jitc.bmj.com/content/7/1/131.abstract
AB Tumor immunology has changed the landscape of cancer treatment. Yet, not all patients benefit as cancer immune responsiveness (CIR) remains a limitation in a considerable proportion of cases. The multifactorial determinants of CIR include the genetic makeup of the patient, the genomic instability central to cancer development, the evolutionary emergence of cancer phenotypes under the influence of immune editing, and external modifiers such as demographics, environment, treatment potency, co-morbidities and cancer-independent alterations including immune homeostasis and polymorphisms in the major and minor histocompatibility molecules, cytokines, and chemokines. Based on the premise that cancer is fundamentally a disorder of the genes arising within a cell biologic process, whose deviations from normality determine the rules of engagement with the host’s response, the Society for Immunotherapy of Cancer (SITC) convened a task force of experts from various disciplines including, immunology, oncology, biophysics, structural biology, molecular and cellular biology, genetics, and bioinformatics to address the complexity of CIR from a holistic view. The task force was launched by a workshop held in San Francisco on May 14–15, 2018 aimed at two preeminent goals: 1) to identify the fundamental questions related to CIR and 2) to create an interactive community of experts that could guide scientific and research priorities by forming a logical progression supported by multiple perspectives to uncover mechanisms of CIR. This workshop was a first step toward a second meeting where the focus would be to address the actionability of some of the questions identified by working groups. In this event, five working groups aimed at defining a path to test hypotheses according to their relevance to human cancer and identifying experimental models closest to human biology, which include: 1) Germline-Genetic, 2) Somatic-Genetic and 3) Genomic-Transcriptional contributions to CIR, 4) Determinant(s) of Immunogenic Cell Death that modulate CIR, and 5) Experimental Models that best represent CIR and its conversion to an immune responsive state. This manuscript summarizes the contributions from each group and should be considered as a first milestone in the path toward a more contemporary understanding of CIR. We appreciate that this effort is far from comprehensive and that other relevant aspects related to CIR such as the microbiome, the individual’s recombined T cell and B cell receptors, and the metabolic status of cancer and immune cells were not fully included. These and other important factors will be included in future activities of the taskforce. The taskforce will focus on prioritization and specific actionable approach to answer the identified questions and implementing the collaborations in the follow-up workshop, which will be held in Houston on September 4–5, 2019.Davide Bedognetti, Rongze Lu, Josue Samayoa, Stefani Spranger and Sarah Warren contributed equally to this work.A correction to this article is available online at https://doi.org/10.1186/s40425-019-0640-y.Abbreviations:ACTAdoptive Cellular TherapyADCCAntibody-Dependent CytotoxicityALKAnaplastic Lymphoma KinaseAPCantigen presenting cellsB2mbeta-2-microglobulinCALRCalreticulinCARChimeric Antigen ReceptorCCRC-C motif chemokine ReceptorccRCCclear cell renal cell cancercfDNACell Free DNACIRCancer Immune ResponsivenessCSFColony-Stimulating FactorCTCCirculating Tumor CellsCTLACytotoxic T-Lymphocyte-Associated proteinDAMPDamage-Associated Molecular PatternDDRDNA Damage ResponseEGFREpidermal Growth Factor ReceptorFcCrystallizable FragmentGM-CSFGranulocyte-Macrophage Colony-stimulating FactorGVHDGraft-Versus-Host DiseaseGWASGenome Wide Association StudiesHLAHuman Leukocyte AntigenHMB1High-Mobility group Box protein 1HSCHematopoietic Stem CellHSPHeat Shock ProteinICDImmunogenic Cell DeathICGCInternational Cancer Genome ConsortiumICIImmune Checkpoint InhibitorICRImmunologic Constant of RejectionIDH1Isocitrate Dehydrogenase 1IFNInterferonILInterleukinIOImmuno-OncologyM-CSFMacrophage Colony-Stimulating FactorMHCMajor Histocompatibility moleculesNGSNext Generation SequencingNKNatural KillerNSGNon-obese-diabetic SCID Gamma miceNSG/SGM3NSG mice/h-Stem Cell Factor, h-Granulocyte Macrophage-Colony Stimulating Factor and h-IL-3 micePD-1Programmed cell Death protein 1PDXPatient-Derived XenograftSCIDSevere Combined ImmunodeficiencySIRPASignal Regulatory Protein AlphaSITCSociety for Immunotherapy of CancerTCDTolerogenic Cell DeathTCGAThe Cancer Genome AtlasTCRT-Cell ReceptorTILTumor-Infiltrating LymphocytesTISTumor Inflammation SignatureTMBTumor Mutational BurdenTMETumor MicroenvironmentTPOThrombopoietinTregRegulatory T cells