Nivolumab for Refractory Anaplastic Large Cell Lymphoma: A Case Report

间变性淋巴瘤激酶 间变性大细胞淋巴瘤 医学 淋巴瘤 癌症研究 肿瘤科 内科学 肺癌 恶性胸腔积液
作者
Holger Hebart,Peter Lang,Wilhelm Woessmann
出处
期刊:Annals of Internal Medicine [American College of Physicians]
卷期号:165 (8): 607-607 被引量:50
标识
DOI:10.7326/l16-0037
摘要

Letters18 October 2016Nivolumab for Refractory Anaplastic Large Cell Lymphoma: A Case ReportHolger Hebart, MD, Peter Lang, MD, and Wilhelm Woessmann, MDHolger Hebart, MDFrom Stauferklinikum Schwaeb. Gmuend, Mutlangen, Germany; Eberhard Karls University Tuebingen, Tuebingen, Germany; and Justus Liebig University Giessen, Giessen, Germany., Peter Lang, MDFrom Stauferklinikum Schwaeb. Gmuend, Mutlangen, Germany; Eberhard Karls University Tuebingen, Tuebingen, Germany; and Justus Liebig University Giessen, Giessen, Germany., and Wilhelm Woessmann, MDFrom Stauferklinikum Schwaeb. Gmuend, Mutlangen, Germany; Eberhard Karls University Tuebingen, Tuebingen, Germany; and Justus Liebig University Giessen, Giessen, Germany.Author, Article, and Disclosure Informationhttps://doi.org/10.7326/L16-0037 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail Background: Anaplastic large cell lymphoma (ALCL) is a rare type of non-Hodgkin lymphoma consisting of T cells. Patients with the systemic form of this cancer are divided into 2 groups, depending on whether an abnormal form of a cellular surface protein called anaplastic lymphoma kinase (ALK) is present. Many of these patients have a chromosome translocation that fuses part of the nucleophosmin (NPM) gene on chromosome 5 with part of the ALK gene on chromosome 2. This combination induces expression of the ligand for the programmed death-1 cell receptor, which is believed to suppress the immune system and allow the ...References1. Mussolin L, Damm-Welk C, Pillon M, Zimmermann M, Franceschetto G, Pulford K, et al. Use of minimal disseminated disease and immunity to NPM-ALK antigen to stratify ALK-positive ALCL patients with different prognosis. Leukemia. 2013;27:416-22. [PMID: 22907048] doi:10.1038/leu.2012.205 CrossrefMedlineGoogle Scholar2. Marzec M, Zhang Q, Goradia A, Raghunath PN, Liu X, Paessler M, et al. Oncogenic kinase NPM/ALK induces through STAT3 expression of immunosuppressive protein CD274 (PD-L1, B7-H1). Proc Natl Acad Sci U S A. 2008;105:20852-7. [PMID: 19088198] doi:10.1073/pnas.0810958105 CrossrefMedlineGoogle Scholar3. Ansell SM, Lesokhin AM, Borrello I, Halwani A, Scott EC, Gutierrez M, et al. PD-1 blockade with nivolumab in relapsed or refractory Hodgkin's lymphoma. N Engl J Med. 2015;372:311-9. [PMID: 25482239] doi:10.1056/NEJMoa1411087 CrossrefMedlineGoogle Scholar4. Damm-Welk C, Busch K, Burkhardt B, Schieferstein J, Viehmann S, Oschlies I, et al. Prognostic significance of circulating tumor cells in bone marrow or peripheral blood as detected by qualitative and quantitative PCR in pediatric NPM-ALK-positive anaplastic large-cell lymphoma. Blood. 2007;110:670-7. [PMID: 17392503] CrossrefMedlineGoogle Scholar5. Amin AD, Rajan SS, Liang WS, Pongtornpipat P, Groysman MJ, Tapia EO, et al. Evidence suggesting that discontinuous dosing of ALK kinase inhibitors may prolong control of ALK+ tumors. Cancer Res. 2015;75:2916-27. [PMID: 26018086] doi:10.1158/0008-5472.CAN-14-3437 CrossrefMedlineGoogle Scholar Author, Article, and Disclosure InformationAffiliations: From Stauferklinikum Schwaeb. Gmuend, Mutlangen, Germany; Eberhard Karls University Tuebingen, Tuebingen, Germany; and Justus Liebig University Giessen, Giessen, Germany.Disclosures: Authors have disclosed no conflicts of interest. Forms can be viewed at www.acponline.org/authors/icmje/ConflictOfInterestForms.do?msNum=L16-0037. PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byAP-1 family transcription factors: a diverse family of proteins that regulate varied cellular activities in classical hodgkin lymphoma and ALK+ ALCLClinicopathological features and prognostic significance of programmed death ligand 1 in pediatric ALK-positive anaplastic large cell lymphoma: results of the ALCL99 treatment in JapanThe Dual Role of Autophagy in Crizotinib-Treated ALK+ ALCL: From the Lymphoma Cells Drug Resistance to Their DemisePharmacological inhibitors of anaplastic lymphoma kinase (ALK) induce immunogenic cell death through on-target effectsThe Spectrum of Anaplastic Large‐cell LymphomaCentral nervous system relapse in a child with anaplastic large cell lymphoma: potential for new therapeutic strategiesMinimal Disease Monitoring in Pediatric Non-Hodgkin's Lymphoma: Current Clinical Application and Future ChallengesNeuro‐meningeal relapse in anaplastic large‐cell lymphoma: incidence, risk factors and prognosis – a report from the European intergroup for childhood non‐Hodgkin lymphomaManagement of ALK positive patients with tumors other than lung cancerNPM-ALK: A Driver of Lymphoma Pathogenesis and a Therapeutic TargetStem Cell Transplantation and Vinblastine Monotherapy for Relapsed Pediatric Anaplastic Large Cell Lymphoma: Results of the International, Prospective ALCL-Relapse TrialCurrent Clinical Applications and Future Perspectives of Immune Checkpoint Inhibitors in Non-Hodgkin LymphomaPD-1/PD-L1 Pathway and Its Blockade in Patients with Classic Hodgkin Lymphoma and Non-Hodgkin Large-Cell LymphomasACCELERATE and European Medicines Agency Paediatric Strategy Forum for medicinal product development of checkpoint inhibitors for use in combination therapy in paediatric patientsPD-L1 expression is associated with ALK positivity and STAT3 activation, but not outcome in patients with systemic anaplastic large cell lymphomaBlockade of programmed cell death protein 1 (PD-1) in Sézary syndrome reduces Th2 phenotype of non-tumoral T lymphocytes but may enhance tumor proliferationFrom bench to bedside: the past, present and future of therapy for systemic paediatric ALCL , ALK +Novel targeted therapeutic agents for the treatment of childhood, adolescent and young adult non‐Hodgkin lymphomaMinimal Disseminated and Minimal Residual Disease in Pediatric Non-Hodgkin LymphomaAnaplastic Large Cell Lymphoma in Children and AdolescentsCheckpoint Inhibitors Hodgkin Lymphoma and Non-Hodgkin LymphomaNouvelles perspectives dans l'immunothérapie des cancers pédiatriquesKaposi's varicelliform eruption in a patient with metastatic melanoma and primary cutaneous anaplastic large cell lymphoma treated with talimogene laherparepvec and nivolumabLymphoma in Adolescents and Young AdultsCurrent Immunotherapeutic Approaches in T Cell Non-Hodgkin LymphomasNHL in adolescents and young adults: A unique populationCNS progression during vinblastine or targeted therapies for high-risk relapsed ALK-positive anaplastic large cell lymphoma: A case seriesCharacterization and diagnostic application of genomic NPM-ALK fusion sequences in anaplastic large-cell lymphomaEfficacy of nivolumab in a patient with systemic refractory ALK+ anaplastic large cell lymphomaTreatment Options for Paediatric Anaplastic Large Cell Lymphoma (ALCL): Current Standard and beyondImmune Response against ALK in Children with ALK-Positive Anaplastic Large Cell LymphomaMonoclonal Antibodies Targeting the Immune SystemFrom Pathology to Precision Medicine in Anaplastic Large Cell Lymphoma Expressing Anaplastic Lymphoma Kinase (ALK+ ALCL)Anaplastic large-cell lymphoma and peripheral T-cell lymphoma: What can pediatricians and adult oncologists learn from each other?NivolumabJudicious Toggling of mTOR Activity to Combat Insulin Resistance and Cancer: Current Evidence and Perspectives 18 October 2016Volume 165, Issue 8Page: 607-608KeywordsBlood cellsCentral nervous systemChemotherapeutic agentsChemotherapyChromosomal translocationsImmune systemLymphomaMacrophagesPolymerase chain reactionStem cell transplantation ePublished: 18 October 2016 Issue Published: 18 October 2016 Copyright & PermissionsCopyright © 2016 by American College of Physicians. 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