Genomic analyses of flow-sorted Hodgkin Reed-Sternberg cells reveal complementary mechanisms of immune evasion

Author:

Wienand Kirsty12ORCID,Chapuy Bjoern123ORCID,Stewart Chip4ORCID,Dunford Andrew J.4ORCID,Wu David5ORCID,Kim Jaegil4,Kamburov Atanas4,Wood Timothy R.4,Cader Fathima Zumla12ORCID,Ducar Matthew D.67,Thorner Aaron R.17,Nag Anwesha17ORCID,Heubeck Alexander T.8,Buonopane Michael J.8,Redd Robert A.9ORCID,Bojarczuk Kamil12ORCID,Lawton Lee N.1ORCID,Armand Philippe12ORCID,Rodig Scott J.10ORCID,Fromm Jonathan R.5ORCID,Getz Gad241112ORCID,Shipp Margaret A.12ORCID

Affiliation:

1. Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, MA;

2. Harvard Medical School, Boston, MA;

3. Department of Hematology and Oncology, University Medical Center Göttingen, Göttingen, Germany;

4. Broad Institute of Harvard and Massachusetts Institute of Technology, Cambridge, MA;

5. Department of Laboratory Medicine, University of Washington, Seattle, WA;

6. Department of Data Science, Knowledge Systems Group, Boston, MA;

7. Center for Cancer Genome Discovery, Boston, MA;

8. Hematologic Neoplasia Flow Cytometry Core and

9. Department of Data Sciences, Dana-Farber Cancer Institute, Boston, MA;

10. Department of Pathology, Brigham and Women’s Hospital, Boston, MA; and

11. Department of Pathology and

12. Center for Cancer Research, Massachusetts General Hospital, Boston, MA

Abstract

Key Points Analyses of recurrent mutations, copy number alterations, and structural variants reveal complementary immune evasion mechanisms in cHL. The mutational burden in EBV– cHLs is among the highest reported, potentially contributing to the efficacy of PD-1 blockade.

Publisher

American Society of Hematology

Subject

Hematology

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