ID

45371

Descrizione

Principal Investigator: Margaret A Shipp, Dana Farber Cancer Institute, Boston MA, USA MeSH: Hodgkin Disease https://www.ncbi.nlm.nih.gov/projects/gap/cgi-bin/study.cgi?study_id=phs000450 Classical Hodgkin lymphoma (cHL) is composed of rare malignant Hodgkin Reed Sternberg (HRS) cells within an extensive, but ineffective, inflammatory/immune cell infiltrate. HRS cells exhibit near-universal somatic copy gains of chromosome 9p/9p24.1 which increase expression of the PD-1 ligands. To define genetic mechanisms of response and resistance to PD-1 blockade and identify complementary treatment targets, we performed whole exome sequencing of flow cytometry-sorted HRS cells from 23 excisional biopsies of newly diagnosed cHLs including 8 EBVsup+/sup tumors. We identified significantly mutated cancer candidate genes (CCGs) as well as somatic copy number alterations and structural variations and characterized their contribution to disease-defining immune evasion mechanisms and NF-KB, JAK/STAT and PI3K signaling pathways. EBV- cHLs had a higher prevalence of genetic alterations in the NF-KB and MHC class I antigen presentation pathways. In this young cHL cohort (median age of 26), we identified a predominant mutational signature of spontaneous deamination of CpGs ("Aging"), in addition to APOBEC, AID and MSI-associated hypermutation. In particular, the mutational burden in EBV- cHLs was among the highest reported, similar to that of carcinogen-induced tumors. Together, the overall high mutational burden, MSI-associated hypermutation and newly identified genetic alterations represent additional potential bases for the efficacy of PD-1 blockade in cHL. Of note, recurrent cHL alterations including *B2M, TNFAIP3, STAT6, GNA13* and *XPO1* mutations and 2p/2p15, 6p21.32, 6q23.2 and 9p/9p24.1 copy number alterations were also identified in 20% of primary mediastinal B-cell lymphomas, highlighting shared pathogenetic mechanisms in these diseases (companion manuscriptsup1/sup). Reprinted from *Blood Advances* 2019;3(23):4065-4080.PMID: 31816062.

collegamento

dbGap-study=phs000450

Keywords

  1. 04/11/22 04/11/22 - Chiara Middel
Titolare del copyright

Margaret A Shipp, Dana Farber Cancer Institute, Boston MA, USA

Caricato su

4 novembre 2022

DOI

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Licenza

Creative Commons BY 4.0

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dbGaP phs000450 Genomic Analyses of Flow-sorted Hodgkin Reed Sternberg Cells Reveal Complementary Mechanisms of Immune Evasion.

Subject ID and consent group of subjects affected with diffuse large B-cell lymphoma and involved in the "Whole Exome Sequencing of Diffuse Large B-Cell Lymphoma" project.

pht002529
Descrizione

pht002529

Subject ID
Descrizione

SUBJECT_ID

Tipo di dati

string

Alias
UMLS CUI [1,1]
C2348585 (Clinical Trial Subject Unique Identifier)
Consent group as determined by DAC
Descrizione

CONSENT

Tipo di dati

text

Alias
UMLS CUI [1,1]
C0021430 (Informed Consent)

Similar models

Subject ID and consent group of subjects affected with diffuse large B-cell lymphoma and involved in the "Whole Exome Sequencing of Diffuse Large B-Cell Lymphoma" project.

Name
genere
Description | Question | Decode (Coded Value)
Tipo di dati
Alias
Item Group
pht002529
SUBJECT_ID
Item
Subject ID
string
C2348585 (UMLS CUI [1,1])
Item
Consent group as determined by DAC
text
C0021430 (UMLS CUI [1,1])
Code List
Consent group as determined by DAC
CL Item
General Research Use (NPU, MDS) (GRU-NPU-MDS) (1)
CL Item
Disease-Specific (Blood and Lymph Disorders, MDS) (DS-BLD-MDS) (2)
CL Item
Disease-Specific (Cancer, MDS) (DS-CA-MDS) (3)
CL Item
Health/Medical/Biomedical (HMB) (4)

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