DNMT3A mutations define a unique biological and prognostic subgroup associated with cytotoxic T cells in PTCL-NOS.


Journal

Blood
ISSN: 1528-0020
Titre abrégé: Blood
Pays: United States
ID NLM: 7603509

Informations de publication

Date de publication:
15 09 2022
Historique:
received: 01 12 2021
accepted: 08 04 2022
pubmed: 1 6 2022
medline: 20 9 2022
entrez: 31 5 2022
Statut: ppublish

Résumé

Peripheral T-cell lymphomas (PTCLs) are heterogenous T-cell neoplasms often associated with epigenetic dysregulation. We investigated de novo DNA methyltransferase 3A (DNMT3A) mutations in common PTCL entities, including angioimmunoblastic T-cell lymphoma and novel molecular subtypes identified within PTCL-not otherwise specified (PTCL-NOS) designated as PTCL-GATA3 and PTCL-TBX21. DNMT3A-mutated PTCL-TBX21 cases showed inferior overall survival (OS), with DNMT3A-mutated residues skewed toward the methyltransferase domain and dimerization motif (S881-R887). Transcriptional profiling demonstrated significant enrichment of activated CD8+ T-cell cytotoxic gene signatures in the DNMT3A-mutant PTCL-TBX21 cases, which was further validated using immunohistochemistry. Genomewide methylation analysis of DNMT3A-mutant vs wild-type (WT) PTCL-TBX21 cases demonstrated hypomethylation in target genes regulating interferon-γ (IFN-γ), T-cell receptor signaling, and EOMES (eomesodermin), a master transcriptional regulator of cytotoxic effector cells. Similar findings were observed in a murine model of PTCL with Dnmt3a loss (in vivo) and further validated in vitro by ectopic expression of DNMT3A mutants (DNMT3A-R882, -Q886, and -V716, vs WT) in CD8+ T-cell line, resulting in T-cell activation and EOMES upregulation. Furthermore, stable, ectopic expression of the DNMT3A mutants in primary CD3+ T-cell cultures resulted in the preferential outgrowth of CD8+ T cells with DNMT3AR882H mutation. Single-cell RNA sequencing(RNA-seq) analysis of CD3+ T cells revealed differential CD8+ T-cell subset polarization, mirroring findings in DNMT3A-mutated PTCL-TBX21 and validating the cytotoxic and T-cell memory transcriptional programs associated with the DNMT3AR882H mutation. Our findings indicate that DNMT3A mutations define a cytotoxic subset in PTCL-TBX21 with prognostic significance and thus may further refine pathological heterogeneity in PTCL-NOS and suggest alternative treatment strategies for this subset.

Identifiants

pubmed: 35639959
pii: S0006-4971(22)00713-3
doi: 10.1182/blood.2021015019
pmc: PMC9479030
doi:

Substances chimiques

Receptors, Antigen, T-Cell 0
Interferon-gamma 82115-62-6
Methyltransferases EC 2.1.1.-

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1278-1290

Subventions

Organisme : NCI NIH HHS
ID : T32 CA009476
Pays : United States

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Auteurs

Tyler A Herek (TA)

Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE.

Alyssa Bouska (A)

Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE.

Waseem Lone (W)

Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE.

Sunandini Sharma (S)

Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE.

Catalina Amador (C)

Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE.

Tayla B Heavican (TB)

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

Yuping Li (Y)

Department of Pathology, City of Hope National Medical Center, Duarte, CA.

Qi Wei (Q)

Department of Pathology, City of Hope National Medical Center, Duarte, CA.

Dylan Jochum (D)

Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE.

Timothy C Greiner (TC)

Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE.

Lynette Smith (L)

Department of Biostatistics, University of Nebraska Medical Center, Omaha, NE.

Stefano Pileri (S)

Division of Diagnostic Hematopathology, European Institute of Oncology-IEO IRCCS, Milan, Italy.

Andrew L Feldman (AL)

Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN.

Andreas Rosenwald (A)

Institute of Pathology, University of Würzburg and Comprehensive Cancer Center Mainfranken, Würzburg, Germany.

German Ott (G)

Department of Clinical Pathology, Robert-Bosch-Krankenhaus, and Dr. Margarete Fischer-Bosch Institute for Clinical Pharmacology, Stuttgart, Germany.

Soon Thye Lim (ST)

Division of Medical Oncology, National Cancer Centre Singapore/Duke-National University of Singapore (NUS) Medical School, Singapore, Singapore.

Choon Kiat Ong (CK)

Division of Medical Oncology, National Cancer Centre Singapore/Duke-National University of Singapore (NUS) Medical School, Singapore, Singapore.

Joo Song (J)

Department of Pathology, City of Hope National Medical Center, Duarte, CA.

Elaine S Jaffe (ES)

Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, MD.

Gang Greg Wang (GG)

Lineberger Comprehensive Cancer Center and.
Department of Biochemistry and Biophysics, University of North Carolina at Chapel Hill, Chapel Hill, NC.

Louis Staudt (L)

Metabolism Branch, Center for Cancer Research, National Cancer Institute, National Institutes of Health, Bethesda, MD.

Lisa M Rimsza (LM)

Department of Laboratory Medicine and Pathology, Mayo Clinic, Scottsdale, AZ.

Julie Vose (J)

Division of Hematology and Oncology, University of Nebraska Medical Center, Omaha, NE; and.

Francesco d'Amore (F)

Department of Haematology, Aarhus University Hospital, Aarhus N, Denmark.

Dennis D Weisenburger (DD)

Department of Pathology, City of Hope National Medical Center, Duarte, CA.

Wing C Chan (WC)

Department of Pathology, City of Hope National Medical Center, Duarte, CA.

Javeed Iqbal (J)

Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE.

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