| Literature DB >> 34164626 |
Alessandra Venanzi1, Andrea Marra1, Gianluca Schiavoni1, Brunangelo Falini2, Enrico Tiacci2, Sara G Milner1, Roberto Limongello1, Alessia Santi1, Valentina Pettirossi1, Simona Ultimo1, Luisa Tasselli1, Alessandra Pucciarini1, Lorenza Falini1, Sofia Sciabolacci1, Maria Paola Martelli1, Paolo Sportoletti1, Stefano Ascani1.
Abstract
Clonal hematopoiesis predisposes to hematological malignancies. However, clonal hematopoiesis is understudied in classical Hodgkin lymphoma (cHL), a mature B-cell neoplasm exhibiting the most abundant microenvironment. We analyzed clonal hematopoiesis in 40 cHL cases by sequencing microdissected tumor cells and matched normal cells from blood and/or lymph nodes. Five patients had blood and/or tissue clonal hematopoiesis. In three of five patients (all failing first-line therapy), clonal hematopoiesis spread through the tissue microenvironment extensively, and featured mutant DNMT3AR882H , KRASG60D and DNMT3AR882H +TET2Q1274 * in 33%, 92% and 60% of non-neoplastic cells, respectively. In the latter case, DNMT3A/TET2-mutant clonal hematopoiesis seeded the neoplastic clone, which was infected by the Epstein-Barr virus and showed almost no other somatic mutations exome-wide. In the former case, DNMT3A-mutant clonal hematopoiesis did not originate the neoplastic clone despite dominating the blood and B-cell lineage (~94% leukocytes; ~96% mature blood B cells), yet led to NPM1-mutated acute myeloid leukemia 6 years after therapy for cHL. Our results expand to cHL the spectrum of hematologic malignancies associated with clonal hematopoiesis.Entities:
Keywords: Acute myeloid leukemia; Clonal hematopoiesis; DNMT3A; Hodgkin lymphoma; Microenvironment; NPM1
Mesh:
Year: 2021 PMID: 34164626 PMCID: PMC7611041 DOI: 10.1158/2643-3230.BCD-20-0203
Source DB: PubMed Journal: Blood Cancer Discov ISSN: 2643-3230