Abstract
Adult T-cell leukemia-lymphoma (ATLL) is an aggressive malignancy driven by human T-cell leukemia virus type 1 (HTLV-1). Although patients from the Western hemisphere (Afro-Caribbean and South American) face worse prognoses, our understanding of ATLL molecular drivers derives mostly from Japanese studies. We performed multi-omic analyses to elucidate the genomic landscape of ATLL in Western cohorts. Recurrent deletions and/or damaging mutations involving FOXO3, ANKRD11, DGKZ, and PTPN6 implicate these genes as potential tumor suppressors. RNA-sequencing, published functional data and in vitro assays support the roles of ANKRD11 and FOXO3 as regulators of T-cell proliferation and apoptosis in ATLL, respectively. Survival data suggest that ANKRD11 mutation may confer a worse prognosis. Japanese and Western cohorts, in addition to acute and lymphomatous subtypes, demonstrated distinct molecular patterns. GATA3 deletion was associated with chronic cases with unfavorable outcomes. IRF4 and CARD11 mutations frequently emerged in relapses after interferon therapy. Our findings reveal novel putative ATLL driver genes and clinically relevant differences between Japanese and Western ATLL patients.
Original language | English (US) |
---|---|
Pages (from-to) | 4021-4039 |
Number of pages | 19 |
Journal | Haematologica |
Volume | 109 |
Issue number | 12 |
DOIs | |
State | Published - Dec 2024 |
Funding
We acknowledge the patients who consented to inclusion in this study, Admera Health, the University of Virginia Comprehensive Cancer Center, the University of Miami Sylvester Comprehensive Cancer Center and its Flow Cytometry Shared Resource and data analysis by Patricia Guevara, and the Northwestern University Flow Cytometry Core and Research Computing Services for their invaluable contributions. JC was supported in part by the National Institutes of Health (R01CA260064-01A1), the Bakewell Foundation and the Leukemia and Lymphoma Society grant 1377-21. JCR was supported in part by the National Institutes of Health/National Cancer Institute (R01CA223232) and the University of Miami-Sylvester Comprehensive Cancer Center (P30CA240139). CSM was supported by the Monticello College Foundation Olin Fellowship. The content of this paper is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health. JC was supported in part by the National Institutes of Health (R01CA260064-01A1), the Bakewell Foundation and the Leukemia and Lymphoma Society grant 1377-21. JCR was supported in part by the National Institutes of Health/National Cancer Institute (R01CA223232) and the University of Miami-Sylvester Comprehensive Cancer Center (P30CA240139). CSM was supported by the Monticello College Foundation Olin Fellowship. The content of this paper is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
ASJC Scopus subject areas
- Hematology