ArticleHaematologica2024
Distinctive genomic features of human T-lymphotropic virus type 1-related adult T-cell leukemia-lymphoma in Western populations.
Article in Haematologica, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed.
- Virus infections and cancers: from mechanisms to therapeutics.Molecular biomedicine · 2026Review
- Immunological decoding of adult T cell leukemia - its cell of origin and oncogenesis.Biomarker research · 2026Review
- Distribution of adult T-cell leukaemia/lymphoma subtypes and survival outcomes across geographical regions: An international retrospective cohort study.British journal of haematology · 2026Article
- The viral and host genomic landscape of human T-cell leukemia virus type I in Peru.Virology journal · 2026Article
- Review
- Characterization of adult T-cell leukemia/lymphoma patients with specific skin lesions in a tertiary dermatological service in Brazil.Frontiers in medicine · 2025Article
- Investigation of exJSRV LTR promoter activity based on transcription factor regulatory networks.Frontiers in veterinary science · 2025Article
- EntitiesHaematologica · 2024Article
Corrections and comments
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Authors and funding
29 authors.
Funding
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.
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