ReviewInternational journal of hematology2026
Viral-driven oncogenesis in T/NK-cell lymphomas: parallels and divergences between HTLV-1 and EBV.
Review in International journal of hematology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors.
Funding
Abstract
Viruses induce approximately 12% of human cancers, including lymphomas. In the case of T/NK cell neoplasms, human T-cell leukemia virus type I (HTLV-1) causes adult T-cell leukemia-lymphoma (ATL), and Epstein-Barr virus (EBV) is associated with extranodal NK/T-cell lymphoma (ENKTCL) and chronic active Epstein-Barr virus disease (CAEBV). Common mechanisms for lymphoma development have been proposed. Viral genes, such as tax and HTLV-1 bZIP factor (HBZ) of HTLV-1, and latent membrane protein 1 (LMP1) and BamHI A rightward transcript microRNA (miRNA-BART) of EBV, contribute to host immune evasion and modulation of host signaling pathways, resulting in the persistence of viral-infected cells. This viral strategy is closely associated with oncogenesis. Furthermore, the long-term survival of infected cells leads to the accumulation of somatic mutations and aberrant epigenetic alterations. These events eventually lead to ATL, ENKTCL, and the lymphoma-like subset of CAEBV. Interrupting these common oncogenic mechanisms is a promising therapeutic strategy for viral-driven lymphomas with poor prognoses.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.