ArticleAIDS (London, England)2026
Mutational profiling of HIV+ diffuse large B-cell lymphoma reveals distinct mutational features with evidence of genomic instability.
Article in AIDS (London, England), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
18 authors.
Funding
Abstract
backgroundPeople with HIV (PWH) remain underrepresented in molecular studies and clinical trials of diffuse large B-cell lymphoma (DLBCL), despite DLBCL being a leading cause of cancer-related death in this population.
methodsWe performed whole-exome sequencing on 30 DLBCL tumors (24 with paired germline) from a Malawian cohort including both HIV-positive (HIV+) and HIV-negative (HIV-) individuals.
resultsKMT2D , BIRC6 , TP53 , and ARID1A were among the most frequently mutated genes. Compared to HIV- DLBCL, the HIV+ DLBCL tumors in this cohort were enriched for mutations in KMT2D , among others, and prior antiretroviral therapy associated with increased tumor mutational burden (TMB) and neoantigen load. Five HIV+ DLBCL tumors exhibited microsatellite instability (MSI), each with strong contributions from mutational signatures related to DNA repair. Furthermore, ARID1A mutations were observed in several MSI samples and in tumors with MSH2 loss. Integration with a published HIV+ DLBCL dataset revealed recurrent driver mutations including LILRB1 p.R30S, MYD88 p.S206C and p.S238N, and NRAS p.Q61K, as well as PTEN mutation as negatively prognostic.
conclusionsTogether, these results highlight distinct tumorigenic mechanisms in HIV+ DLBCL and underscore the need for mutational profiling of HIV+ DLBCL cohorts worldwide to identify biomarkers and therapeutic targets.
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.