ArticleBMC cancer2026
Elevated m
Article in BMC cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Pharmacological METTL3 inhibition attenuates HIV-1 latency reversal in CD4Antimicrobial agents and chemotherapy · 2026Article
- Pharmacological METTL3 inhibition attenuates HIV-1 latency reversal in CD4bioRxiv : the preprint server for biology · 2026Article
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4 authors.
Funding
Abstract
backgroundN6-methyladenosine (m6A) modifications of human immunodeficiency virus type 1 (HIV-1) and cellular RNA contribute to regulation of viral and host gene expression. RNA m6A dysregulation has been implicated in multiple cancers. However, the role of m6A modifications in HIV-1-associated cancers remains unclear. Here, we aim to address this important question using clinical samples.
methodsUsing enzyme-linked immunosorbent assay (ELISA), RNA m6A levels were quantified in peripheral blood mononuclear cells (PBMCs) from 43 de-identified people living with HIV-1 (PLWH), comparing those with cancer (n = 15) to those without cancer (n = 28). Correlation analyses were performed to evaluate the associations between m6A levels and HIV-1 RNA copies, CD4+ T-cell counts, and age of PLWH. The mRNA and protein expression of m6A regulatory genes was measured by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot, respectively. Furthermore, quantitative transcriptomic profiling of 84 type I interferon (IFN-I)-responsive genes was performed using an RT-qPCR array.
resultsWe observed that HIV-1 viral load in the cancer group was higher than the non-cancer group. m6A levels of PBMCs were 2.8-fold higher in the cancer group and correlated with the expression of some m6A regulatory genes and proteins. Higher m6A levels were positively associated with HIV-1 RNA copies and negatively associated with CD4+ T-cell counts and age. Transcriptomic analysis of 84 IFN-I-responsive genes revealed upregulation of many pro-inflammatory and interferon-stimulated genes, along with downregulation of some genes in PLWH with cancer.
conclusionsOur findings suggest that HIV-1 infection and cancer-mediated m6A reprogramming may contribute to multifaceted chronic immune activation and malignancy in PLWH. Our results also highlight a post-transcriptional mechanism linking HIV-1 persistence to cancer risk.
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