ReviewCell death discovery2025
The expression, regulation, and function of human endogenous retroviruses in genitourinary cancers.
Review in Cell death discovery, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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
6 citing papers in PubMed.
- Differential Expression and Co-Variation of HERV-Associated Transcripts, IL-17 Cytokines, and NFκB in Paired Colorectal Cancer Tissues.Biomedicines · 2026Article
- The HIV-1 restriction factor RPRD2 does not inhibit transcription of HIV-1 or endogenous retroelements.bioRxiv : the preprint server for biology · 2026Article
- LINE-1 Retrotransposons and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2026Review
- HERV2365 upregulates FGF1 expression by sponging miR-326 to promote the progression of intrahepatic cholangiocarcinoma.iScience · 2026Article
- CirculatingCancers · 2026Article
- Activation of endogenous retroviruses in tumor cells and their immunomodulatory mechanisms: from molecular basis to clinical translation.Frontiers in oncology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Human endogenous retroviruses (HERVs), constituting approximately 8% of the human genome, represent genomic remnants of ancestral retroviral infections that colonized the germline through evolutionary processes. While most HERVs remain epigenetically silenced, their reactivation through environmental stimuli or epigenetic dysregulation enables participation in oncogenesis via viral mimicry, immunomodulation, and insertional mutagenesis. Substantial evidence now implicates aberrant HERVs activity across urologic malignancies-including prostate cancer, renal cell carcinoma (RCC), bladder cancer, and testicular germ cell tumors-where cancer-type-specific mechanisms drive tumor development and progression. These encompass androgen-responsive HERV-K activation in prostate malignancies, hypoxia-inducible factor-mediated ERV immunogenicity in RCC, HERV-derived microRNA silencing of tumor suppressors in bladder cancer, and DNA hypomethylation-associated HERV expression in testicular germ cell tumors. This review synthesizes fundamental HERV biology with recent advances in their diagnostic and therapeutic applications for urologic neoplasms. Key clinical translations include ERV-based stratification models predicting immune checkpoint inhibitor response in metastatic RCC, HERV-E-targeted adoptive T cell therapies, and noncoding RNA biomarkers for early bladder cancer detection. We further discuss unresolved mechanistic paradoxes such as contradictory prognostic associations between HERV superfamily expression and PBRM1 inactivation in RCC, concluding with priorities for future research: validating HERV-derived neoantigens in immunotherapy platforms, optimizing epigenetic priming strategies to enhance viral mimicry effects, and establishing standardized HERV signatures as clinical biomarkers through multi-institutional cohorts.
Identifiers
What Socratic 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 Socratic graph.