ReviewMobile DNA2016
Endogenous retroviral promoter exaptation in human cancer.
Review in Mobile DNA, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 157 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
157 citing papers in PubMed, 246 citations in OpenAlex.
- Endogenous retrovirus control of calbindin is essential for human early embryogenesis.Science advances · 2026Article
- THE1 repeats: Ancient endogenous retroviruses rampaging behind sarcoid myopathy.Journal of human genetics · 2026Review
- Transcriptional Activation of Transposable Element (TE)-Associated Genes Is Frequently Associated with Altered Promoter Methylation in Placenta and Melanoma.International journal of molecular sciences · 2026Article
- Transposable elements shape stemness in normal and leukemic hematopoiesis.Nature genetics · 2026Article
- Epigenetic Deregulation of Transposable Elements Links Developmental Processes and Tumorigenesis.International journal of molecular sciences · 2026Review
- Article
- Review
- TEITbase: a database for transposable element (TE)-initiated transcripts in human cancers.Database : the journal of biological databases and curation · 2026Article
- Review
- TE-SCALE: a comprehensive database for exploring transposable element expression across human cancers at single-cell resolution.Nucleic acids research · 2026Article
- Investigating the Physiological Regulation of Transposable Elements In Vivo: Nuclei Preparation from Primary Mouse Tissues for Epigenomic Analyses and Computational Approaches to Interrogate the Repeat Genome.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Leveraging cfDNA fragmentomic features for the early detection of colorectal cancer.Frontiers in immunology · 2026Article
- How Oncovirus Affects Drug Resistance in Cancer Cells.Recent patents on anti-cancer drug discovery · 2026Review
- Non-canonical and induced neoantigens as emerging sources of cancer-specific immunotherapy targets.Frontiers in immunology · 2026Review
- Endogenous retroviruses and response to immune checkpoint inhibitors: mechanisms, clinical evidence, and therapeutic implications.Frontiers in immunology · 2026Review
- Endogenous retroviruses in aging and cancer: from genomic defense to oncogenic activation.Mobile DNA · 2025Review
- Revisiting Clonal Evolution Through the Light of Retrotransposons.BioEssays : news and reviews in molecular, cellular and developmental biology · 2025Review
- The expression, regulation, and function of human endogenous retroviruses in genitourinary cancers.Cell death discovery · 2025Review
- Haplotype-Resolved Chromatin Conformation Data Reveals Relationship Between Transposable Elements and Chromosomal Pairing.Genome biology and evolution · 2025Article
- The increased expression levels of human endogenous retrovirus-K envelope and human endogenous retrovirus-H polymerase transcripts in laryngeal squamous cell carcinoma.Virology journal · 2025Article
97 more citing papers are in PubMed but not listed here.
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cancer arises from a series of genetic and epigenetic changes, which result in abnormal expression or mutational activation of oncogenes, as well as suppression/inactivation of tumor suppressor genes. Aberrant expression of coding genes or long non-coding RNAs (lncRNAs) with oncogenic properties can be caused by translocations, gene amplifications, point mutations or other less characterized mechanisms. One such mechanism is the inappropriate usage of normally dormant, tissue-restricted or cryptic enhancers or promoters that serve to drive oncogenic gene expression. Dispersed across the human genome, endogenous retroviruses (ERVs) provide an enormous reservoir of autonomous gene regulatory modules, some of which have been co-opted by the host during evolution to play important roles in normal regulation of genes and gene networks. This review focuses on the "dark side" of such ERV regulatory capacity. Specifically, we discuss a growing number of examples of normally dormant or epigenetically repressed ERVs that have been harnessed to drive oncogenes in human cancer, a process we term onco-exaptation, and we propose potential mechanisms that may underlie this phenomenon.
Indexed as
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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.