ReviewTrends in genetics : TIG2019
Off to a Bad Start: Cancer Initiation by Pluripotency Regulator PRDM14.
Review in Trends in genetics : TIG, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed.
- Interaction Between PRDM14 and CBFA2T2 Supports Pluripotency and Proliferation in Germ Cell Tumors.Cancers · 2026Article
- PRDM Family Proteins in Immune Regulation: Epigenetic Control and Implications in Immune-Related Diseases.Biology · 2026Review
- Functional and molecular single-cell analyses implicate PRDM14 in the initiation of B cell leukemia in mice.Scientific reports · 2025Article
- Article
- PRDM14 extinction enables the initiation of trophoblast stem cell formation.Cellular and molecular life sciences : CMLS · 2024Article
- Germline stem cells in human.Signal transduction and targeted therapy · 2022Review
- Whole-genome analysis of Nigerian patients with breast cancer reveals ethnic-driven somatic evolution and distinct genomic subtypes.Nature communications · 2021Observational
- Immune-related protein signature in serum stratify relapsed mantle cell lymphoma patients based on risk.BMC cancer · 2020Article
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
Despite advances in chemotherapies that improve cancer survival, most patients who relapse succumb to the disease due to the presence of cancer stem cells (CSCs), which are highly chemoresistant. The pluripotency factor PR domain 14 (PRDM14) has a key role in initiating many types of cancer. Normally, PRDM14 uses epigenetic mechanisms to establish and maintain the pluripotency of embryonic cells, and its role in cancer is similar. This important link between cancer and induced pluripotency is a key revelation for how CSCs may form: pluripotency genes, such as PRDM14, can expand stem-like cells as they promote ongoing DNA damage. PRDM14 and its protein-binding partners, the ETO/CBFA2T family, are ideal candidates for eliminating CSCs from relevant cancers, preventing relapse and improving long-term survival.
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.