ArticleOncogene2019
The induction of core pluripotency master regulators in cancers defines poor clinical outcomes and treatment resistance.
Article in Oncogene, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 54 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
54 citing papers in PubMed, 92 citations in OpenAlex.
- SET1B Drives Sustained HIF Activity and Disease Progression in Clear-Cell Renal Cell Carcinoma.Cancer research · 2026Article
- From Environmental Risk to Cancer Stemness: Epigenetic Regulation in Oral Squamous Cell Carcinoma.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Lamin A/C directs nucleosome-scale chromatin remodeling to define early lineage segregation in mammals.bioRxiv : the preprint server for biology · 2026Article
- CRISPR-RfxCas13d screening uncovers Bckdk as a post-translational regulator of maternal-to-zygotic transition in teleosts.The EMBO journal · 2025Article
- (Non)canonical Wnt signaling, cytoarchitecture and stemness: new insights from primary nonmetastatic, primary metastatic, regional and distant metastatic models of adrenocortical carcinoma.Experimental & molecular medicine · 2025Article
- Unlocking the Role of OCT4 in Cancer Lineage Plasticity: A Cross-Cancer Perspective with an Emphasis on Prostate Cancer.Biomedicines · 2025Review
- The thyroid hormone activating enzyme, DIO2, is a potential pan-cancer biomarker and immunotherapy target.Journal of endocrinological investigation · 2025Article
- Article
- Metformin enhances alpelisib sensitivity in HER2+ breast cancer by suppressing cancer stemness and oncogenic signaling.Frontiers in oncology · 2025Article
- WTAP/IGF2BP3 mediated m6A modification of the EGR1/PTEN axis regulates the malignant phenotypes of endometrial cancer stem cells.Journal of experimental & clinical cancer research : CR · 2024Article
- SIX2 promotes cell plasticity via Wnt/β-catenin signalling in androgen receptor independent prostate cancer.Nucleic acids research · 2024Article
- Possible Strategies to Reduce the Tumorigenic Risk of Reprogrammed Normal and Cancer Cells.International journal of molecular sciences · 2024Review
- Whole-genome bisulfite sequencing identifies stage- and subtype-specific DNA methylation signatures in pancreatic cancer.iScience · 2024Article
- Are embryonic stem cell markers and ALDH1A1 relevant in the context of breast cancer estrogen positivity?Cancer medicine · 2024Article
- The transcription factor sex-determining region Y-box 2 (SOX2) in bladder cancer.American journal of clinical and experimental urology · 2024Article
- Prostate cancer research: tools, cell types, and molecular targets.Frontiers in oncology · 2024Review
- Exploring the promising potential of induced pluripotent stem cells in cancer research and therapy.Molecular cancer · 2023Review
- Reactivation of embryonic genetic programs in tissue regeneration and disease.Nature genetics · 2023Review
- Restricting epigenetic activity promotes the reprogramming of transformed cells to pluripotency in a line-specific manner.Cell death discovery · 2023Article
- Review
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
14 authors at 5 institutions in 1 country.
Funding
Abstract
Stem cell characteristics have been associated with treatment resistance and poor prognosis across many cancer types. The ability to induce and regulate the pathways that sustain these characteristic hallmarks of lethal cancers in a novel in vitro model would greatly enhance our understanding of cancer progression and treatment resistance. In this work, we present such a model, based simply on applying standard pluripotency/embryonic stem cell media alone. Core pluripotency stem cell master regulators (OCT4, SOX2 and NANOG) along with epithelial-mesenchymal transition (EMT) markers (Snail, Slug, vimentin and N-cadherin) were induced in human prostate, breast, lung, bladder, colorectal, and renal cancer cells. RNA sequencing revealed pathways activated by pluripotency inducing culture that were shared across all cancers examined. These pathways highlight a potential core mechanism of treatment resistance. With a focus on prostate cancer, the culture-based induction of core pluripotent stem cell regulators was shown to promote survival in castrate conditions-mimicking first line treatment resistance with hormonal therapies. This acquired phenotype was shown to be mediated through the upregulation of iodothyronine deiodinase DIO2, a critical modulator of the thyroid hormone signalling pathway. Subsequent inhibition of DIO2 was shown to supress expression of prostate specific antigen, the cardinal clinical biomarker of prostate cancer progression and highlighted a novel target for clinical translation in this otherwise fatal disease. This study identifies a new and widely accessible simple preclinical model to recreate and explore underpinning pathways of lethal disease and treatment resistance.
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.