ArticleNature genetics2024
Interaction between MED12 and ΔNp63 activates basal identity in pancreatic ductal adenocarcinoma.
Article in Nature genetics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Lineage master regulator and cancer-selective partner transcription factors rewire 3D genome topology for tumor-specific gene control.Science advances · 2026Article
- Ampullary Amphicrine Carcinoma: A Rare Case Report With Review of Literature.International journal of surgical pathology · 2026Review
- KMT2D loss drives adeno-to-squamous transition and sensitizes TKI-resistant lung cancer to AURKA inhibition.Cell death and differentiation · 2026Article
- GATA4 loss promotes mutantbioRxiv : the preprint server for biology · 2026Article
- Isoform-specific cofactor recruitment through the intrinsically disordered N-terminus of p63 underlies differential transcriptional activities.bioRxiv : the preprint server for biology · 2026Article
- Identification of HSPE1 as a new actionable cancer vulnerability leads to an innovative and effective combination therapy for pancreatic ductal adenocarcinoma.Molecular cancer · 2026Article
- Epigenetic and transcriptional control of classical and basal-like cell states in pancreatic ductal adenocarcinoma.Gastroenterology report · 2026Review
- KLF5 enables dichotomous lineage programs in pancreatic cancer via the AAA+ ATPase coactivators RUVBL1 and RUVBL2.Nature communications · 2025Article
- Luminal and Basal Subtypes Across Carcinomas: Molecular Programs Beyond Tissue of Origin.Cancers · 2025Review
- Differential Transcriptional Activity of ΔNp63β Is Encoded by an Isoform-Specific C-Terminus.Molecular and cellular biology · 2025Article
- A Case Report of Gastric Squamous Cell Carcinoma Associated with Pancreatic Adenocarcinoma and Literature Review.Case reports in gastroenterologyArticle
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20 authors.
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Abstract
The presence of basal lineage characteristics signifies hyperaggressive human adenocarcinomas of the breast, bladder and pancreas. However, the biochemical mechanisms that maintain this aberrant cell state are poorly understood. Here we performed marker-based genetic screens in search of factors needed to maintain basal identity in pancreatic ductal adenocarcinoma (PDAC). This approach revealed MED12 as a powerful regulator of the basal cell state in this disease. Using biochemical reconstitution and epigenomics, we show that MED12 carries out this function by bridging the transcription factor ΔNp63, a known master regulator of the basal lineage, with the Mediator complex to activate lineage-specific enhancer elements. Consistent with this finding, the growth of basal-like PDAC is hypersensitive to MED12 loss when compared to PDAC cells lacking basal characteristics. Taken together, our genetic screens have revealed a biochemical interaction that sustains basal identity in human cancer, which could serve as a target for tumor lineage-directed therapeutics.
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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.