ArticleInternational journal of biological sciences2024
BET inhibition induces synthetic lethality in PTEN deficient colorectal cancers via dual action on p21
Article in International journal of biological sciences, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 4 citations in OpenAlex.
- Hyperprogressive disease in carcinoma induced by immune checkpoint inhibitor therapy: a systematic review.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2026Pooled it
- Targeting Phosphatase and Tensin Homolog Deleted on Chromosome 10q23.3 (PTEN) as a Potential Theragnostic Biomarker in Tumors.Recent patents on anti-cancer drug discovery · 2026Article
- Biology of PEST-containing nuclear proteins as potential targets in ovarian cancer (Review).Oncology letters · 2026Review
- KAT6A acetyltransferase accelerates colorectal cancer progression through upregulating BRD1 protein expression via acetylation modification.Cancer cell international · 2025Article
- MicroRNA 195, lactate dehydrogenase 5, phosphatase and tensin homologue in colorectal cancer: Clinicopathology and prognosis.World journal of gastrointestinal surgery · 2025Article
- PTEN-deficient, chromosomal instability colorectal cancer is hypersensitive to STAT3 inhibition.International journal of biological sciences · 2025Article
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Loss of PTEN tumor suppressor is an important event during colorectal cancer (CRC) development and is a target for therapeutic exploitation. This study reports that bromodomain and extra-terminal motif (BET) is a synthetic lethal partner of PTEN in CRC. BET inhibition (BETi) selectively induced G1 cell cycle arrest and apoptosis in
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.