ReviewNature2026
A mechanism for adaptive genome regulation in cancer.
Review in Nature, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- TKTL1 mediates metabolic adaptation and stress resistance in pancreatic cancer cells under nutrient-deprived conditions.Oncogene · 2026Article
- Article
- Challenges and advances in drug resistance and tolerance in cancer.Journal of experimental & clinical cancer research : CR · 2026Review
- Covariate-adjusted AP-1 motif architecture and footprinting track olaparib-adaptive chromatin remodelling.Frontiers in systems biology · 2026Article
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
The ability of cancer cells to consistently escape therapy highlights their remarkable adaptive potential. A longstanding debate in cancer research concerns whether drug resistance originates primarily from mutational processes or through cellular plasticity. Emerging evidence has suggested that adaptive cellular states arise through phenotypic plasticity triggered by intracellular stress signals. Here we propose a theoretical framework for how such cellular adaptation in cancer drug resistance could be 'learned' by the AP-1 family of transcription factors. We highlight key AP-1 properties, including regulatory combinatorics, stress-induced feedback and cellular memory, and argue that this system constitutes a molecular framework for establishing drug-resistant cellular states. Finally, we discuss the potentially broad relevance of this adaptation mechanism beyond cancer.
Indexed as
Identifiers
41986626What 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.