ArticleCell death and differentiation2026
m
Article in Cell death and differentiation, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
16 authors.
Funding
Abstract
Radiotherapy is a mainstay of cancer treatment, yet its efficacy is still substantially restricted due to radioresistance. The mechanisms underlying radioresistance remain elusive, impeding drug development and therapeutics. Here, using a high-throughput random gene perturbation method based on piggyBac transposon, we screened and identified CABLES1, an adaptor protein, as a key regulator of tumor radioresistance. The function of CABLES1 in radioresistance was further validated in multiple human cell lines in vitro and a mouse xenograft model in vivo. High expression of CABLES1 is significantly correlated with radioresistance in cancer patients. Mechanistically, CABLES1 interacts with XRCC6/XRCC5 heterodimer and activates DNA-PKcs by promoting DNA-PK holoenzyme formation, thus facilitating the efficiency of nonhomologous end-joining (NHEJ) repair and radioresistance. Notably, YTHDF1 recognizes METTL14-deposited m
Identifiers
42103895What 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.