ReviewNeoplasia (New York, N.Y.)2026
Ataxia telangiectasia mutated (ATM) kinase as a predictive biomarker in clinical oncology: implications for a precision treatment approach.
Review in Neoplasia (New York, N.Y.), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- DNER drives glycolytic reprogramming in renal cell carcinoma by activating the JAK2/STAT3 signaling pathway.Frontiers in immunology · 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
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
ATM (ataxia telangiectasia mutated) kinase is a central mediator of the DNA damage response (DDR), with established roles in maintaining genomic integrity in response to genotoxic insults. Both germline and somatic alterations in ATM occur frequently in tumors, with pathogenic variants affecting an estimated 1 in 100 individuals worldwide. Emerging evidence has shown its utility as a biomarker for therapeutic sensitivity. ATM-deficient tumors exhibit increased sensitivity to radiotherapy, chemotherapy and present opportunities for synthetic lethality approaches. Notably, ATM loss sensitizes tumors to ATR and PARP inhibitors. This review summarizes the structure and function of ATM kinase and its interacting partners, while addressing critical knowledge gaps in recently described rationale for drug combinations that induce selective synthetic lethality in tumors cells. We examine how these approaches can be leveraged to improve standard chemotherapeutic and immunotherapeutic treatments in cancer. Additionally, we highlight the key preclinical and clinical studies evaluating ATM as a predictive biomarker and discuss its evolving role in precision oncology.
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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.