Document Type

Article

Publication Date

11-22-2023

Comments

This article is the author's final published version in Science Advances, Volume 9, Issue 47, 22 Nov 2023, Article number eadg2263.

The published versions is available at https://doi.org/10.1126/sciadv.adg2263. Copyright © 2023 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science.

Abstract

Ataxia-telangiectasia mutated (ATM) plays a central role in the cellular response to DNA damage and ATM alterations are common in several tumor types including bladder cancer. However, the specific impact of ATM alterations on therapy response in bladder cancer is uncertain. Here, we combine preclinical modeling and clinical analyses to comprehensively define the impact of ATM alterations on bladder cancer. We show that ATM loss is sufficient to increase sensitivity to DNA-damaging agents including cisplatin and radiation. Furthermore, ATM loss drives sensitivity to DNA repair-targeted agents including poly(ADP-ribose) polymerase (PARP) and Ataxia telangiectasia and Rad3 related (ATR) inhibitors. ATM loss alters the immune microenvironment and improves anti-PD1 response in preclinical bladder models but is not associated with improved anti-PD1/PD-L1 response in clinical cohorts. Last, we show that ATM expression by immunohistochemistry is strongly correlated with response to chemoradiotherapy. Together, these data define a potential role for ATM as a predictive biomarker in bladder cancer.

Creative Commons License

Creative Commons License
This work is licensed under a Creative Commons Attribution-Noncommercial 4.0 License

sciadv.adg2263_sm.pdf (2085 kB)
Figs. S1 to S9, Legends for tables S1 to S5, References

sciadv.adg2263_tables_s1_to_s5.zip (1183 kB)
Tables S1 to S5

Language

English

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