Targeting ATR in Cancer Medicine.

AT-rich interactive domain-containing protein 1A (ARID1A) deficiency ATR inhibitors Ataxia telangiectasia and Rad3-related protein (ATR) Ataxia telangiectasia-mutated (ATM) deficiency DNA damage response (DDR) PARP inhibitors

Journal

Cancer treatment and research
ISSN: 0927-3042
Titre abrégé: Cancer Treat Res
Pays: United States
ID NLM: 8008541

Informations de publication

Date de publication:
2023
Historique:
medline: 27 11 2023
pubmed: 18 11 2023
entrez: 17 11 2023
Statut: ppublish

Résumé

As a key component of the DNA Damage Response, the Ataxia telangiectasia and Rad3-related (ATR) protein is a promising druggable target that is currently widely evaluated in phase I-II-III clinical trials as monotherapy and in combinations with other rational antitumor agents, including immunotherapy, DNA repair inhibitors, chemo- and radiotherapy. Ongoing clinical studies for this drug class must address the optimization of the therapeutic window to limit overlapping toxicities and refine the target population that will most likely benefit from ATR inhibition. With advances in the development of personalized treatment strategies for patients with advanced solid tumors, many ongoing ATR inhibitor trials have been recruiting patients based on their germline and somatic molecular alterations, rather than relying solely on specific tumor subtypes. Although a spectrum of molecular alterations have already been identified as potential predictive biomarkers of response that may sensitize to ATR inhibition, these biomarkers must be analytically validated and feasible to measure robustly to allow for successful integration into the clinic. While several ATR inhibitors in development are poised to address a clinically unmet need, no ATR inhibitor has yet received FDA-approval. This chapter details the underlying rationale for targeting ATR and summarizes the current preclinical and clinical landscape of ATR inhibitors currently in evaluation, as their regulatory approval potentially lies close in sight.

Identifiants

pubmed: 37978140
doi: 10.1007/978-3-031-30065-3_14
doi:

Substances chimiques

Ataxia Telangiectasia Mutated Proteins EC 2.7.11.1
Antineoplastic Agents 0
Biomarkers 0
ATR protein, human EC 2.7.11.1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

239-283

Informations de copyright

© 2023. The Author(s), under exclusive license to Springer Nature Switzerland AG.

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Auteurs

Carolina Salguero (C)

Department of Investigational Cancer Therapeutics (Phase I Program), Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Christian Valladolid (C)

Department of Investigational Cancer Therapeutics (Phase I Program), Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA.

Helen M R Robinson (HMR)

Artios Pharma, The Glenn Berge Building, Babraham Research Campus, Cambridge, UK.

Graeme C M Smith (GCM)

Artios Pharma, The Glenn Berge Building, Babraham Research Campus, Cambridge, UK.

Timothy A Yap (TA)

Department of Investigational Cancer Therapeutics (Phase I Program), Division of Cancer Medicine, The University of Texas MD Anderson Cancer Center, Houston, TX, USA. tyap@mdanderson.org.
The Institute for Applied Cancer Science, and Institute for Personalized Cancer Therapy, The University of Texas MD Anderson Cancer Center, 1400 Holcombe Boulevard, TX, 77030, Houston, USA. tyap@mdanderson.org.

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