Therapeutic Options Targeting the Ataxia-Telangiectasia Mutated (ATM)-mediated DNA Damage Response, Macropinocytosis, and Adaptive Immunity in Ovarian Cancer

Copyright © 2024 International Institute of Anticancer Research (Dr. George J. Delinasios), All rights reserved..

Ataxia-telangiectasia mutated (ATM) is a pivotal protein with versatile kinase activity that responds to DNA damage. While its well-established role as a DNA repair protein is widely recognized, the understanding of its noncanonical functions in ovarian cancer remains limited. Numerous studies have investigated the potential of targeting ATM for ovarian cancer treatment. In addition to its involvement in homologous recombination repair (HRR), an increasing body of research suggests that ATM plays a role in cellular metabolism and adaptive immunity. This review focuses on the current evidence and provides a perspective on how targeting ATM in ovarian cancer can address HRR-deficient genotypes, influence macropinocytosis, and enhance immune checkpoint blockade (ICB) therapy. It underscores the diverse avenues through which targeting ATM is a potential tailored treatment for ovarian cancer.

Medienart:

E-Artikel

Erscheinungsjahr:

2024

Erschienen:

2024

Enthalten in:

Zur Gesamtaufnahme - volume:44

Enthalten in:

Anticancer research - 44(2024), 4 vom: 25. Apr., Seite 1353-1364

Sprache:

Englisch

Beteiligte Personen:

Tseng, Cai-Chieh [VerfasserIn]
Ku, Min-Hsi [VerfasserIn]
Wu, Yun-Chieh [VerfasserIn]
Huang, Wei-Lun [VerfasserIn]
Wu, Wei-Ming [VerfasserIn]
Pai, Ching Hua [VerfasserIn]
Chen, Chi-Wei [VerfasserIn]

Links:

Volltext

Themen:

ATM
ATM protein, human
Adaptive immunity
Ataxia Telangiectasia Mutated Proteins
Cell Cycle Proteins
DNA damage response
DNA-Binding Proteins
EC 2.7.11.1
Journal Article
Macropinocytosis
Ovarian cancer
Protein Serine-Threonine Kinases
Review
Tumor Suppressor Proteins

Anmerkungen:

Date Completed 29.03.2024

Date Revised 03.04.2024

published: Print

Citation Status MEDLINE

doi:

10.21873/anticanres.16931

funding:

Förderinstitution / Projekttitel:

PPN (Katalog-ID):

NLM370275373