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Updated: Feb 17, 2026

Author Spotlight: Deciphering the Role of ATM in Ataxia-Telangiectasia and the Associated Cerebellar Degeneration
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Author Spotlight: Deciphering the Role of ATM in Ataxia-Telangiectasia and the Associated Cerebellar Degeneration

Published on: December 27, 2024

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Ataxia-Telangiectasia Mutated Modulation of Carbon Metabolism in Cancer

Erika S Dahl1, Katherine M Aird1

  • 1Department of Cellular and Molecular Physiology, Penn State College of Medicine, Hershey, PA, United States.

Frontiers in Oncology
|December 15, 2017
PubMed

Insights

Ataxia-telangiectasia mutated (ATM) protein kinase regulates carbon metabolism, a process often altered in cancer. This review explores ATM

Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Metabolic Pathways

Background:

  • The ataxia-telangiectasia mutated (ATM) protein kinase is crucial for DNA damage response and linked to ataxia telangiectasia.
  • Emerging evidence implicates ATM in regulating cellular carbon metabolism.
  • Cancer cells exhibit dysregulated carbon metabolism to support biomass production.

Purpose of the Study:

  • To review the current understanding of ATM's role in regulating carbon metabolism.
  • To discuss the implications of ATM-mediated carbon metabolism in cancer.
  • To highlight the therapeutic potential of ATM inhibitors in cancer treatment.

Main Methods:

  • Literature review of studies on ATM, carbon metabolism, and cancer.
  • Analysis of recent research on non-canonical ATM functions.
  • Synthesis of information on ATM inhibitors as cancer therapeutics.

Main Results:

  • ATM plays a significant, non-canonical role in regulating key carbon metabolic pathways.
  • Dysregulation of ATM-controlled metabolism is observed in various cancers.
  • ATM inhibitors show promise as targeted cancer therapies.

Conclusions:

  • ATM is a critical regulator of carbon metabolism with implications for cancer.
  • Targeting ATM-dependent metabolic pathways offers a potential therapeutic strategy for cancer treatment.
Keywords:
AKTataxia-telangiectasia mutatedc-myccancercellular metabolismp53reactive oxygen speciessenescence

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