Targeting the Ataxia Telangiectasia Mutated Protein in Cancer Therapy

Donatella Vecchio, Guido Frosina1

  • 1IRCCS AOU San Martino - IST, Mutagenesis Unit, Largo Rosanna Benzi 10, 16132 Genova, Italy. guido.frosina@hsanmartino.it.

Current Drug Targets
|November 11, 2014
PubMed

Insights

This review explores ATM inhibitors, which target DNA damage response pathways in cancer. These inhibitors show promise for improving cancer therapy outcomes when used alone or with other treatments.

Area of Science:

  • Oncology
  • Molecular Biology
  • Biochemistry

Background:

  • Genotoxic anticancer drugs induce DNA damage, activating the DNA Damage Response (DDR) network.
  • Ataxia Telangiectasia Mutated (ATM) protein is a key regulator of DDR, controlling cell cycle arrest, DNA repair, and apoptosis.
  • ATM is a significant target for enhancing tumor radio- and chemosensitization.

Purpose of the Study:

  • To review ATM inhibitors developed for cancer therapy.
  • To discuss recent findings on the antineoplastic potential of ATM inhibitors.

Main Methods:

  • Literature review of preclinical studies on ATM inhibitors.
  • Analysis of small molecules developed to inhibit ATM specificity.
  • Evaluation of ATM inhibitors' efficacy alone and in combination therapies.

Main Results:

  • Development of specific small molecule ATM inhibitors by pharmaceutical industries and research labs.
  • Preclinical evidence suggests ATM inhibitors can improve therapeutic outcomes.
  • ATM inhibitors demonstrate potential in enhancing cancer treatment efficacy.

Conclusions:

  • ATM inhibitors are a promising therapeutic strategy in oncology.
  • Further research into ATM inhibitors may lead to improved cancer treatment protocols.
  • Targeting ATM offers a viable approach for overcoming resistance and enhancing existing cancer therapies.

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