Targeting the Ataxia Telangiectasia Mutated protein in cancer therapy

Donatella Vecchio, Guido Frosina

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Genotoxic anticancer drugs explicate their effects damaging DNA, thus triggering a coordinated signal-transduction network called DNA Damage Response (DDR). Ataxia Telangiectasia Mutated (ATM) protein plays a central role in this response: activated by DNA damage, ATM phosphorylates itself and downstream effectors that arrest cell cycle allowing for DNA repair or, should DNA damage be too severe and not retrievable, inducing apoptosis. ATM is a worth-investigating target for tumor radio and chemosensitization. During last years, pharmaceutical industries and research laboratories have developed a series of small molecules, capable to inhibit ATM with increasing specificity. Several preclinical studies have demonstrated that these inhibitors alone or in association with other treatments may improve therapeutic outcomes. In this review we discuss ATM inhibitors so far developed, focussing on recent acquisitions on their potential antineoplastic usefulness.

Original languageEnglish
Pages (from-to)139-153
Number of pages15
JournalCurrent Drug Targets
Volume17
Issue number2
Publication statusPublished - Feb 1 2016

Fingerprint

Ataxia Telangiectasia Mutated Proteins
Ataxia Telangiectasia
DNA Damage
DNA
Neoplasms
Drug Industry
Therapeutics
Cell Cycle Checkpoints
Signal transduction
Radio
DNA Repair
Antineoplastic Agents
Signal Transduction
Research laboratories
Pharmaceutical Preparations
Apoptosis
Tumors
Repair
Cells
Association reactions

Keywords

  • ATM
  • Chemotherapy
  • Glioma
  • Inhibitor
  • Radiotherapy
  • Resistance
  • Sensitization

ASJC Scopus subject areas

  • Drug Discovery
  • Pharmacology
  • Clinical Biochemistry
  • Molecular Medicine

Cite this

Targeting the Ataxia Telangiectasia Mutated protein in cancer therapy. / Vecchio, Donatella; Frosina, Guido.

In: Current Drug Targets, Vol. 17, No. 2, 01.02.2016, p. 139-153.

Research output: Contribution to journalArticle

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