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Somatic and germline ATM variants in non-small-cell lung cancer: Therapeutic implications

Juan-Manuel Hernandez-Martinez1, Rafael Rosell2, Oscar Arrieta3

  • 1Thoracic Oncology Unit and Experimental Oncology Laboratory, Instituto Nacional de Cancerología de México (INCan), Mexico; CONACYT-Instituto Nacional de Cancerología, Mexico City, Mexico.

Critical Reviews in Oncology/Hematology
|June 21, 2023
PubMed

Insights

Germline and somatic ATM alterations increase lung adenocarcinoma (LUAD) risk and impact immune function. Understanding these ATM variants is crucial for developing targeted therapies for ATM-deficient lung cancers.

Area of Science:

  • Oncology
  • Genetics
  • Immunology

Background:

  • ATM kinase is vital for DNA double-strand break repair.
  • Germline ATM variants (gATM) and somatic ATM mutations (sATM) are implicated in lung adenocarcinoma (LUAD) pathogenesis.
  • Immune dysfunction in gATM carriers and clinicopathological features of LUAD with ATM alterations require further investigation.

Purpose of the Study:

  • To review the role of ATM in LUAD development.
  • To explore the impact of ATM alterations on immune function in LUAD patients.
  • To examine the clinicopathological characteristics of LUAD with gATM or sATM.
  • To re-evaluate therapeutic strategies for ATM-deficient LUAD.

Main Methods:

  • Literature review of studies on ATM, DNA damage response, and lung cancer.
  • Analysis of existing data on germline and somatic ATM variants in LUAD.
  • Synthesis of information on immunological abnormalities associated with ATM alterations.
  • Review of clinical trial data for targeted therapies and immunotherapies in LUAD.

Main Results:

  • ATM is a key kinase in DNA repair, and its alterations are linked to LUAD.
  • gATM and sATM are associated with increased LUAD risk and potential immune dysfunction.
  • Limited data exists on the specific clinicopathological features of LUAD patients with ATM alterations.
  • The therapeutic landscape for LUAD is evolving with targeted and immunotherapies.

Conclusions:

  • ATM plays a significant role in LUAD pathogenesis.
  • Further research is needed to understand the immune consequences of ATM alterations in LUAD.
  • Characterizing LUAD patients with ATM alterations is essential for personalized treatment.
  • Optimizing therapeutic approaches for ATM-deficient LUAD is a critical unmet need.
Keywords:
ATMAtaxia-telangiectasia mutatedChemotherapyHomologous recombination repairImmunotherapyLung cancer susceptibilityRadiotherapyTargeted therapies

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