Abnormal expression of p-ATM/CHK2 in nasal extranodal NK/T cell lymphoma, nasal type, is correlated with poor prognosis

J Clin Pathol. 2021 Apr;74(4):223-227. doi: 10.1136/jclinpath-2020-206476. Epub 2020 Mar 27.

Abstract

Aims: The aim of this study is to investigate the expression profiles of cell cycle related proteins in nasal extranodal NK/T cell lymphoma, nasal type (ENKTCL).

Methods: The expression profiles of cell cycle related proteins were assessed with a cell cycle antibody array and validated by immunohistochemistry. Correlations between the expression levels of proteins and clinical outcomes of patients with nasal ENKTCL were evaluated.

Results: The expression of full length ataxia telangiectasia mutated (ATM) in nasal ENKTCL significantly decreased compared with that in nasal benign lymphoid proliferative disease (NBLPD), but the expression levels of p-ATM, CHK2 and RAD51 significantly increased in nasal ENKTCL compared with that in NBLPD. Kaplan-Meier analysis showed that the expression levels of p-ATM and CHK2 in nasal ENKTCL were inversely related to overall survival (p=0.011 and p=0.025, respectively).

Conclusion: Abnormalities in the ATM pathway may play a crucial role in the oncogenesis and chemoradiotherapy resistance of nasal ENKTCL.

Keywords: cell cycle regulation; immunohistochemistry; lymphoma.

MeSH terms

  • Ataxia Telangiectasia Mutated Proteins / analysis*
  • Biomarkers, Tumor / analysis*
  • Cell Proliferation
  • Checkpoint Kinase 2 / analysis*
  • Drug Resistance, Neoplasm
  • Humans
  • Immunohistochemistry
  • Lymphoma, Extranodal NK-T-Cell / enzymology*
  • Lymphoma, Extranodal NK-T-Cell / mortality
  • Lymphoma, Extranodal NK-T-Cell / pathology
  • Lymphoma, Extranodal NK-T-Cell / therapy
  • Neoplasm Grading
  • Phosphorylation
  • Rad51 Recombinase / analysis
  • Radiation Tolerance
  • Risk Factors
  • Time Factors
  • Treatment Outcome
  • Up-Regulation

Substances

  • Biomarkers, Tumor
  • Checkpoint Kinase 2
  • ATM protein, human
  • Ataxia Telangiectasia Mutated Proteins
  • CHEK2 protein, human
  • RAD51 protein, human
  • Rad51 Recombinase