DNA-Dependent protein kinase activity correlates with clinical and in vitro sensitivity of chronic lymphocytic leukemia lymphocytes to nitrogen mustards

Blood. 1998 Oct 1;92(7):2213-9.

Abstract

The objective of this study is to investigate the role of DNA-dependent protein kinase (DNA-PK) in the chronic lymphocytic leukemia (CLL) lymphocyte response to nitrogen mustard therapy. DNA-PK is a nuclear serine/threonine kinase that functions in DNA double-strand break repair and in the joining process in recombination mechanisms. In a series of 34 patients with B-CLL, either untreated (n = 16) or resistant to chlorambucil (n = 18), the kinase activity of the complex, as determined by its capacity to phosphorylate a peptide substrate in vitro, is increased in the resistant samples as compared with the untreated ones (24.4 +/- 2.6 arbitrary units [a.u.] [range, 12.7 to 55.8 a.u.] versus 8.1 +/- 2.8 a.u. [range, 0.9 to 44.5 a.u.], respectively (P < .0001]), independent of other clinical and biological factors. Linear regression analysis shows an excellent correlation between the level of DNA-PK activity and the inherent in vitro sensitivity of CLL lymphocytes to chlorambucil (r = .875, P =.0001). The regulation of DNA-PK activity was associated with increased DNA-binding activity of its regulatory subunit, the Ku heterodimer, in resistant samples. These results suggest that this activity is a determinant in the cellular response to chlorambucil and participates in the development of nitrogen mustard-resistant disease. The increase in DNA-PK activity might contribute to the enhanced cross-link repair that we previously postulated to be a primary mechanism of resistance to nitrogen mustards in CLL.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Aged
  • Aged, 80 and over
  • Amino Acid Sequence
  • Antineoplastic Agents, Alkylating / pharmacology*
  • Antineoplastic Agents, Alkylating / therapeutic use
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Chlorambucil / pharmacology
  • Chlorambucil / therapeutic use
  • Cross-Linking Reagents / pharmacology*
  • Cross-Linking Reagents / therapeutic use
  • Cyclophosphamide / administration & dosage
  • Cyclophosphamide / pharmacology
  • Cyclophosphamide / therapeutic use
  • DNA Damage
  • DNA Repair / drug effects*
  • DNA, Neoplasm / drug effects
  • DNA, Neoplasm / metabolism*
  • DNA-Activated Protein Kinase
  • DNA-Binding Proteins*
  • Doxorubicin / administration & dosage
  • Drug Resistance, Neoplasm
  • Female
  • Humans
  • Leukemia, Lymphocytic, Chronic, B-Cell / drug therapy*
  • Leukemia, Lymphocytic, Chronic, B-Cell / pathology
  • Male
  • Middle Aged
  • Molecular Sequence Data
  • Neoplasm Proteins / metabolism*
  • Neoplastic Stem Cells / drug effects*
  • Neoplastic Stem Cells / enzymology
  • Nitrogen Mustard Compounds / pharmacology*
  • Nitrogen Mustard Compounds / therapeutic use
  • Nuclear Proteins
  • Peptides / metabolism
  • Phosphorylation
  • Prednisone / administration & dosage
  • Protein Processing, Post-Translational
  • Protein Serine-Threonine Kinases / metabolism*
  • Recombination, Genetic / drug effects*
  • Treatment Outcome
  • Tumor Cells, Cultured / drug effects
  • Vincristine / administration & dosage

Substances

  • Antineoplastic Agents, Alkylating
  • Cross-Linking Reagents
  • DNA, Neoplasm
  • DNA-Binding Proteins
  • Neoplasm Proteins
  • Nitrogen Mustard Compounds
  • Nuclear Proteins
  • Peptides
  • Chlorambucil
  • Vincristine
  • Doxorubicin
  • Cyclophosphamide
  • DNA-Activated Protein Kinase
  • PRKDC protein, human
  • Protein Serine-Threonine Kinases
  • Prednisone

Supplementary concepts

  • CHOP protocol
  • COP protocol 2