The impact of NOTCH1, FBW7 and PTEN mutations on prognosis and downstream signaling in pediatric T-cell acute lymphoblastic leukemia: a report from the Children's Oncology Group

Leukemia. 2009 Aug;23(8):1417-25. doi: 10.1038/leu.2009.64. Epub 2009 Apr 2.

Abstract

We explored the impact of mutations in the NOTCH1, FBW7 and PTEN genes on prognosis and downstream signaling in a well-defined cohort of 47 patients with pediatric T-cell acute lymphoblastic leukemia (T-ALL). In T-ALL lymphoblasts, we identified high-frequency mutations in NOTCH1 (n=16), FBW7 (n=5) and PTEN (n=26). NOTCH1 mutations resulted in 1.3- to 3.3-fold increased transactivation of an HES1 reporter construct over wild-type NOTCH1; mutant FBW7 resulted in further augmentation of reporter gene activity. NOTCH1 and FBW7 mutations were accompanied by increased median transcripts for NOTCH1 target genes (HES1, DELTEX1 and cMYC). However, none of these mutations were associated with treatment outcome. Elevated HES1, DELTEX1 and cMYC transcripts were associated with significant increases in transcript levels of several chemotherapy relevant genes, including MDR1, ABCC5, reduced folate carrier, asparagine synthetase, thiopurine methyltransferase, BCL2 and dihydrofolate reductase. PTEN transcripts positively correlated with HES1 and cMYC transcript levels. Our results suggest that (1) multiple factors should be considered with attempting to identify molecular-based prognostic factors for pediatric T-ALL, and (2) depending on the NOTCH1 signaling status, modifications in the types or dosing of standard chemotherapy drugs for T-ALL, or combinations of agents capable of targeting NOTCH1, AKT and/or mTOR with standard chemotherapy agents may be warranted.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Antineoplastic Combined Chemotherapy Protocols / pharmacokinetics
  • Antineoplastic Combined Chemotherapy Protocols / therapeutic use
  • Basic Helix-Loop-Helix Transcription Factors / biosynthesis
  • Basic Helix-Loop-Helix Transcription Factors / genetics
  • Cell Cycle Proteins / genetics*
  • Cell Cycle Proteins / physiology
  • Child
  • Child, Preschool
  • Cohort Studies
  • DNA Mutational Analysis
  • DNA, Neoplasm / genetics
  • F-Box Proteins / genetics*
  • F-Box Proteins / physiology
  • F-Box-WD Repeat-Containing Protein 7
  • Female
  • Gene Expression Regulation, Leukemic / genetics*
  • Genes, Reporter
  • Homeodomain Proteins / biosynthesis
  • Homeodomain Proteins / genetics
  • Humans
  • Infant
  • Male
  • Mutation*
  • Neoplasm Proteins / genetics*
  • Neoplasm Proteins / physiology
  • PTEN Phosphohydrolase / genetics*
  • PTEN Phosphohydrolase / physiology
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / drug therapy
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / genetics*
  • Precursor T-Cell Lymphoblastic Leukemia-Lymphoma / mortality
  • Prognosis
  • Receptor, Notch1 / genetics*
  • Receptor, Notch1 / physiology
  • Signal Transduction / genetics
  • Transcription Factor HES-1
  • Treatment Outcome
  • Ubiquitin-Protein Ligases / genetics*
  • Ubiquitin-Protein Ligases / physiology
  • Young Adult

Substances

  • Basic Helix-Loop-Helix Transcription Factors
  • Cell Cycle Proteins
  • DNA, Neoplasm
  • F-Box Proteins
  • F-Box-WD Repeat-Containing Protein 7
  • FBXW7 protein, human
  • Homeodomain Proteins
  • NOTCH1 protein, human
  • Neoplasm Proteins
  • Receptor, Notch1
  • Transcription Factor HES-1
  • HES1 protein, human
  • Ubiquitin-Protein Ligases
  • PTEN Phosphohydrolase
  • PTEN protein, human