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Involvement of CDKN2 (p16INK4A/MTS1) and p15INK4B/MTS2 in human leukemias and lymphomas

T Otsuki1, H M Clark, A Wellmann

  • 1Hematopathology Section, National Cancer Institute, NIH, Bethesda, Maryland 20892.

Cancer Research
|April 1, 1995
PubMed

Insights

CDKN2 and p15INK4B genes, potential tumor suppressors, were analyzed in lymphoid tumors. Homozygous deletions were frequent in T-cell acute lymphoblastic leukemia, suggesting their role in its development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • CDKN2 (p16INK4A/MTS1) and p15INK4B/MTS2 are potent inhibitors of the cyclin D/cyclin-dependent kinase 4 complex.
  • Both genes are implicated as candidate tumor suppressor genes located at chromosome 9p21.

Purpose of the Study:

  • To investigate deletions and mutations in CDKN2 and p15INK4B genes within hematopoietic cell lines and primary lymphoid tumors.
  • To assess the role of these genes in the pathogenesis of lymphoid malignancies.

Main Methods:

  • Analysis of 14 hematopoietic cell lines and 117 primary lymphoid tumors (65 T-cell, 52 B-cell malignancies).
  • Examination for homozygous deletions and mutations using PCR-single strand conformational polymorphism (PCR-SSCP).

Main Results:

  • Homozygous deletions of CDKN2 were observed in all 4 T-cell acute lymphoblastic leukemia (T-ALL) cell lines studied.
  • Homozygous deletions of both CDKN2 and MTS2 occurred in 35% of T-ALL/lymphoblastic lymphoma cases and 1 of 3 precursor B-ALLs.
  • No mutations were detected in CDKN2 or MTS2 exons in T- or B-cell malignancies, with few exceptions.

Conclusions:

  • CDKN2 and/or MTS2 deletions are frequent in T-ALL/lymphoblastic lymphoma, indicating their involvement in the pathogenesis of these cancers.
  • The findings support the role of CDKN2 and MTS2 as tumor suppressors in lymphoid malignancies.

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