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Low frequency of p16(INK4a) alterations in insulinomas

D K Bartsch1, M Kersting, A Wild

  • 1Department of Surgery, Philipps University, Marburg, Germany. bartsch@mailer.uni-marburg.de

Digestion
|October 12, 2000
PubMed
Abstract

Insights

The p16(INK4a) tumor-suppressor gene plays a role in a small fraction of insulinoma tumorigenesis. Genetic alterations like deletion and methylation of p16(INK4a) were found in 17% of tumors studied.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Insulinoma tumorigenesis mechanisms are not fully understood.
  • The p16(INK4a) tumor-suppressor gene is crucial in cell cycle regulation and is implicated in various cancers.
  • Previous studies linked p16(INK4a) inactivation to gastrinomas and pancreatic carcinomas.

Purpose of the Study:

  • To investigate the role of the p16(INK4a) tumor-suppressor gene in the development of insulinomas.
  • To evaluate genetic alterations and expression of p16(INK4a) in insulinoma samples.

Main Methods:

  • Seventeen insulinoma samples (14 benign, 3 malignant) were analyzed.
  • Genetic alterations in p16(INK4a) were assessed using Single-Strand Conformation Polymorphism (SSCP), PCR-based deletion assays, and methylation-specific assays.
  • p16 protein expression was evaluated via immunohistochemistry.

Main Results:

  • Aberrant methylation of the p16(INK4a) promoter was observed in two benign insulinomas.
  • A homozygous deletion of p16(INK4a) was detected in one malignant insulinoma.
  • All three tumors with genetic alterations showed a lack of p16 expression; no intragenic mutations were found. Overall, 17% of insulinomas exhibited p16(INK4a) alterations.

Conclusions:

  • The p16(INK4a) tumor-suppressor gene is involved in the tumorigenesis of a small subset of insulinomas.
  • Genetic alterations, specifically deletion and promoter methylation, contribute to p16(INK4a) inactivation in some insulinomas.

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