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Isolation and Functional Assessment of Human Breast Cancer Stem Cells from Cell and Tissue Samples
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High frequency of aberrant p16(INK4A) expression in human breast cancer

J Geradts1, P A Wilson

  • 1Department of Pathology and Laboratory Medicine, University of North Carolina School of Medicine, Chapel Hill, USA.

The American Journal of Pathology
|July 1, 1996
PubMed

Insights

Aberrant p16(INK4A) expression is common in breast cancer. This cell cycle regulator, encoded by the CDKN2/MTS1 gene, is frequently inactivated, impacting tumor development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cell Cycle Regulation

Background:

  • The CDKN2/MTS1 gene product, p16(INK4A), is a crucial negative cell cycle regulator that inhibits retinoblastoma protein (pRB) phosphorylation.
  • Inactivation of p16(INK4A) is observed in various human malignancies, including breast cancer, suggesting its role in tumorigenesis.

Purpose of the Study:

  • To investigate the expression patterns of p16(INK4A) and pRB in a cohort of archival breast tumors.
  • To determine the frequency and potential correlations of aberrant p16(INK4A) expression with histopathological features in breast cancer.

Main Methods:

  • Immunohistochemistry was employed to assess the expression levels of p16(INK4A) and pRB proteins in 104 archival breast tumor specimens.
  • Tumor specimens included ductal, lobular, and mixed carcinomas, with evaluation for both protein expression and abnormalities.

Main Results:

  • While retinoblastoma protein (pRB) expression was largely normal (only 6 tumors showed abnormalities), a significant proportion of breast carcinomas exhibited abnormal p16(INK4A) expression.
  • Approximately 49% of the 87 interpretable cases (43 tumors) were completely or focally negative for p16(INK4A).
  • No significant correlation was found between abnormal p16(INK4A) expression and common histopathological parameters.

Conclusions:

  • Aberrant p16(INK4A) expression, particularly loss of expression, is a frequent molecular abnormality in human breast cancer.
  • The findings highlight the potential significance of p16(INK4A) dysregulation in the pathogenesis of breast cancer.

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