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De novo programmed cell death in oral cancer

D Ravi1, K Ramadas, B S Mathew

  • 1Division of Laboratory Medicine, Regional Cancer Centre, Thiruvananthapuram, Kerala State, India.

Histopathology
|April 27, 1999
PubMed
Abstract

Insights

Apoptosis, programmed cell death, decreases with increasing oral cancer abnormality. This is linked to altered apoptosis regulatory proteins and deregulated proliferation during tumor progression.

Area of Science:

  • Oncology
  • Cell Biology
  • Molecular Pathology

Background:

  • Apoptosis is crucial for tissue homeostasis.
  • Dysregulation of apoptosis is implicated in oral cancer pathogenesis.

Purpose of the Study:

  • To analyze apoptosis in oral cancer.
  • To investigate the relationship between apoptosis, regulatory proteins, proliferation, and tumor histology.

Main Methods:

  • Morphological assessment and TUNEL assay for apoptosis.
  • Immunocytochemistry for p53, bax, bcl-2, and cyclin D1.
  • ELISA for mutant p53 detection.

Main Results:

  • Apoptosis inversely correlated with lesion histology.
  • Apoptosis correlated with p53, bcl-2, and bax expression.
  • Mutant p53 inversely correlated with apoptosis.
  • Bax/bcl-2 ratio and cyclin D1 correlated with apoptosis.

Conclusions:

  • Apoptosis decreases as histological abnormality increases in oral lesions.
  • Apoptosis regulatory proteins change in a histology-dependent manner.
  • Deregulated proliferation and decreased apoptosis occur during oral tumor progression.

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