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Related Concept Videos

Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes I: Proto-oncogenes01:33

Cancer-Critical Genes I: Proto-oncogenes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Abnormal Proliferation02:23

Abnormal Proliferation

Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the daughter...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...

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DEK proto-oncogene expression interferes with the normal epithelial differentiation program.

Trisha M Wise-Draper1, Richard J Morreale, Teresa A Morris

  • 1Division of Pediatric Hematology/Oncology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio 45229, USA.

The American Journal of Pathology
|November 28, 2008
PubMed
Summary
This summary is machine-generated.

Overexpression of the DEK gene disrupts normal cell differentiation and promotes proliferation, contributing to skin hyperplasia and potentially cancer development. This occurs independently of p53 pathways, highlighting DEK

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Area of Science:

  • Oncology
  • Molecular Biology
  • Dermatology

Background:

  • DEK gene overexpression is linked to various human cancers.
  • The DEK oncogene's precise role in cancer is not fully understood.
  • DEK transcription is induced by human papillomavirus (HPV) E7 oncogene.

Purpose of the Study:

  • To investigate the role of DEK overexpression in cellular differentiation and proliferation.
  • To determine if DEK's effects are dependent on p53 or apoptosis pathways.
  • To examine DEK protein levels in HPV-associated skin conditions and squamous cell carcinomas.

Main Methods:

  • Studied DEK expression during keratinocyte differentiation.
  • Utilized an organotypic raft model to assess epidermal hyperplasia from stable DEK overexpression.
  • Analyzed p53 and p63 expression in DEK-overexpressing models.
  • Examined DEK protein levels in HPV-positive murine skin and human squamous cell carcinomas.

Main Results:

  • DEK expression is repressed during normal keratinocyte differentiation.
  • Stable DEK overexpression caused epidermal thickening and delayed keratinocyte differentiation.
  • DEK overexpression led to increased proliferation and basal cell expansion, independent of p53 destabilization.
  • Elevated p63 expression was observed with DEK overexpression.
  • Increased DEK protein levels were found in HPV-positive hyperplastic skin and a subset of squamous cell carcinomas.

Conclusions:

  • DEK overexpression disrupts normal differentiation and promotes proliferation, contributing to skin hyperplasia.
  • DEK's oncogenic activity in this context is independent of p53 destabilization.
  • DEK up-regulation may drive carcinoma development by increasing proliferation and hindering differentiation.