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Related Concept Videos

Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
Loss of Tumor Suppressor Gene Functions01:12

Loss of Tumor Suppressor Gene Functions

Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
When the tumor suppressor genes develop mutations or are lost, cells start growing out of control, leading to cancer. However, a single functional copy of the tumor suppressor gene is enough for the cells to maintain their normal functions and cell...
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...
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...
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...

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Related Experiment Video

Updated: May 20, 2026

SUMO-Binding Entities (SUBEs) as Tools for the Enrichment, Isolation, Identification, and Characterization of the SUMO Proteome in Liver Cancer
08:29

SUMO-Binding Entities (SUBEs) as Tools for the Enrichment, Isolation, Identification, and Characterization of the SUMO Proteome in Liver Cancer

Published on: November 1, 2019

SUMO, PTEN and Tumor Suppression.

Michael J Matunis1, Catherine M Guzzo

  • 1Johns Hopkins University Guzzo, Catherine; Johns Hopkins University, Biochemistry and Molecular, Biology.

Pigment Cell & Melanoma Research
|August 1, 2012
PubMed
Summary
This summary is machine-generated.

Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a tumor suppressor gene frequently altered in cancers. Loss of PTEN function is common in melanoma, impacting its development.

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Last Updated: May 20, 2026

SUMO-Binding Entities (SUBEs) as Tools for the Enrichment, Isolation, Identification, and Characterization of the SUMO Proteome in Liver Cancer
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Published on: April 17, 2026

Area of Science:

  • Oncology
  • Genetics
  • Molecular Biology

Background:

  • Phosphatase and tensin homologue deleted on chromosome 10 (PTEN) identified as a tumor suppressor gene in 1997.
  • PTEN is frequently mutated or deleted in various human cancers.
  • Loss of PTEN function is implicated in cancer predisposition syndromes like Cowden disease.

Purpose of the Study:

  • To investigate the role and frequency of PTEN alterations in human cancers, with a focus on melanoma.
  • To understand the implications of PTEN mutations, deletions, and epigenetic silencing in melanoma development.

Main Methods:

  • Gene mapping to identify homozygous mutations in tumor types and cancer predisposition syndromes.
  • Analysis of mutation and deletion frequencies in melanoma cell lines.
  • Assessment of epigenetic silencing of PTEN in malignant melanomas.

Main Results:

  • PTEN is one of the most frequently mutated or deleted genes in human cancers.
  • Loss of PTEN function through mutation or deletion observed in up to 70% of melanoma cell lines.
  • Epigenetic silencing of PTEN detected in 30-40% of malignant melanomas.

Conclusions:

  • PTEN plays a critical role as a tumor suppressor in human skin cancers, particularly melanoma.
  • Alterations in PTEN, including mutations, deletions, and epigenetic silencing, are significant events in melanoma pathogenesis.
  • Understanding PTEN's role is crucial for advancing melanoma research and treatment strategies.