Related Experiment Video

Updated: Aug 3, 2026

A 3D Organotypic Melanoma Spheroid Skin Model
08:49

A 3D Organotypic Melanoma Spheroid Skin Model

Published on: May 18, 2018

[p16(INK4A)/CDKN2--the "melanoma gene"? Status of research and outlook]

T Bogenrieder1, M Landthaler, W Stolz

  • 1Dermatologische Klinik und Poliklinik, Universität Regensburg.

Der Hautarzt; Zeitschrift Fur Dermatologie, Venerologie, Und Verwandte Gebiete
|April 29, 1998
PubMed

Insights

The p16INK4A gene, a tumor suppressor, is frequently altered in melanoma. This review clarifies its role in melanocytic tumor development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Context:

  • The p16INK4A (CDKN2/MTS1) gene is a candidate tumor suppressor on chromosome 9p21.
  • This region is frequently deleted in various human cancers, including malignant melanoma.
  • Conflicting data exists on p16INK4A's role in melanoma, necessitating a comprehensive review.

Purpose:

  • To consolidate current knowledge on the p16INK4A gene.
  • To analyze the frequency of homozygous deletions and mutations of p16INK4A in melanoma.
  • To discuss the biological significance of p16INK4A in the pathogenesis of melanocytic tumors.

Summary:

  • p16INK4A, a cyclin-dependent kinase 4 inhibitor, is located on the frequently deleted 9p21 region.
  • The review synthesizes existing data on p16INK4A alterations in malignant melanoma.
  • It evaluates the gene's importance in the development of melanocytic tumors.

Impact:

  • Provides a clear understanding of p16INK4A's function in melanoma.
  • Aids in clarifying the conflicting data regarding its role in tumor development.
  • Offers insights into the pathogenesis of melanocytic tumors for future research and therapeutic strategies.

More Related Videos

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells06:09

Spatial and Temporal Control of Murine Melanoma Initiation from Mutant Melanocyte Stem Cells

Published on: June 7, 2019

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma08:18

Analysis of Lymph Node Volume by Ultra-High-Frequency Ultrasound Imaging in the Braf/Pten Genetically Engineered Mouse Model of Melanoma

Published on: September 8, 2021

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
M cyclin...
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...
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
Skin Cancer01:30

Skin Cancer

Skin cancer is a type of cancer that occurs when there is an abnormal growth of skin cells, usually triggered by damage to the DNA within the skin cells. It is primarily caused by exposure to ultraviolet (UV) radiation from the sun or artificial sources like tanning beds. Skin cancer is the most common type of cancer worldwide, and its incidence continues to rise.
Basal Cell Carcinoma (BCC): BCC is the most common type of skin cancer, accounting for about 80% of cases. It typically develops in...