Related Experiment Video

Updated: Oct 4, 2026

Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence
08:55

Murine Model for Non-invasive Imaging to Detect and Monitor Ovarian Cancer Recurrence

Published on: November 2, 2014

Alterations of the p16INK4A gene in human ovarian cancers

T Kanuma1, J Nishida, T Gima

  • 1Department of Reproductive Physiology and Endocrinology, Kyushu University, Beppu, Japan.

Molecular Carcinogenesis
|March 1, 1997
PubMed

Insights

Alterations in the p16INK4A gene, a tumor suppressor, were found in ovarian cancers. These genetic changes, including deletions and mutations, suggest p16INK4A is a target in ovarian carcinogenesis.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • The p16INK4A gene encodes a protein that regulates the cell cycle.
  • p16INK4A is considered a potential tumor-suppressor gene.
  • Ovarian cancer is a significant health concern with complex genetic underpinnings.

Purpose of the Study:

  • To investigate alterations of the p16INK4A gene in primary ovarian cancers and cell lines.
  • To determine if p16INK4A gene mutations and deletions are associated with ovarian carcinogenesis.
  • To assess the functional impact of observed p16INK4A alterations.

Main Methods:

  • Analysis of p16INK4A gene status (deletions, mutations) in 30 primary ovarian cancers.
  • Examination of p16INK4A gene alterations in 11 ovarian cancer cell lines.
  • Assessment of p16INK4A gene transcription levels in cell lines.

Main Results:

  • Loss of both p16INK4A genes was observed in 16.7% of primary ovarian cancers.
  • Missense mutations and a one-base deletion in p16INK4A were found in 13.3% of primary cancers.
  • Homozygous deletions and intragenic mutations of p16INK4A were detected in cell lines, along with suppressed transcription.

Conclusions:

  • p16INK4A alterations, including genetic and transcriptional changes, are frequent in ovarian cancer.
  • These findings support p16INK4A as a functional target in ovarian carcinogenesis.
  • The observed alterations suggest a role for p16INK4A in the development of primary ovarian cancers.

More Related Videos

Transplantation Into the Mouse Ovarian Fat Pad09:25

Transplantation Into the Mouse Ovarian Fat Pad

Published on: September 7, 2016

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts10:27

Testing Targeted Therapies in Cancer using Structural DNA Alteration Analysis and Patient-Derived Xenografts

Published on: July 25, 2020

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...
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...
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...
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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,...