Related Experiment Video

Updated: May 12, 2026

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer
06:01

A Genetically Engineered Mouse Model of Sporadic Colorectal Cancer

Published on: July 6, 2017

Multistage carcinogenesis induced by ras and myc oncogenes in a reconstituted organ

T C Thompson1, J Southgate, G Kitchener

  • 1Imperial Cancer Research Fund, London, England.

Cell
|March 24, 1989
PubMed

Insights

Activating single oncogenes (RAS or MYC) in mouse prostate cells caused distinct premalignant lesions. Consecutive oncogene activation and gene amplification drive tumor progression and carcinoma development.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Oncogenes play a critical role in cancer development.
  • Understanding the specific roles of oncogenes in tumorigenesis is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the distinct phenotypic alterations induced by RAS and MYC oncogenes in mouse prostate glands.
  • To explore the role of oncogene activation and gene amplification in tumor progression and multistep tumorigenesis.

Main Methods:

  • Introduction of RAS and MYC oncogenes into mouse prostate gland progenitor cells.
  • Analysis of phenotypic alterations, including dysplasia, hyperplasia, and carcinoma formation.
  • Investigation of genetic alterations, such as gene amplification, during tumor progression.

Main Results:

  • RAS oncogene induced dysplasia and angiogenesis.
  • MYC oncogene induced hyperplasia in a normally developed organ.
  • Co-expression of RAS and MYC primarily led to carcinomas.
  • Tumor progression was associated with gene amplification.

Conclusions:

  • Distinct premalignant lesions can arise from the activation of specific single oncogenes.
  • Consecutive activation of multiple oncogenes is a potential causal event in the step-wise progression of tumorigenesis.
  • Gene amplification contributes to tumor progression.

More Related Videos

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)04:12

Chemical-Induced Skin Carcinogenesis Model Using Dimethylbenz[a]Anthracene and 12-O-Tetradecanoyl Phorbol-13-Acetate (DMBA-TPA)

Published on: December 19, 2019

Establishment and Histological Analysis of Esophageal Organoids Modeling the Progression from Normal to Cancerous Tissues05:57

Establishment and Histological Analysis of Esophageal Organoids Modeling the Progression from Normal to Cancerous Tissues

Published on: May 30, 2025

Related Concept Videos

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...
Cancers Originate from Somatic Mutations in a Single Cell02:21

Cancers Originate from Somatic Mutations in a Single Cell

Cancer arises from mutations in the critical genes that allow healthy cells to escape cell cycle regulation and acquire the ability to proliferate indefinitely. Though originating from a single mutation event in one of the originator cells, cancer progresses when the mutant cell lines continue to gain more and more mutations, and finally, become malignant. For example, chronic myelogenous leukemia (CML) develops initially as a non-lethal increase in white blood cells, which progressively...
The Ras Gene02:38

The Ras Gene

The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
Ras is a superfamily...
Induced Pluripotent Stem Cells01:06

Induced Pluripotent Stem Cells

Stem cells are undifferentiated cells that divide and produce different cell types. Ordinarily, cells that have differentiated into a specific cell type are terminally differentiated; however, scientists have found a way to reprogram these mature cells so that they dedifferentiate and return to an unspecialized, proliferative state. These cells are pluripotent like embryonic stem cells—able to produce all cell types—and are called induced pluripotent stem cells (iPSCs).
Somatic cells are...
Mutagenicity and Carcinogenicity01:25

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...