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Lethal Alleles

Lethal Alleles

Agouti: A Lethal Allele
Lucien Cuénot discovered lethal alleles in 1905 while studying the inheritance of coat color in mice. The agouti gene is responsible for the color of the coat in mice. This gene codes for an agouti-signaling protein, which is responsible for melanin distribution in mammals. The wild-type allele gives rise to gray-brown coat color in mice, while the mutant allele gives rise to yellow coat color. In addition to coat color, the agouti gene is associated with the yellow...

Abnormal Proliferation

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...

Cancer-Critical Genes II: Tumor Suppressor Genes

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...

In-vitro Mutagenesis

In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.

Loss of Tumor Suppressor Gene Functions

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...

The Intrinsic Apoptotic Pathway

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...

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Related Experiment Video

Updated: Apr 14, 2026

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions

Published on: May 27, 2021

[Synthetic lethal genes to mutant p53].

Tong-Yang Liu^1,2, Hai-Qiang Guo³, Mei-Yan Zhu³

¹1.School of Life Science and Biotechnology, Kunming University of Science and Technology, Kunming 650500, China.

Yi Chuan = Hereditas

|April 18, 2015

Summary

Targeted cancer therapy is advancing with research into synthetic lethal interactions. Understanding these interactions with mutant p53 (a key cancer gene) can reveal new tumor-specific treatments.

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Last Updated: Apr 14, 2026

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions

A Data Integration Workflow to Identify Drug Combinations Targeting Synthetic Lethal Interactions

Published on: May 27, 2021

Yeast As a Chassis for Developing Functional Assays to Study Human P53

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Published on: August 4, 2019

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Detection of Aggregation-Prone Behavior in Mutant P53 V157F Breast Cancer Cells Using Multipoint Thioflavin T Fluorescence

Published on: December 30, 2025

Area of Science:

Oncology
Molecular Biology
Genetics

Context:

Targeted therapy is a cornerstone of modern cancer treatment.
Mutant p53 is a significant factor in tumorigenesis and tumor progression.
Identifying synthetic lethal interactions with mutant p53 is crucial for personalized medicine.

Purpose:

To review synthetic lethal interactions involving mutant p53.
To categorize these interactions into cell cycle regulators and non-cell cycle regulators.
To explore the therapeutic potential of these interactions in cancer treatment.

Summary:

This review examines synthetic lethal interactions with mutant p53, a common driver in cancer.
These interactions involve both cell cycle regulators and non-cell cycle regulators.
The findings highlight potential new strategies for targeted anticancer therapies.

Impact:

Advances understanding of mutant p53's role in cancer.
Provides a framework for developing novel tumor-specific synthetic lethal therapies.
Facilitates personalized treatment approaches for p53-mutant cancers.