Related Experiment Video
Updated: Feb 26, 2026
08:53
Identifying the Effects of BRCA1 Mutations on Homologous Recombination using Cells that Express Endogenous Wild-type BRCA1
Published on: February 17, 2011
15.1K
Genetic Redundancy, Functional Compensation, and Cancer Vulnerability
Matteo Cereda1, Thanos P Mourikis1, Francesca D Ciccarelli1
1Division of Cancer Studies, King's College London, London SE1 1UL, UK.
Trends in Cancer
|July 26, 2017
Summary
Cancer genomes accumulate genetic changes, inactivating genes without harming cancer cells due to redundancy. This creates vulnerabilities, known as synthetic dependencies, that researchers can target for new cancer therapies.
Area of Science:
- Genomics
- Cancer Biology
- Molecular Oncology
Background:
- Somatic alterations in cancer genomes vary significantly across cancer types.
- Genetic redundancy allows cancer cells to tolerate gene inactivation without immediate negative consequences.
Purpose of the Study:
- To explore the concept of cancer synthetic dependencies arising from gene inactivation.
- To discuss the therapeutic potential of exploiting these synthetic dependencies.
Main Methods:
- Review of existing literature on cancer genomics and genetic redundancy.
- Conceptual analysis of synthetic lethality principles in the context of cancer.
Main Results:
- Identification of genetic redundancy as a key factor enabling cancer cell survival despite gene inactivation.
- Elucidation of synthetic dependencies as exploitable vulnerabilities in cancer.
Conclusions:
- Cancer cells' reliance on genetic redundancy creates specific dependencies.
- Targeting these synthetic dependencies offers a promising avenue for novel cancer treatments.
Keywords:
cancer genomicsfunctional redundancyparalog dependencypersonalized medicinesynthetic lethalityMore Related Videos
Related Concept Videos
01:20Mismatch Repair
6.8K
Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
6.8K
01:36Mismatch Repair
44.1K
Overview
44.1K
02:53Adaptive Mechanisms in Cancer Cells
7.2K
Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
7.2K
01:05Cancer-Critical Genes II: Tumor Suppressor Genes
9.9K
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...
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...
9.9K
01:12Loss of Tumor Suppressor Gene Functions
6.2K
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...
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...
6.2K
02:21Cancers Originate from Somatic Mutations in a Single Cell
15.1K
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...
15.1K