Genome evolution in yeast reveals connections between rare mutations in human cancers.

Xinchen Teng,Marie Hardwick

doi:10.15698/mic2014.06.153

Abstract

Cancer cells are riddled with mutations. Less than one percent of these are thought to be mutations that drive cancer phenotypes. However, a recent study conducted on the yeast knockout collections by Teng et al. [Mol. Cell (2013) 52: 485-494] provides hard evidence that single gene deletions/mutations in most non-essential genes can drive the selection for cancer-like mutations.

Highlights

A recent study conducted on the yeast knockout collections by Teng et al [Mol
Cell (2013) 52: 485–494] provides hard evidence that single gene deletions/mutations in most non-essential genes can drive the selection for cancerlike mutations
Problems arise when one of these rare mutations provides some growth and/or survival advantage that escapes the checks and balances designed to eliminate potentially dangerous cells. All of these mutations reduce overall fitness, yet cells carrying such a mutation can become more abundant in a given niche, and logic follows that greater genetic diversity provides a greater chance that at least one cell in a population will prevail under a given selection pressure, such as chemotherapy

Summary

Introduction

Genome evolution in yeast reveals connections between rare mutations in human cancers Xinchen Teng1,2,* and J. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland 21205 USA. A recent study conducted on the yeast knockout collections by Teng et al [Mol. Cell (2013) 52: 485–494] provides hard evidence that single gene deletions/mutations in most non-essential genes can drive the selection for cancerlike mutations.

Results

Conclusion