Cell death in genome evolution.
Inappropriate survival of abnormal cells underlies tumorigenesis. Most discoveries about programmed cell death have come from studying model organisms. Revisiting the experimental contexts that inspired these discoveries helps explain confounding biases that inevitably accompany such discoveries. Amending early biases has added a newcomer to the collection of cell death models. Analysis of gene-dependent death in yeast revealed the surprising influence of single gene mutations on subsequent eukaryotic genome evolution. Similar events may influence the selection for mutations during early tumorigenesis. The possibility that any early random mutation might drive the selection for a cancer driver mutation is conceivable but difficult to demonstrate. This was tested in yeast, revealing that mutation of almost any gene appears to specify the selection for a new second mutation. Some human tumors contain pairs of mutant genes homologous to co-occurring mutant genes in yeast. Here we consider how yeast again provide novel insights into tumorigenesis.
College of Pharmaceutical Sciences, Soochow University, Suzhou, Jiangsu Province 215123, PR China; W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA. Electronic address: xcteng@suda.edu.cn.
Xinchen
X
Teng
W. Harry Feinstone Department of Molecular Microbiology and Immunology, Johns Hopkins University Bloomberg School of Public Health, Baltimore, MD 21205, USA. Electronic address: hardwick@jhu.edu.
J Marie
JM
Hardwick
D000818:Animals; D005075:Biological Evolution; D016923:Cell Death; D006801:Humans; D008675:Metamorphosis, Biological; D009154:Mutation; D009369:Neoplasms / Q000188:drug therapy / Q000235:genetics* / Q000473:pathology*; D012441:Saccharomyces cerevisiae / Q000166:cytology* / Q000235:genetics*; D059016:Tumor Microenvironment
Apoptosis; Cancer progression; Evolution; Programmed cell death; Tumorigenesis; Yeast