Interview with the retinoblastoma family members: do they help each other?
The ultimate destiny of a cell to undergo division, differentiation, survival, and death results from an intricate balance between multiple regulators including oncogenes, tumor suppressor genes, and cell cycle associated proteins. Deregulation of the cell cycle machinery switches the phenotype from a normal cell to a cancerous cell. Fundamental alterations of tumor suppressor genes may result in an unregulated cell cycle with the accumulation of mutations and eventual neoplastic transformation. As such, one may define cancer as a genetic disease of the cell cycle. In this review, we will emphasize our current understanding of how the cell cycle machinery maintains cellular homeostasis by studying the consequences of its deregulation.
Sbarro Institute for Cancer Research and Molecular Medicine, Center for Biotechnology, Temple University, Philadelphia, Pennsylvania, USA.
Tiziana
T
Tonini
Christina
C
Hillson
Pier Paolo
PP
Claudio
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D018797:Cell Cycle Proteins; D002454:Cell Differentiation / Q000502:physiology*; D018844:Cyclin-Dependent Kinases / Q000378:metabolism / Q000502:physiology; D016213:Cyclins / Q000378:metabolism / Q000502:physiology; D004268:DNA-Binding Proteins; D050684:E2F Transcription Factors; D006801:Humans; D016160:Retinoblastoma Protein / Q000235:genetics* / Q000378:metabolism / Q000502:physiology; D014157:Transcription Factors / Q000378:metabolism* / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000378:metabolism* / Q000502:physiology
D018797:Cell Cycle Proteins; D016213:Cyclins; D004268:DNA-Binding Proteins; D050684:E2F Transcription Factors; D016160:Retinoblastoma Protein; D014157:Transcription Factors; D016159:Tumor Suppressor Protein p53; D018844:Cyclin-Dependent Kinases