Cyclins, Cdks, E2f, Skp2, and more at the first international RB Tumor Suppressor Meeting.
The RB1 gene was cloned because its inactivation causes the childhood ocular tumor, retinoblastoma. It is widely expressed, inactivated in most human malignancies, and present in diverse organisms from mammals to plants. Initially, retinoblastoma protein (pRB) was linked to cell cycle regulation, but it also regulates senescence, apoptosis, autophagy, differentiation, genome stability, immunity, telomere function, stem cell biology, and embryonic development. In the 23 years since the gene was cloned, a formal international symposium focused on the RB pathway has not been held. The "First International RB Tumor Suppressor Meeting" (Toronto, Canada, November 19-21, 2009) established a biennial event to bring experts in the field together to discuss how the RB family ("pocket proteins"), as well as its regulators and effectors, influence biology and human disease. We summarize major new breakthroughs and emerging trends presented at the meeting.
Bremner
Rod
R
Toronto Western Research Institute, Toronto, Ontario, Canada. rbremner@uhnres.utoronto.ca
Zacksenhaus
Eldad
E
D018844:Cyclin-Dependent Kinases / Q000502:physiology*; D016213:Cyclins / Q000502:physiology*; D050684:E2F Transcription Factors / Q000502:physiology*; D016147:Genes, Tumor Suppressor; D006801:Humans; D009369:Neoplasms / Q000235:genetics / Q000503:physiopathology*; D016160:Retinoblastoma Protein / Q000235:genetics / Q000502:physiology*; D044786:S-Phase Kinase-Associated Proteins / Q000502:physiology*
D016213:Cyclins; D050684:E2F Transcription Factors; D016160:Retinoblastoma Protein; D044786:S-Phase Kinase-Associated Proteins; D018844:Cyclin-Dependent Kinases