Alternative reading frame supports an alternative model for retinoblastoma.
The recent observation by Tyler Jacks' group that loss of ARF accelerates pituitary tumors in Rb(+/-):Arf(-/-) mice by inducing proliferation without affecting apoptosis allows one to speculate about an alternative model for retinoblastoma. Retinoblasts in human and pituitary gland melanotrophs in the mouse might be uniquely susceptible to bi-allelic inactivation of Rb because upon loss-of-heterozygosity, these tissues are able to slowly proliferate without effectively activating the cell death machinery, and respond to an additional oncogenic signal. But what is the nature of this proliferation-permissive oncogenic alteration?
Zacksenhaus
Eldad
E
Department of Medicine, Division of Cell and Molecular Biology, Toronto General Research Institute-University Health Network, University of Toronto, 67 College Street, Rm. 407, Toronto, Ontario M5G-2M1 Canada. eldad.zacksenhaus@utoronto.ca
D000818:Animals; D002471:Cell Transformation, Neoplastic / Q000235:genetics* / Q000378:metabolism; D004195:Disease Models, Animal; D016147:Genes, Tumor Suppressor / Q000502:physiology*; D006801:Humans; D051379:Mice; D018345:Mice, Knockout / Q000235:genetics; D016366:Open Reading Frames / Q000235:genetics*; D010911:Pituitary Neoplasms / Q000235:genetics / Q000378:metabolism; D012175:Retinoblastoma / Q000235:genetics* / Q000378:metabolism; D016160:Retinoblastoma Protein / Q000172:deficiency* / Q000235:genetics; D025521:Tumor Suppressor Proteins / Q000235:genetics* / Q000378:metabolism
D016160:Retinoblastoma Protein; D025521:Tumor Suppressor Proteins