Abstract
The retinoblastoma tumour suppressor (RB) is a crucial regulator of cell-cycle progression that is invoked in response to a myriad of anti-mitogenic signals. It has been hypothesized that perturbations of the RB pathway confer a synonymous proliferative advantage to tumour cells; however, recent findings demonstrate context-specific outcomes associated with such lesions. Particularly, loss of RB function is associated with differential response to wide-ranging therapeutic agents. Thus, the status of this tumour suppressor may be particularly informative in directing treatment regimens.
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Acknowledgements
The authors would like to thank all of their colleagues for thought-provoking discussions that provide the basis for the current Perspective. In particular the authors appreciate the contributions of W. Cavenee, R. Bremner, and T. Tlsty to the preparation of the manuscript. A concerted effort was made to provide a highly inclusive discussion of the field: any omission was accidental and the authors apologize for not being able to cite all of the outstanding studies in the literature. The authors are supported by grants from the NIH: CA10617 and CA104213 to E.S.K. and CA099996 and CA116777 to K.E.K.
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Knudsen, E., Knudsen, K. Tailoring to RB: tumour suppressor status and therapeutic response. Nat Rev Cancer 8, 714–724 (2008). https://doi.org/10.1038/nrc2401
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DOI: https://doi.org/10.1038/nrc2401
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