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Rb suppresses human cone-precursor-derived retinoblastoma tumours

Xiaoliang L. Xu, Hardeep P. Singh, Lu Wang, Dong-Lai Qi, Bradford K. Poulos, David H. Abramson, Suresh C. Jhanwar () and David Cobrinik ()
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Xiaoliang L. Xu: Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
Hardeep P. Singh: The Vision Center, Children’s Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, California 90027, USA
Lu Wang: Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
Dong-Lai Qi: The Vision Center, Children’s Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, California 90027, USA
Bradford K. Poulos: Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461, USA
David H. Abramson: Ophthalmic Oncology Service, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
Suresh C. Jhanwar: Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10021, USA
David Cobrinik: The Vision Center, Children’s Hospital Los Angeles, 4650 Sunset Boulevard, Los Angeles, California 90027, USA

Nature, 2014, vol. 514, issue 7522, 385-388

Abstract: The nature of the retinal cell-type-specific circuitry that predisposes to retinoblastoma is demonstrated, in which a program that is unique to post-mitotic human cone precursors sensitizes to the oncogenic effects of retinoblastoma (Rb) protein depletion; hence, the loss of Rb collaborates with the molecular framework of cone precursors to initiate tumorigenesis.

Date: 2014
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DOI: 10.1038/nature13813

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