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 ()
Additional contact information
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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Persistent link: https://EconPapers.repec.org/RePEc:nat:nature:v:514:y:2014:i:7522:d:10.1038_nature13813
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DOI: 10.1038/nature13813
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