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Genomic Amplification in Retinoblastoma Narrowed to 0.6 Megabase on Chromosome 6p Containing a Kinesin-like Gene, RBKIN¹

Divisions of Cancer Informatics [D. C., S. P., A. D., V. D. B., B. L. G.] and Cellular and Molecular Biology [D. C., S. P., A. D., V. D. B., B. L. G., J. A. S.], Ontario Cancer Institute/Princess Margaret Hospital, University Health Network, Toronto, M5G 2M9 Canada; Departments of Ophthalmology [B. L. G.], Laboratory Medicine and Pathobiology [J. A. S.], and Medical Biophysics [B. L. G., J. A. S.], University of Toronto, Toronto, M5G 2M9 Canada; and Department of Ophthalmology, First Affiliated Hospital, West China University of Medical Sciences, Chengdu 610041, People’s Republic of China [D. C.]

All retinoblastomas (RBs) show genomic changes in addition to loss of both RB1 alleles. Quantitative-multiplex PCR analysis identified in 41 of 70 (59%) RBs a 0.6-Mb minimal region of chromosome 6p22 gain from which we cloned the human kinesin gene, RBKIN/KIF13A, by rapid amplification of retinal cDNA. RBKIN is expressed ubiquitously in adult tissues, at low levels in fetal tissues, and at high levels in RB. Antisense RBKIN oligonucleotide reduced the growth rate of RB cell lines. RBKIN and/or another closely linked gene are candidate oncogenes contributing to malignant progression of RB.

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