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[Cancer Research 59, 3911-3914, August 1, 1999]
© 1999 American Association for Cancer Research
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[Cancer Research 59, 3911-3914, August 15, 1999]
© 1999 American Association for Cancer Research

Advances in Brief

Hammerhead Ribozyme-mediated Inactivation of Mutant RET in Medullary Thyroid Carcinoma1

Ranjani Parthasarathy, Gilbert J. Cote and Robert F. Gagel2

Section of Endocrine Neoplasia and Hormonal Disorders, Department of Internal Medicine Specialties, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

Activating mutations of the RET proto-oncogene cause hereditary medullary thyroid carcinoma. To examine whether selective inactivation of mutant RET could prevent transformation, a hammerhead ribozyme was designed to cleave RET mRNA containing a transforming mutation of codon 634 TGC -> TAC (Cys634Tyr). In vitro RNA cleavage assay demonstrated that the ribozyme selectively cleaved RET RNA with a Cys634Tyr but not Cys634Arg or the normal sequence. Expression of ribozyme in NIH/3T3 cells prevented RET-mediated colony formation in soft agar. This inhibition required catalytically active ribozyme and was specific for the TAC mutation. Therefore, ribozymes designed to selectively target mutant RET RNA may provide an effective therapeutic in the treatment of this syndrome.




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Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
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Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1999 by the American Association for Cancer Research.