This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kovacs, M. S. Articles by Brown, J. M. Search for Related Content PubMed Articles by Kovacs, M. S. Articles by Brown, J. M.

Stable Translocations Detected by Fluorescence in Situ Hybridization: A Rapid Surrogate End Point to Evaluate the Efficacy of a Potentiator of Tumor Response to Radiotherapy¹

Department of Radiation Oncology, Cancer Biology Research Laboratory, Stanford University, Stanford, California 94305

Testing potential modifiers of the response of tumors to radiation therapy requires large, expensive, and time-consuming clinical trials. It would, therefore, be of value to have a rapid surrogate end point of tumor response that could be used to evaluate such modifiers. We here propose that radiation-induced stable chromosome translocations measured by fluorescence in situ hybridization (FISH) could fulfill this purpose. The assay requires that the ratio of nonlethal stable translocations to lethal dicentric aberrations be unity and not change with radiation dose and that radiation-induced stable translocations remain in the tumor cell population essentially indefinitely after irradiation. We have tested these assumptions with four human tumor cell lines in vitro at doses of 1–5 Gy and found them to be valid. We also modified the response to fractionated irradiation of a human tumor xenograft in three different ways and quantitated the tumor response using clonogenic cell survival and using the FISH stable translocation assay. Both assays gave similar values for the extent of radiation modification. These data suggest that this assay could allow clinical evaluation of potential radiation sensitizers with fewer patients and in shorter times than is the case with conventional clinical trials.

¹ This work was supported by NIH Grants CA 15201 and CA 67166.

² Present address: Department of Orthopedic Surgery, Faculty of Medicine, Toyama Medical and Pharmaceutical University, 2630 Sugitani, Toyama, 930-01, Japan.

³ To whom requests for reprints should be addressed.

Received 8/28/96. Accepted 12/19/96.

This article has been cited by other articles:

				J. M. Brown Drug Resistance: The Role of Genes Involved in Apoptosis Am. Assoc. Cancer Res. Educ. Book, April 1, 2005; 2005(1): 119 - 122. [Full Text] [PDF]