Cancer Research Infection and Cancer: Biology, Therapeutics, and Prevention  AACR Conference on Molecular Diagnostics - 2008
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[Cancer Research 50, 278-283, January 15, 1990]
© 1990 American Association for Cancer Research

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Absence of IFNA and IFNB Genes from Human Malignant Glioma Cell Lines and Lack of Correlation with Cellular Sensitivity to Interferons1

Junji Miyakoshi2, Kelly D. Dobler, Joan Allalunis-Turner, John D. S. McKean, Kenneth Petruk, Peter B. R. Allen, Keith N. Aronyk, Bryce Weir, Debbie Huyser-Wierenga, Dorcas Fulton, Raul C. Urtasun and Rufus S. Day, III3

Molecular Genetics and Carcinogenesis Laboratory, Department of Medicine [J. M., K. D., R. S. D.], Radiobiology Laboratory, Department of Radiation Oncology [J. A-T.], and Department of Radiation Oncology [D. H-W., D. F., R. C. U.], Cross Cancer Institute, Edmonton, Alberta T6G 1Z2, and Division of Neurosurgery, Faculty of Medicine, University of Alberta, Edmonton, Alberta T6G 2G3, Canada [J. D. S. M., K. P., P. B. R. A., K. N. A., B. W.]

We report that 5 of 19 human malignant glioma cell lines have neither interferon {alpha} (IFNA) nor interferon ß (IFNB) genes that are detectable by Southern blotting. Of 5 other of these malignant glioma lines that have a single IFNB gene copy, 3 lack the IFNA genes entirely and two have one copy. One of the lines that lacks the IFNA genes entirely but has one copy of the IFNB gene has a rearrangement near the IFNB gene that is most easily interpreted as an insertion of a large segment of DNA (at least 50 kilobases) the 3' end of which is <1.3 kilobases 5' to the known regulatory sequences of the IFNB gene. In spite of the rearrangement, IFNB-specific RNA is highly inducible in this line by poly(I)-poly(C). The ability of interferon {alpha} or interferon ß to inhibit cell growth does not depend upon the presence or absence of the respective gene. This finding adds solid tumors to those tumor cell lines (acute lymphocytic leukemia, chronic myelogeneous leukemia) previously determined to lack the IFNA and IFNB genes (Diaz et al., Proc. Natl. Acad. Sci. USA, 85: 5259–5263, 1988).

1 This study was supported by an Establishment/Scholarship Grant from the Alberta Heritage Foundation for Medical Research (AHFMR) to R. Day and AHFMR and Alberta Cancer Board fellowships to J. Miyakoshi.

2 Present address: Department of Experimental Radiology, Faculty of Medicine, Kyoto University, Kyoto 606, Japan.

3 To whom requests for reprints should be addressed, at Molecular Genetics and Carcinogenesis Laboratory, Department of Medicine, Cross Cancer Institute, 11560 University Ave., Edmonton, Alberta T6G 1Z2.

Received 5/30/89. Revised 9/20/89. Accepted 10/10/89.




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Copyright © 1990 by the American Association for Cancer Research.