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Institute for Cancer Research, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111 [P. A. L.], and Laboratory of Biology, Division of Cancer Etiology, National Cancer Institute, Bethesda, Maryland 20892 [J. A. D., N. C. P.]
The human papillomavirus type 18 integrated in the HeLa cell genome is amplified on chromosome 8. E6, E7, and E1 open reading frames are amplified 5-fold, and the late viral DNA region, the viral long control region, and cellular flanking sequences are amplified 15-fold. The common 5'-flanking cellular DNA was localized by in situ hybridization of normal and HeLa cells only on chromosome 8 band q24. This flanking probe is included in the amplification unit of Colo320 cells, but in the case of HeLa the amplified region does not include the myc gene which is structurally conserved. Viral integration on chromosome 8 represents an independent event and not a rearrangement of viral DNA located on other chromosomes. The amplification of HPV-18 E6 and E7 open reading frames and the constitutive expression of the myc protooncogene may contribute to immortalization and/or proliferative capacity of HeLa cells.
1 Supported by NIH Grants CA-06927 and RR-05539, an appropriation from the Commonwealth of Pennsylvania to the Fox Chase Cancer Center, and a fellowship from the Cancer Research Institute, Inc., New York (P. A. L.).
2 To whom requests for reprints should be addressed, at Laboratory of Biology, Division of Cancer Etiology, National Cancer Institute, Bethesda, MD 20892.
Received 8/ 1/88. Revised 11/14/88. Revised 4/19/89. Accepted 4/24/89.
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