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[Cancer Research 48, 7164-7172, December 1, 1988]
© 1988 American Association for Cancer Research

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Isolation of a New Type of Human Papillomavirus (HPV52b) with a Transforming Activity from Cervical Cancer Tissue

Hajime Yajima, Tetsuo Noda, Ethel-Michele de Villiers, Akira Yajima, Kaiichiro Yamamoto, Kiichiro Noda and Yoshiaki Ito1

Institute for Virus Research, Kyoto University, Kyoto 606, Japan [H. Y., T. N., Y. I.]; Reference Center for Human Pathogenic Papillomavirus, German Cancer Center, 6900 Heidelberg, Federal Republic of Germany [E-M. de V.] Department of Gynecology and Obstetrics, Tohoku University School of Medicine, Sendai 980, Japan [H. Y., A. Y.]; Department of Gynecology and Obstetrics, Kinki University School of Medicine, Osaka-Sayama 586, Japan [K. Y., K. N.]

Substantial evidence has implicated human papillomaviruses (HPVs) as etiological agents of human cervical cancer. We detected and cloned an unidentified HPV genome in cellular DNA extracted from a surgical specimen of a Japanese patient with cervical cancer. Hybridization studies suggested that this HPV was the most homologous to HPV33 among more than 51 types of HPV ever identified. A recently identified new HPV, isolated by W. Lancaster and designated HPV52, is also most homologous to HPV33 (W. Lancaster et al., unpublished data). Our HPV was found to be homologous but not identical to HPV52 and hence was designated HPV52b. By introducing it into NIH3T3 cells, we found that HPV52b DNA had growth-stimulating activity as HPV16 DNA. This newly identified HPV52b DNA was present as episomes in cervical cancer cells of two out of two specimens so far examined and the integrated copies were not detected. HPV52b was present in three out of 15 (20%) specimens in Japan. In addition, the presence of three additional unidentified HPV sequences homologous to HPV52b was detected in three other specimens. The results suggest that this group of HPV may be prevalent and involved in carcinogenesis of cervical cancer in Japan.

1 To whom requests for reprints should be addressed.

Received 4/15/88. Revised 9/13/88. Accepted 9/19/88.







HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Cancer Research Clinical Cancer Research
Cancer Epidemiology Biomarkers & Prevention Molecular Cancer Therapeutics
Molecular Cancer Research Cancer Prevention Research
Cancer Prevention Journals Portal Cancer Reviews Online
Annual Meeting Education Book Meeting Abstracts Online
Copyright © 1988 by the American Association for Cancer Research.