We have previously demonstrated the presence of human papillomavirus (HPV) DNA in several gynecological cancers using conventional PCR. In the present study, to further understand the role of HPV in malignant transformation of these cancers, the infection rates and viral loads of HPV 16 and 18 in gynecological cancers were analyzed using real-time quantitative PCR (qPCR). HPV 16 DNA was detected in 61.0% (58/95), 15.2% (7/46) and 32.1% (18/56) of cases of cervical, endometrial and ovarian cancers, respectively. On the other hand, HPV 18 DNA was detected in 23.2% (22/95) of cervical cancers, 1.8% (1/56) of ovarian cancers, and in no cases of endometrial cancer. Thus, HPV 16 is much more prevalent than HPV 18 in malignancies of the female genital tract. We also found that both HPV 16 and 18 were significantly (p < 0.05) less frequently present in endometrial and ovarian cancers than in cervical cancer. The median copy numbers of HPV 16 DNA in endometrial and ovarian cancers were 3,500 and 7,590 copies/microg DNA, respectively. These amounts were also significantly (p < 0.05) lower than HPV 16 DNA in cervical cancer (492,800 copies/microg DNA). Thus, HPV 16 could be detected in all three types of gynecological cancer, whilst HPV 18 is extremely rare in endometrial and ovarian cancers. The lower HPV 16 infection rates and lower copy numbers when compared with cervical cancer tend to suggest that HPV plays a less essential role in the development of endometrial cancer and ovarian cancer.
Copyright 2003 S. Karger AG, Basel