In a study of 197 cases of histologically confirmed invasive cervical cancer, 61% of biopsies were positive for human papillomavirus (HPV) DNA by Southern or dot-blot hybridization. An association between detection of HPV DNA and oral contraceptive use was observed when HPV-positive and -negative cases were compared. Women reporting recent or long-term (greater than 4 yrs) oral contraceptive use were at 2.3 and 2.9-fold increased risks of HPV positivity, respectively. An increased risk of HPV positivity was also associated with formal education and with urban residence, while long-term smoking was negatively associated with HPV detection. A non-significant trend of increasing risk of HPV positivity with increasing number of sexual partners of the women and of the male partners of monogamous women was observed. Detection of HPV DNA was not associated with other cervical cancer risk factors examined, including age at first coitus, number of pregnancies, and Pap smear screening history. Our findings suggest either an interaction between HPV infection and oral contraceptive use in the genesis of cervical cancer or an increased expression of HPV genome in neoplasms of oral contraceptive users. These observations also support a multifactorial model of cervical cancer causation.
PIP: 197 cases of invasive cervical cancer were biopsied and tested for presence of human papilloma virus (HPV) DNA, and virus-positive and - negative cases were compared as to oral contraceptive use and other risk factors. These cases were all histologically confirmed invasive cervical cancers seen in the Panamanian National Oncology Institute ascertained from July 1985-June 1987. HPV DNA was identified by Southern or dot-blot hybridization, using probes for HPV-16, -18 and - 33. 61% of the cases were considered positive for at least 1 of the tests. Women reporting oral contraceptive use within the last year, or long-term (44 years) use, were 2.3 and 2.9-fold more likely to he HPV- positive than were non-users. Increased risk of HPV was also associated with urban residence and some, rather than no, formal education. Smoking was negatively associated with HPV. A non-significant trend was evident for multiple sexual partners of the women, or for monogamous women, of her partner. HPV was not linked with other cervical cancer risk factors, such as age at 1st coitus, parity, or Pap screen history. The possibility of an interaction between HPV infection and oral contraceptive use in the genesis of cervical cancer, or an increased expression of HPV genome in neoplasms of oral contraceptive users, was discussed, suggesting a multifactorial model of cervical cancer causation.