During the 19th century, studies indicated that reproductive events were involved in
cervical cancer. Human papillomavirus (HPV)
infection is a prerequisite for development of
cancer, but co-factors, among them the action of sexual
steroid hormones, are necessary. Childbirth has been an important risk factor but now probably plays a minor role in the industrialized world, where parity is low. Long-term
oral contraceptive use has been thoroughly studied epidemiologically, and correlates to
cervical cancer in most studies. In vitro studies on cervical cell lines transfected with HPV and animal studies indicate that
sex steroid hormones are capable to induce
cancer. In in vivo
cervical cancer tissue studies there have been observations that endogenous
progesterone in serum correlates to a negative pattern of expression of cellular and extracellular
proteins,
tumor markers. Immune response could be another mechanism.
Estradiol might be associated with a positive pattern and high
estradiol and low
progesterone levels increase duration of survival in
cervical cancer. Studies where treatment of compounds that influence
sex steroid hormones have been given are rare and have been disappointing.