Oral contraceptives and breast cancer: what has 20 years of research shown?
Buehring, G.C.
Biomedicine and PharmacoTherapy 42(8): 525-530
1988
ISSN/ISBN: 0753-3322 PMID: 3066414 Document Number: 325844
Animal model, histologic, and epidemiologic studies over a 20 year period do not support an increased risk of breast cancer with oral contraceptive (OC) use. Even though the US Food and Drug Administration required using the dog, the monkey, and the rodent as animal models for OC testing at the end of the 1970s, research showed that theses models do not adequately match humans. For example, primates rarely get breast cancer yet the incidence for humans ranges from 7%-10%. The beagle experiences 1-2 estrus cycles/year while humans have 12 menstrual cycles/year. Although rodents have a breast cancer incidence similar to humans, study results varied widely depending on strains, doses, and/or administration routes. As of 1988, no case control or cohort studies had demonstrated a statistically significant overall increase in breast cancer incidence in OC users vs. never users. Yet at least 18 studies in which the investigator corrected for major confounding variables showed an insignificant increased risk of breast cancer among certain subsets of women associated with OC use. Various studies supported the theory that OCs may augment multiplication of already altered cells. For example, OCs induced an increased incidence of mammary cancer only in animal models and strains which had an incidence of mammary cancer at least as high as humans. Further, mammographic studies of breast dysplasia revealed that OC users have 18 times the risk of developing breast cancer than do nonusers. Additionally, in breast tissue culture studies, combination OCs containing norethynodrel-mestranol and norgestrel-ethinyl estradiol triggered cancerous cells to multiply faster than normal cells. Research must continue so as to know how to alter OCs to reduce any tumor promotion capabilities without foregoing contraceptive efficiency.