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Does HRT modify risk of gynecological cancers?
Int J Fertil Menopausal Stud 1995; 40 Suppl 1:40-53IJ

Abstract

A substantial body of recent experimental, clinical and epidemiological evidence indicates that hormones play a major role in the etiology of several human cancers. The ability of hormones to stimulate cell division in certain target organs such as the breast, endometrium, prostate and the ovary, may lead following repeated cell divisions to accumulation of random genetic errors that ultimately produce the neoplastic phenotype. Hormone-related cancers account for more than 30% of all newly diagnosed female cancers in the United States. While most non-hormone-dependent adult cancers rise continuously with age, hormone-responsive cancers of the breast, the ovary and the endometrium rise with age until menopause, and then distinctly level off to a plateau. These epidemiologic characteristics may indicate that the key etiologic events for these cancers occur in the premenopausal period. Prevention strategies that intervene during the premenopausal period can be expected to have a greater long-term impact in reducing risk than those implemented for an equivalent length of time in the postmenopausal years. Epidemiological studies demonstrate a reduction in endometrial cancer risk of about 11.7% per year of combination oral contraceptive (COC) use; ovarian cancer risk may be reduced by 7.5% per year of COC use, while breast cancer studies have produced mixed results. A comparison of age-adjusted incidence and mortality rates for women less than 50 years of age between the years 1973-1974 and 1986-1987 demonstrate a change in the average rate of breast cancer of plus 9.6% incidence and minus 8.2% mortality; the rates reflect the cancer burden of women who would and would not have had access to COCs during the majority of their child-bearing years. The use of hormone replacement therapy (HRT) is well established to provide short-term relief of symptoms related to menopause and long-term protection from the consequences of estrogen deficiency, such as postmenopausal osteoporosis and cardiovascular disease. Besides COCs, use of HRT constitutes the other major setting in which exogenous steroid hormones are widely used in essentially healthy women and has had a remarkable impact on cancer incidence and mortality. Estrogen replacement therapy (ERT) and endometrial cancer risk are strongly associated with respect to both dose and duration. Endometrial cell mitotic activity during continuous high-dose estrogen monotherapy equals that observed during the follicular phase of the menstrual cycle, and the total mitotic activity over a 28-day period amounts to roughly double that of a premenopausal woman as long as there is no opposition by a progestogen.(

ABSTRACT

TRUNCATED AT 400 WORDS)

Authors+Show Affiliations

Department of Obstetrics, University of Muenster, Germany.No affiliation info available

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

7581588

Citation

Schneider, H P., and M Birkhauser. "Does HRT Modify Risk of Gynecological Cancers?" International Journal of Fertility and Menopausal Studies, vol. 40 Suppl 1, 1995, pp. 40-53.
Schneider HP, Birkhauser M. Does HRT modify risk of gynecological cancers? Int J Fertil Menopausal Stud. 1995;40 Suppl 1:40-53.
Schneider, H. P., & Birkhauser, M. (1995). Does HRT modify risk of gynecological cancers? International Journal of Fertility and Menopausal Studies, 40 Suppl 1, pp. 40-53.
Schneider HP, Birkhauser M. Does HRT Modify Risk of Gynecological Cancers. Int J Fertil Menopausal Stud. 1995;40 Suppl 1:40-53. PubMed PMID: 7581588.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Does HRT modify risk of gynecological cancers? AU - Schneider,H P, AU - Birkhauser,M, PY - 1995/1/1/pubmed PY - 1995/1/1/medline PY - 1995/1/1/entrez SP - 40 EP - 53 JF - International journal of fertility and menopausal studies JO - Int J Fertil Menopausal Stud VL - 40 Suppl 1 N2 - A substantial body of recent experimental, clinical and epidemiological evidence indicates that hormones play a major role in the etiology of several human cancers. The ability of hormones to stimulate cell division in certain target organs such as the breast, endometrium, prostate and the ovary, may lead following repeated cell divisions to accumulation of random genetic errors that ultimately produce the neoplastic phenotype. Hormone-related cancers account for more than 30% of all newly diagnosed female cancers in the United States. While most non-hormone-dependent adult cancers rise continuously with age, hormone-responsive cancers of the breast, the ovary and the endometrium rise with age until menopause, and then distinctly level off to a plateau. These epidemiologic characteristics may indicate that the key etiologic events for these cancers occur in the premenopausal period. Prevention strategies that intervene during the premenopausal period can be expected to have a greater long-term impact in reducing risk than those implemented for an equivalent length of time in the postmenopausal years. Epidemiological studies demonstrate a reduction in endometrial cancer risk of about 11.7% per year of combination oral contraceptive (COC) use; ovarian cancer risk may be reduced by 7.5% per year of COC use, while breast cancer studies have produced mixed results. A comparison of age-adjusted incidence and mortality rates for women less than 50 years of age between the years 1973-1974 and 1986-1987 demonstrate a change in the average rate of breast cancer of plus 9.6% incidence and minus 8.2% mortality; the rates reflect the cancer burden of women who would and would not have had access to COCs during the majority of their child-bearing years. The use of hormone replacement therapy (HRT) is well established to provide short-term relief of symptoms related to menopause and long-term protection from the consequences of estrogen deficiency, such as postmenopausal osteoporosis and cardiovascular disease. Besides COCs, use of HRT constitutes the other major setting in which exogenous steroid hormones are widely used in essentially healthy women and has had a remarkable impact on cancer incidence and mortality. Estrogen replacement therapy (ERT) and endometrial cancer risk are strongly associated with respect to both dose and duration. Endometrial cell mitotic activity during continuous high-dose estrogen monotherapy equals that observed during the follicular phase of the menstrual cycle, and the total mitotic activity over a 28-day period amounts to roughly double that of a premenopausal woman as long as there is no opposition by a progestogen.(ABSTRACT TRUNCATED AT 400 WORDS) SN - 1069-3130 UR - https://www.unboundmedicine.com/medline/citation/7581588/Does_HRT_modify_risk_of_gynecological_cancers L2 - https://www.lens.org/lens/search?q=citation_id:7581588 DB - PRIME DP - Unbound Medicine ER -