PMID- 7999456
DCOM- 19950124
LR  - 20131121
IS  - 1052-6773 (Print)
IS  - 1052-6773 (Linking)
IP  - 16
DP  - 1994
TI  - Sex steroids and breast cancer prevention.
PG  - 139-47
AB  - Mitogenesis and mutagenesis are major driving forces in neoplastic development.
      Little is known about important breast mutagens, but much is known about breast
      mitogens. "Blocking" the effect of breast cell mitogens, by reducing the actual
      exposure of the breast to them, is an obvious strategy for breast cancer
      prevention. The ovarian hormones, estrogens and progesterone, are major effective
      (direct or indirect) breast cell mitogens. There is overwhelming epidemiologic
      evidence that breast cancer risk is closely related to exposure to estrogens and 
      progestogens. A woman's exposure to endogenous ovarian estrogens and progesterone
      is drastically reduced by the use of combination-type oral contraceptives (COCs),
      but the exogenous synthetic estrogen and progestogen in the COC effectively
      replace the ovarian estrogen and progesterone, so that no decrease in breast cell
      exposure to these hormones is obtained. Doses of estrogen and progestogen in
      modern COCs are close to the minimum attainable, while still retaining both
      contraceptive efficacy and ovarian suppression (so that endogenous estrogen and
      progesterone do not add to the dose of estrogen and progestogen from the COC).
      Considerably lower effective breast cell exposure to estrogen and progestogen
      can, however, be achieved by using a gonadotropin-releasing hormone agonist to
      suppress ovarian function and compensating for the resulting hypoestrogenemia
      with low-dose hormone replacement. Such a contraceptive is predicted to reduce
      lifetime breast cancer risk by more than 50% if used for 10 years and by as much 
      as 70% following 15 years of use. Contraception represents a unique opportunity
      to have a substantial beneficial impact on women's health; more than 10 million
      women use COCs daily in the United States.(ABSTRACT TRUNCATED AT 250 WORDS)
FAU - Spicer, D V
AU  - Spicer DV
AD  - Department of Medicine, School of Medicine, University of Southern California,
      Los Angeles.
FAU - Pike, M C
AU  - Pike MC
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - J Natl Cancer Inst Monogr
JT  - Journal of the National Cancer Institute. Monographs
JID - 9011255
RN  - 0 (Contraceptives, Oral, Combined)
RN  - 0 (Contraceptives, Oral, Hormonal)
RN  - 0 (Estrogens)
RN  - 0 (Progestins)
RN  - 33515-09-2 (Gonadotropin-Releasing Hormone)
RN  - 3XMK78S47O (Testosterone)
RN  - 4G7DS2Q64Y (Progesterone)
RN  - EFY6W0M8TG (Leuprolide)
SB  - IM
MH  - Adult
MH  - Age Factors
MH  - Bone Density/drug effects
MH  - Breast Neoplasms/chemically induced/epidemiology/*prevention & control
MH  - Cardiovascular Diseases/prevention & control
MH  - Case-Control Studies
MH  - Cell Division/drug effects
MH  - Contraceptives, Oral, Combined/adverse effects/*therapeutic use
MH  - Contraceptives, Oral, Hormonal/adverse effects/*therapeutic use
MH  - Drug Utilization
MH  - Endometrial Neoplasms/chemically induced/epidemiology/prevention & control
MH  - Endometrium/drug effects/pathology
MH  - Estrogen Replacement Therapy/adverse effects
MH  - *Estrogens
MH  - Female
MH  - Gonadotropin-Releasing Hormone/*agonists
MH  - Humans
MH  - Hyperplasia
MH  - Incidence
MH  - Leuprolide/pharmacology/therapeutic use
MH  - Middle Aged
MH  - Neoplasms, Hormone-Dependent/*prevention & control
MH  - Osteoporosis/chemically induced
MH  - Ovarian Neoplasms/epidemiology/prevention & control
MH  - Pilot Projects
MH  - Premenopause
MH  - *Progesterone
MH  - Progestins/administration & dosage/adverse effects/*therapeutic use
MH  - Reproductive History
MH  - Risk Factors
MH  - Testosterone/*therapeutic use
RF  - 100
EDAT- 1994/01/01 00:00
MHDA- 1994/01/01 00:01
CRDT- 1994/01/01 00:00
PHST- 1994/01/01 00:00 [pubmed]
PHST- 1994/01/01 00:01 [medline]
PHST- 1994/01/01 00:00 [entrez]
PST - ppublish
SO  - J Natl Cancer Inst Monogr. 1994;(16):139-47.