title: Characteristics of women with a family history of ovarian cancer. II. Follicular phase hormone levels.
abstract: BACKGROUND
  Although there is a basis for linking pituitary or ovarian hormones with experimentally induced ovarian cancer, establishing their role in women is complicated because the usual case-control methods cannot be applied. In this study, hormonal levels in women with a family history of ovarian cancer (FOC) and who are at higher risk for the disease are compared with women without such a history.
  
  
  METHODS
  The authors studied 106 unrelated women (FOC patients) with at least one primary or two second-degree relatives with ovarian cancer compared with 116 age- and residence-matched controls without a family history of ovarian cancer (FOC control subjects). All women were premenopausal, between the ages of 25 and 49 years, not currently using oral contraceptives, and had blood drawn during the early follicular phase for gonadotropins, estradiol (E2), and CA-125.
  
  
  RESULTS
  Women with a family history of ovarian cancer and control subjects did not differ significantly in follicle stimulating hormone (FSH) levels, E2, or CA-125. Patients with a family history of ovarian cancer had significantly lower luteinizing hormone (LH) levels compared with control subjects and produced more E2 and FSH relative to their level of LH. The ratios of LH to E2 and LH to FSH were correlated with the enzymatic activity of galactose-1-phosphate uridyl transferase, which was shown previously to differ between FOC patients and control subjects.
  
  
  CONCLUSIONS
  Lower LH and higher E2 are reported in women with breast, endometrial, and ovarian cancer (before surgery). The authors speculate that these observations reflect greater LH binding and estradiol production in ovaries at risk for these cancers--the ovarian cortical hyperplasia postulated in older gynecologic literature as the precursor to estrogen dependent neoplasia.
authors.affiliation: Familial Ovarian Cancer Clinic, Obstetrics and Gynecology Epidemiology Center, Boston, Massachusetts.
authors.forename: D W
authors.initials: DW
authors.lastname: Cramer
authors.forename: R L
authors.initials: RL
authors.lastname: Barbieri
authors.forename: M G
authors.initials: MG
authors.lastname: Muto
authors.forename: A
authors.initials: A
authors.lastname: Kelly
authors.forename: J P
authors.initials: JP
authors.lastname: Brucks
authors.forename: B L
authors.initials: BL
authors.lastname: Harlow
mesh_terms: D000328:Adult; D015295:Antigens, Tumor-Associated, Carbohydrate / Q000097:blood; D014408:Biomarkers, Tumor / Q000097:blood; D016022:Case-Control Studies; D004958:Estradiol / Q000097:blood; D005260:Female; D005640:Follicle Stimulating Hormone / Q000097:blood; D005498:Follicular Phase / Q000097:blood*; D006062:Gonadotropins / Q000097:blood*; D006801:Humans; D007986:Luteinizing Hormone / Q000097:blood; D008598:Menstruation / Q000097:blood; D008875:Middle Aged; D010051:Ovarian Neoplasms / Q000097:blood* / Q000235:genetics*; D012307:Risk Factors; D005694:UTP-Hexose-1-Phosphate Uridylyltransferase / Q000097:blood
chemical_list: D015295:Antigens, Tumor-Associated, Carbohydrate; D014408:Biomarkers, Tumor; D006062:Gonadotropins; D004958:Estradiol; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D005694:UTP-Hexose-1-Phosphate Uridylyltransferase