Table 1.
Name of Hormone | Formulation Name and Dose | Observation Time | Study Model | Results | References |
---|---|---|---|---|---|
ER antagonist | 0.15 mL Faslodex and 1.5 mg of raloxifene | Faslodex twice a week for a month and raloxifene for a month, 5 days a week | K14E7 and K14E6 transgenic mice | Raloxifene, ER antagonist and selective ER modulator, efficiently clears cancer and its precursor lesions in both the cervix and the vagina | [79] |
Non-steroid synthetic estrogen with synthetic progestagen | Dienestrol—1 tablet (5 mg) and Chlormadinon—1 tablet (2 mg) |
5 years | 120 patients after surgery and/or radiotherapy | Only 20% and 32% incidence of cancer recurrences and survival without cancer symptoms was found in 80% and 65% of cases, respectively in the hormonally treated group and in the control group | [90] |
Estrogen and progesterone | HT formulation (estrogen alone, progesterone alone, combination of estrogen/progesterone) | 3 groups (≤1, 2–4, ≥5 years) | 261 ICC and 804 CIN3/CIS cases of post- and perimenopausal women | Significantly decreased the risk of ICC in peri- and postmenopausal women, but menopausal estrogens alone were associated with an increased risk of CIN3/CIS and combined HT was inversely associated with ICC | [81] |
ERT | — | 1–10 years | 645 women | Exogenous estrogens decreased the risk of cervical cancer | [78] |
Estrogens progestin | Oral conjugated equine estrogens, 0.625 mg/day, plus medroxyprogesterone acetate, 2.5 mg/day | 2 years | 2561 women | Did not significantly affect the incidence of cytologic abnormalities | [76] |
Anti-estrogen | Triphenylethylene antiestrogen tamoxifen | 10 days (20 or 40 mg/day) | 19 patients | Certain cervical carcinomas had changes in their proliferation and differentiation levels following tamoxifen administration | [82] |
Anti-estrogen | Tamoxifen | 10 mg per orally twice a day | 34 patients | The objective response rate was 11.1%, so tamoxifen appears to have minimal activity in non-squamous cell carcinoma of the cervix | [83] |
Progestagen | Combined oral contraceptives | <5 years and >5 years | 16,573 women | The risk of invasive cervical cancer increased with increasing duration of use, not for short time use | [84] |
Estrone, estradiol and progesterone |
SHBG (20 nmol·L−1) estradiol (5 pg·mL−1) estrone (5 pg·mL−1) estrone sulphate (100 pg·mL−1) DHEAS 10 μg·dl−1 and progesterone 100·pg·mL−1 | 5–10 years of study | 11,742 women | Elevated plasma levels of endogenous estrogens or progesterone decrease the risk of cervical neoplasia | [85] |
HRT | — | 1 January, 2005 to 31 December 31 2015 | 222 women | 48% patients received counseling for HRT and then improved efforts to reduce disparities in the distribution of survivorship care | [86] |
ER modulator, Tamoxifen | 5% dextran-charcoal treated fetal bovine serum (D5) and 0, 1, 2.5, 5, 7.5, or 10 μM tamoxifen | 6 days | In vitro growth of three cell lines derived from carcinoma of the uterine cervix (HeLa, CaSki, ME-180) | Inhibited cell growth of the cervical carcinoma cell lines; 2.5 μM tamoxifen induced more than 60% growth inhibition where 5 μM tamoxifen was cytotoxic | [87] |
Estrogens and progestogens | Contraceptives (G03A), estrogens (G03C), progestogens (G03D), and progestogens and estrogens in combination (G03F). | 0.5 to 1 year after diagnosis | 171 (67%) of 257 women had at least one dispensing of HT (Hormonal Therapy) | Fewer than half of cervical cancer survivors with therapy-induced early menopause used HT | [88] |
Estradiol | 30 to 35 μg ethinylestradiol | From 1995 to 2014 | women aged 15 to 49 | The risk pattern among any hormonal and combined contraceptive users generally increased with longer duration of use and declined after stopping | [89] |