Tamoxifen and medroxyprogesterone therapy for advanced endometrial carcinoma

Rendina, George; Donadio, Carlo; Fabri, M; Mazzoni, Pietro; Nazzicone, P.

doi:10.1016/0028-2243(84)90071-6

Cited by 58 publications

(30 citation statements)

References 5 publications

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“…Endometrial carcinoma with secretory changes and deep myometrial invasion can also be seen with this therapy (Fig. 14) (40,41). Carcinosarcomas (malignant mixed müllerian tumors) of the uterus have been reported as well, representing the second most FIGURE 10.…”

Section: Tamoxifen Therapy For Breast Neoplasmsmentioning

confidence: 98%

Hormonal Pathology of the Endometrium

2000

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The endometrial tissue is a sensitive target for steroid sex hormones and is able to modify its structural characteristics with promptness and versatility. This article discusses briefly endogenous hormonal effects (cyclic changes, luteal phase defect, unopposed estrogen effect) and describes the histologic patterns encountered in the most commonly used hormone therapies: oral contraceptives, ovulation stimulation, hormone replacement therapy, and antitumoral hormone therapy.Oral contraceptives exert a predominant progestational effect on the endometriun, inducing an arrest of glandular proliferation, pseudosecretion, and stromal edema followed by decidualized stroma with granulocytes and thin sinusoidal blood vessels. Prolonged use results in progressive endometrial atrophy.Ovulation induction therapy accelerates the maturation of the stroma and is often associated with a discrepancy between early secretory glands and an edematous or decidualized stroma with spiral arterioles.Hormone replacement therapy with estrogen alone may result in continuous endometrial proliferation, hyperplasia, and neoplasia. The use of both estrogen and progesterone elicits a wide range of histologic patterns, seen in various combinations: proliferative and secretory changes, often mixed in the same tissue sample; glandular hyperplasia (in polyps or diffuse) ranging from simple to complex atypical; stromal hyperplasia and/or decidual transformation; epithelial metaplasia (eosinophilic, ciliated, mucinous); and inactive and atrophic endometrium.Progesterone therapy for endometrial hyperplasia and neoplasia induces glandular secretory changes, decidual reaction, and spiral arterioles. Glandular proliferation is usually arrested, but neoplastic changes may persist and coexist with secretory changes.Lupron therapy produces a shrinking of uterine leiomyomas by accelerating their hyaline degeneration, similar to that in postmenopausal involution. It generally produces endometrial atrophy.Tamoxifen for breast carcinoma has an estrogenagonist effect on the uterus in approximately 20% of patients, who develop endometrial polyps, glandular hyperplasia, adenomyosis, and/or leiomyomata. Both endometrioid and nonendometrioid carcinomas are seen, often in polyps. Their causal relationship to tamoxifen therapy is debatable. Mod Pathol 2000;13(3):285-294Hormone therapy is widely used throughout the world by women of all ages for a variety of reasons, ranging from oral contraception and ovulation stimulation for family planning to hormone replacement therapy in menopause, to adjuvant therapy of tumors of the breast and uterus. The histopathologic changes of the uterus, and particularly of the endometrium, associated with these therapies encompass a variety of morphologic features that are often difficult to interpret. The endometrium is a sensitive target tissue for steroid sex hormones and is able to modify its structural characteristics with promptness and versatility. The physiologic changes of the endometrium during reproductive life and after men...

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Section: Tamoxifen Therapy For Breast Neoplasmsmentioning

confidence: 98%

Hormonal Pathology of the Endometrium

2000

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“…51 In addition, body weight gain accounted for 67.7% of the adverse effects recorded in patients with advanced-stage EC during oral progestin treatment. 52 One study reported thrombophlebitis in 5% of patients (96.7% were aged 950 years) with advanced or recurrent EC treated with oral progestin. 53 Nevertheless, no such event occurred in young patients receiving oral progestin treatment.…”

Section: Safety Issuesmentioning

confidence: 99%

Oral Progestin Treatment for Early-Stage Endometrial Cancer: A Systematic Review and Meta-analysis

Qin¹,

Yu²,

Yang³

et al. 2016

Int J Gynecol Cancer

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“…Various hormonal agents have been used (progestins, selective estrogen receptor modulators, aromatase inhibitors, synthetic steroid derivatives, and gonadotropin-releasing (GN-RH) hormone analogs) with a response rate of 9% to 55% in different studies (Kokka et al 2010). Cochrane Database Systematic Review of hormonal therapy in advanced or recurrent endometrial cancer assessed 542 patients from 6 different randomized trials (Stolyarova I ;Rendina et al 1984;Ayoub et al 1988;Urbanski et al 1993;Thigpen et al 1999;Pandya et al 2001) (Table 8). The results indicated that hormonal therapy did not prolong overall survival or progression free survival in women with advanced or recurrent endometrial cancer (Kokka et al 2010).…”

Section: Recurrent Endometrial Cancermentioning

confidence: 99%