Reevaluating the safety of fertility-sparing hormonal therapy for early endometrial cancer.
OBJECTIVE
To evaluate the safety of fertility-sparing hormonal therapy for endometrial cancer in young patients.


METHODS
Six patients diagnosed with endometrial adenocarcinoma grade I and had undergone progestin treatment were reviewed. Four patients failed progestin treatment and were then found at surgery to have both endometrial and ovarian cancers. A clonality assay using the human androgen receptor gene as the X-linked polymorphic marker and immunohistochemistry for steroid hormone receptor expression were used to delineate the relation between the endometrial and ovarian lesions and to explore possible causes of treatment failure.


RESULTS
The patients were followed for a mean of 48.8 months. Four of the six responded to the treatment at a mean of 3.5 months. Two of these patients had a recurrence within a mean of 4.5 months after their initial response. Two patients did not respond to progestin treatment. At surgery in those 4, both endometrial and ovarian tumors were found. All 6 are still alive, and 2 successfully delivered healthy infants. The clonality assay revealed an independent cell origin for the endometrial and ovarian lesions in 2 of the 4 women who failed progestin treatment. Progesterone receptors were absent in both endometrial and ovarian tumors in 2 of these 4 patients.


CONCLUSIONS
The absence of progesterone receptors may relate to the failure of progestin treatment. The use of progestin treatment for well-differentiated early endometrial carcinoma should be cautious and requires very careful clinical evaluation before and after treatment.
Yang
Yuh-Cheng
YC
Department of Obstetrics and Gynecology, Mackay Memorial Hospital, 92 Sec. 2 Chung-San North Road, Taipei 104, Taiwan. eugene@ms2.mmh.org.tw
Wu
Chao-Chih
CC
Chen
Chie-Pein
CP
Chang
Chih-Long
CL
Wang
Kung-Liang
KL
D000328:Adult; D018931:Antineoplastic Agents, Hormonal / Q000627:therapeutic use*; D018269:Carcinoma, Endometrioid / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000601:surgery; D041321:Chromosomes, Human, X / Q000235:genetics; D016889:Endometrial Neoplasms / Q000188:drug therapy* / Q000235:genetics / Q000378:metabolism / Q000601:surgery; D047628:Estrogen Receptor alpha / Q000096:biosynthesis; D005260:Female; D005298:Fertility; D006801:Humans; D007150:Immunohistochemistry; D019290:Megestrol Acetate / Q000627:therapeutic use*; D009364:Neoplasm Recurrence, Local; D010051:Ovarian Neoplasms / Q000235:genetics / Q000378:metabolism / Q000601:surgery; D011446:Prospective Studies; D011944:Receptors, Androgen / Q000235:genetics; D011980:Receptors, Progesterone / Q000096:biosynthesis; D017211:Treatment Failure; D049951:X Chromosome Inactivation
D018931:Antineoplastic Agents, Hormonal; D047628:Estrogen Receptor alpha; D011944:Receptors, Androgen; D011980:Receptors, Progesterone; D019290:Megestrol Acetate