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Cancer Types / Gynecologic Cancers / Gestational Trophoblastic Disease and Choriocarcinoma / NCI Resources

NCI CANCERLIT^® Search: Gestational Trophoblastic Neoplasms - May 2002

National Cancer Institute^®
Last Modified: May 1, 2002

Comparative genomic hybridization studies in hydatidiform moles and choriocarcinoma: amplification of 7q21-q31 and loss of 8p12-p21 in

Choriocarcinoma and epithelial trophoblastic tumor: successful treatment of relapse with hysterectomy and high-dose chemotherapy with peripheral

Is lack of response to single-agent chemotherapy in gestational trophoblastic disease associated with dose scheduling or chemotherapy

17alpha-methyl testosterone is a competitive inhibitor of aromatase activity in Jar choriocarcinoma cells and macrophage-like THP-1 cells in

Thyrotoxicosis of a rare aetiology.

Epithelioid trophoblastic tumor of the uterus: cytological and immunohistochemical observation of a case.

Table of Contents

1
UI - 10616525
AU - Ahmed MN; Kim K; Haddad B; Berchuck A; Qumsiyeh MB
TI - Comparative genomic hybridization studies in hydatidiform moles and choriocarcinoma: amplification of 7q21-q31 and loss of 8p12-p21 in choriocarcinoma.
SO - Cancer Genet Cytogenet 2000 Jan 1;116(1):10-5
AD - Department of Pathology, Duke University Medical Center, Durham, NC 27710, USA.
Comparative genomic hybridization (CGH) was utilized to investigate genetic changes from archived cases of choriocarcinoma (n = 12) and hydatidiform moles (n = 7). Test DNA was extracted from paraffin-embedded tissues, amplified using total universal PCR, and co-hybridized with control DNA to normal metaphases. Comparative genomic hybridization findings showed chromosomal imbalances in 9 of 12 cases of choriocarcinoma. By contrast, all hydatidiform moles showed normal CGH profiles. Consistent findings in choriocarcinoma included deletion at 8p (5 cases) and amplification at 7q (4 cases). A tumor suppressor gene (e.g., N33) at 8p and/or a growth regulator at 7q could play a role in the initiation of choriocarcinoma and its progression. This is the first study showing specific alterations in choriocarcinomas by CGH, and illustrates the utility of this technique in elucidating genetic changes in gynecological tumors.

2
UI - 11925147
AU - Knox S; Brooks SE; Wong-You-Cheong J; Ioffe O; Meisenberg B; Goldstein
TI - DP Choriocarcinoma and epithelial trophoblastic tumor: successful treatment of relapse with hysterectomy and high-dose chemotherapy with peripheral stem cell support: a case report.
SO - Gynecol Oncol 2002 Apr;85(1):204-8
AD - Department of Obstetrics and Gynecology and Reproductive Sciences, School of Medicine, Baltimore, Maryland 21201, USA.
BACKGROUND: Post-termchoriocarcinoma is a rare complication of pregnancy. The presence of epithelioid trophoblastic elements may lead to the persistence of locally invasive disease which is unresponsive to multiagent chemotherapy. Relapse is associated with an estimated mortality rate of 30%. CASE: We present a case of Stage IC post-term choriocarcinoma and epithelioid trophoblastic tumor. While the metastatic sites in the lungs responded to multiagent chemotherapy, a hysterectomy was required to treat persistent disease in the uterus. The patient relapsed within 4 months of completion of chemotherapy. Relapse was treated with high-dose chemotherapy with peripheral stem cell support. The patient is alive with no evidence of disease 23 months posttransplant. CONCLUSIONS: The application of multimodality treatment and high-dose chemotherapy resulted in a successful outcome for this patient, indicating a potential role for high-dose therapy in patients who suffer a relapse of choriocarcinoma.

3
UI - 11925117
AU - Kohorn EI
TI - Is lack of response to single-agent chemotherapy in gestational trophoblastic disease associated with dose scheduling or chemotherapy resistance?
SO - Gynecol Oncol 2002 Apr;85(1):36-9
AD - Yale Trophoblast Center, Yale University School of Medicine, New Haven, Connecticut 06510, USA. ernest.kohorn@yale.edu
OBJECTIVE: The aim of this study was to determine whether in the management of low-risk gestational trophoblastic neoplasia (GTN) the administration of 5-day courses of 12 microg/kg actinomycin D is effective following the failure of 1.25 mg/m(2) "pulsed" actinomycin D. METHODS: Patients with low-risk GTN who failed to respond to 1.25 mg/m(2) pulsed actinomycin were switched to the 5-day course of 12 microg/kg actinomycin. RESULTS: Patients with low-risk GTN who failed to respond to pulsed actinomycin were changed to the same chemotherapy agent, actinomycin D, given as a 5-day course at 12 microg/kg. Four of the five responded and one required methotrexate to achieve remission. CONCLUSIONS: Pulsed biweekly actinomycin and pulsed weekly methotrexate have been shown to have a higher failure rate than the 5-day regimens of the same medications. This study demonstrates that failure of pulsed actinomycin may be successfully treated by a 5-day course of the same medication. It appears that with the pulsed regimens cytotoxic exposure of trophoblastic cells to the medication is too brief and the 5-day course permits more cells to be in cycle. It is suggested that, following failure of a pulsed regimen, the patient is given the same chemotherapy as a 5-day course, rather than switching from actinomycin to methotrexate or vice versa. This conserves options for chemotherapy in GTN.

4
UI - 11850230
AU - Mor G; Eliza M; Song J; Wiita B; Chen S; Naftolin F
TI - 17alpha-methyl testosterone is a competitive inhibitor of aromatase activity in Jar choriocarcinoma cells and macrophage-like THP-1 cells in culture.
SO - J Steroid Biochem Mol Biol 2001 Dec;79(1-5):239-46
AD - Department of Obstetrics and Gynecology, Center for Research in Reproductive Biology and Reproductive Neuroscience Unit, Yale University Medical School, 333 Cedar Street, FMB 335, New Haven, CT 06520 8063, USA.
17alpha-methyl testosterone is a synthetic androgen with affinity for the androgen receptor. 17alpha-methyl testosterone is used widely as a component of hormone replacement therapy. Previous reports have indicated that contrary to testosterone, 17alpha-methyl testosterone is not aromatized. However, 17alpha-methyl testosterone still could affect local estrogen formation by regulating aromatase expression or by inhibiting aromatase action. Both possibilities have important clinical implications. To evaluate the effect of 17alpha-methyl testosterone on the expression and activity of aromatase, we tested the choriocarcinoma Jar cell line, a cell line that express high levels of P450 aromatase, and the macrophage-like THP-1 cells, which express aromatase only after undergoing differentiation. We found that in both cell lines, 17alpha-methyl testosterone inhibits aromatase activity in a dose-related manner. The curve of inhibition parallels that of letrozole and gives complete inhibition at 10(-4) M 17alpha-methyl testosterone, determined by the tritium release assay. 17alpha-methyl testosterone does not have detectable effects on aromatase RNA and protein expression by Jar cells. Undifferentiated THP-1 cells had no aromatase activity and showed no effect of 17alpha-methyl testosterone, but differentiated THP-1 (macrophage-like) cells had a similar inhibition of aromatase activity by 17alpha-methyl testosterone to that seen in Jar cells. The Lineweaver-Burke plot shows 17alpha-methyl testosterone to be a competitive aromatase inhibitor. Our results show for the first time that 17alpha-methyl testosterone acts as an aromatase inhibitor. These findings are relevant for understanding the effects of 17alpha-methyl testosterone as a component of hormone replacement therapy. 17alpha-methyl testosterone may, as a functional androgen and orally active steroidal inhibitor of endogenous estrogen production, also offer special possibilities for the prevention/treatment of hormone-sensitive cancers.

5
UI - 11085778
AU - Ismail M; Bhat RV
TI - Thyrotoxicosis of a rare aetiology.
SO - Postgrad Med J 2000 Dec;76(902):799, 806
AD - Department of Medicine, Kasturba Medical College, Mangalore 575 001, India.

6
UI - 11940211
AU - Kamoi S; Ohaki Y; Mori O; Yokoyama M; Kawamoto Y; Kawamura T; Araki T
TI - Epithelioid trophoblastic tumor of the uterus: cytological and immunohistochemical observation of a case.
SO - Pathol Int 2002 Jan;52(1):75-81
AD - Department of Obstetrics and Gynecology, Nippon Medical School, Tokyo, Japan. skamoi@nms.ac.jp
Epithelioid trophoblastic tumor (ETT) is a new entity of trophoblastic tumor and 14 such cases were reported by Shih and Kurman in 1998. However, only three subsequent cases supporting ETT have been reported. Recently, we experienced a case of ETT in a 37-year-old woman whose preoperative endometrial brushings showed atypical mononucleate giant cells and who underwent hysterectomy with the diagnosis of a uterine fibroid. The specimens revealed a 2.5 x 3.0 cm yellow-tan intramural nodule located in the lower uterine segment, which was composed of a neoplastic proliferation of intermediate trophoblasts in epithelioid arrangements. Immunohistochemically, the tumor cells were diffusely positive for cytokeratin and inhibin-alpha, and focally positive for human chorionic gonadotropin and human placental lactogen. She presented

The above citations and abstracts reflect those newly added to CANCERLIT for the month and topic listed in the title. The citations have been retrieved from CANCERLIT using a predefined search strategy of indexed subject terms. Although the search strategy has been refined as best as possible, citations may appear that are not directly related to the topic, and occasionally relevant references may be omitted.

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