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

Imprima English

National Cancer Institute^®
Ultima Vez Modificado: 1 de junio del 2002

Nursing practice in gestational trophoblastic disease.
Gestational trophoblastic disease: one more risk in adolescent pregnancy.
Malignant placental site trophoblastic tumor: a cytogenetic study using comparative genomic hybridization and chromosome in situ hybridization.
[Inhibin in pregnancy--a new screening marker for prenatal diagnosis?]
Regulation by human chorionic gonadotropin of sodium/iodide symporter gene expression in the JAr human choriocarcinoma cell line.
Treatment of gestational trophoblastic tumors.

Table of Contents

1
UI - 11968642
AU - Strickland S
TI - Nursing practice in gestational trophoblastic disease.
SO - Nurs Times 2000 Oct 5-11;96(40):37-9
AD - Charing Cross Hospital, London.

2
UI - 11952469
AU - Uberti EM; Diestel Mdo C; Guimaraes FE; Goloubkova T; Rosa MW; De Napoli
TI - G Gestational trophoblastic disease: one more risk in adolescent pregnancy.
SO - Acta Obstet Gynecol Scand 2002 Apr;81(4):356-63
AD - Centro de Doencas Trofoblasticas, Mario Totta Maternity Ward, Hospital Irmandade da Santa Casa de Misericordia de Porto Alegre, RS, Brazil. elzauberti@cpovo.net
BACKGROUND: An evaluation of the performance of a Referral Center in the diagnosis, treatment and follow up of adolescents with gestational trophoblastic disease. METHODS: In a 13-year prospective cohort study, trophoblastic disease were followed up and/or treated by a multidisciplinary team. Adolescents underwent strict clinical and laboratory control after mole evacuation to guarantee adhesion to follow up, early diagnosis, and prompt treatment of persistent disease. The Student-Fischer t-test and the chi-square test were used for the statistic analysis of the results. RESULTS: Adolescents represented 21.3% of the 583 patients with gestational trophoblastic disease: 102 (82.3%) had uncomplicated hydatidiform moles, and 22 (17.7%) underwent chemotherapy for persistent gestational trophoblastic disease or a gestational trophoblastic tumor. Complications were diagnosed earlier (p < 0.001) in patients managed and treated at the referral center. Of the adolescents with complications, 81.8% were low risk, 54.5% were at the International Federation of Gynecology and Obstetrics stage I, and 90.9% were treated with chemotherapy only. Time to remission and follow up were shorter for uncomplicated hydatidiform moles (9.8 +/- 3.4 weeks and 8.8 +/- 1.8 months, respectively) than for persistent disease (16.2 +/- 5.8 weeks and 45 +/- 24.5 months, respectively). Adhesion to follow up was similar in the two groups (84.2% and 91.8%). To this date, 50% of the adolescents have had one or more gestations, and 82% of these pregnancies were normal. CONCLUSIONS: Adolescents comprise approximately 20% of all gestational trophoblastic disease patients and have high adhesion to follow up. The disease did not affect their reproductive capacity, and chances of a normal subsequent gestation were high.

3
UI - 12001129
AU - Xue WC; Guan XY; Ngan HY; Shen DH; Khoo US; Cheung AN
TI - Malignant placental site trophoblastic tumor: a cytogenetic study using comparative genomic hybridization and chromosome in situ hybridization.
SO - Cancer 2002 Apr 15;94(8):2288-94
AD - Department of Pathology, People's Hospital, Peking University, Beijing, China.
BACKGROUND: Placental site trophoblastic tumor (PSTT) is a rare form of gestational trophoblastic neoplasm composed predominantly of intermediate trophoblast. Most showed benign behavior whereas 10-15% of PSTTs were clinically malignant with later recurrence and metastasis. Currently, there are no reliable means to predict clinical outcome, and cytogenetic information is scanty. METHODS: The clinicopathologic features of two cases of malignant PSTT were analyzed. Cytogenetic analysis was performed by comparative genomic hybridization (CGH) and chromosome in situ hybridization (CISH) using frozen tissue and paraffin embedded sections, respectively. RESULTS: Both patients were 32 years old at time of diagnosis. One patient with PSTT presented with menorrhagia, and the other presented with symptoms of missed abortion. Elevated serum human chorionic gonadotropin (HCG) was detected in both patients. Histologic examination showed the typical features of PSTT with high mitotic count (> 5/10 high-power fields). Ovarian and lung metastasis occurred in both patients. Immunohistochemical staining revealed an equal distribution of HCG and human placental lactogen. Cytogenetic studies by CISH showed that karyotypes of these two malignant PSTTs were diploid. Analysis of the tumor tissue by CGH did not show any changes in DNA copy numbers. CONCLUSIONS: The authors' study indicated that the two metastasizing PSTTs had balanced diploid karyotype. The malignant behavior of PSTTs may be not related to the DNA copy number changes. Such cytogenetic study may be useful in distinguishing metastatic PSTT from choriocarcinoma. Copyright 2002 American Cancer Society.

4
UI - 11987577
AU - Chada M; Lisa L; Prusa R
TI - [Inhibin in pregnancy--a new screening marker for prenatal diagnosis?]
SO - Ceska Gynekol 2002 Mar;67(2):93-6
AD - Ustav klinicke biochemie a patobiochemie UK, 2. LF a FN Motol, Praha.

5
UI - 12021185
AU - Arturi F; Lacroix L; Presta I; Scarpelli D; Caillou B; Schlumberger M;
TI - Russo D; Bidart JM; Filetti S Regulation by human chorionic gonadotropin of sodium/iodide symporter gene expression in the JAr human choriocarcinoma cell line.
SO - Endocrinology 2002 Jun;143(6):2216-20
AD - Dipartimento di Medicina Sperimentale e Clinica, Universita di Catanzaro, Magna Graecia 88100 Catanzaro, Italy.
Sodium/iodide symporter (NIS) gene and protein expressions have been recently described in human cytotrophoblasts, emphasizing its potential function in the active transport of iodide from the mother to the fetus. In this study we analyzed NIS expression and function in the human JAr placental choriocarcinoma cell line. Using real-time quantitative RT-PCR, we first demonstrated that NIS transcripts are expressed at a high level in JAr cells compared with other cell lines, including thyroid cancer cells. Functional analysis clearly showed that Jar cells are able to concentrate iodide in presence of hCG. Iodide accumulation increased after 2-h exposure to 5 IU/ml hCG, to 6-fold over the basal level after 8 h. This effect was reproduced using forskolin, the cAMP analog (Bu)(2)-cAMP, and phorbol acetate. Moreover, hCG increased both NIS mRNA after 2 h and NIS protein levels after 4 h, reaching a maximum after 8 h in both cases. In conclusion, our data demonstrate that 1) NIS is expressed in JAr cells; 2) iodide transport in JAr cells is regulated by hCG and by cAMP-dependent and -independent mechanisms; 3) the stimulation of iodide uptake is due to an increase in both NIS mRNA and protein levels; and 4) JAr cells may represent an excellent in vitro model suitable to analyze the molecular mechanisms involved in iodide transport from mother to fetus.

6
UI - 12057074
AU - Lurain JR
TI - Treatment of gestational trophoblastic tumors.
SO - Curr Treat Options Oncol 2002 Apr;3(2):113-24
AD - John I. Brewer Trophoblastic Disease Center, Department of Obstetrics and Gynecology, Northwestern University Medical School, Prentice Women's Hospital, 333 East Superior Street, Suite 420, Chicago, IL 60611, USA. jlurain@nmh.org
Gestational trophoblastic tumors (invasive mole, choriocarcinoma, and placental site trophoblastic tumor) should be classified according to the National Cancer Institute (NCI), World Health Organization (WHO), and International Federation of Gynecology and Obstetrics (FIGO) criteria into nonmetastatic, low-risk metastatic, and high-risk metastatic categories. Nonmetastatic tumors (FIGO Stage I) can be treated with a variety of single-agent methotrexate or actinomycin D protocols, resulting in cure of essentially all patients. Metastatic low-risk tumors (FIGO Stages II and III, WHO score < 8) should be treated with 5-day dosage schedules of methotrexate or actinomycin D, with cure rates approaching 100%. Metastatic high-risk tumors (FIGO Stage IV, WHO score > 7) require combination chemotherapy with etoposide, methotrexate, actinomycin D, cyclophosphamide, and vincristine (EMA-CO) with or without adjuvant radiation therapy and surgery to achieve cure rates of 80% to 90%.

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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