UI - 11968642
AU - Strickland S
Nursing practice in gestational trophoblastic disease.
SO - Nurs Times 2000 Oct 5-11;96(40):37-9
AD - Charing Cross Hospital, London.
UI - 11952469
AU - Uberti EM; Diestel Mdo C; Guimaraes FE; Goloubkova T; Rosa MW; De Napoli
Gestational trophoblastic disease: one more risk in adolescent
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.
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.
UI - 12001129
AU - Xue WC; Guan XY; Ngan HY; Shen DH; Khoo US; Cheung AN
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,
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.
UI - 11987577
AU - Chada M; Lisa L; Prusa R
[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.
UI - 12021185
AU - Arturi F; Lacroix L; Presta I; Scarpelli D; Caillou B; Schlumberger M;
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.
UI - 12057074
AU - Lurain JR
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.
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%.
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