National Cancer Institute®
Last Modified: September 1, 2002
1
UI - 12065138
AU - Chama CM; Nggada HA; Nuhu A
TI -
Cutaneous metastasis of gestational choriocarcinoma.
SO - Int J Gynaecol Obstet 2002 Jun;77(3):249-50
AD - Department of Obstetrics and Gynaecology, University of Maiduguri
Teaching Hospital, Nigeria.
A 40-year-old woman presented with subcutaneous masses on her chest
wall, abnormal vaginal bleeding and an enlarged uterus. Chest X-ray and
liver ultrasound revealed metastatic disease to these sites,
respectively. A urine human chorionic gonadotrophin assay was positive.
A biopsy of the chest wall lesion and endometrium revealed
choriocarcinoma. Treatment with methotrexate, actinomycin-D and
cyclophosphamide led to complete resolution of the disease on
examination, X-ray and ultrasound scans. The urinary pregnancy test
became negative.
2
UI - 12065144
AU - FIGO Oncology Committee
TI -
FIGO staging for gestational trophoblastic neoplasia 2000. FIGO Oncology
Committee.
SO - Int J Gynaecol Obstet 2002 Jun;77(3):285-7
3
UI - 12186481
AU - Mamelak AN; Withers GJ; Wang X
TI -
Choriocarcinoma brain metastasis in a patient with viable intrauterine
pregnancy. Case report.
SO - J Neurosurg 2002 Aug;97(2):477-81
AD - Department of Neurosurgery, Huntington Memorial Hospital, Pasadena,
California, USA. amamelak@coh.org
The authors report the case of a woman who presented during her 30th
week of pregnancy with a large brain metastasis from a previously
undetected metastatic choriocarcinoma. The metastasis caused significant
neurological deficit due to mass effect, necessitating rapid
intervention. Medical management included a regimen of high-dose
corticosteroid medications for 36 hours, followed by cesarean delivery
of the fetus and craniotomy to remove the metastatic tumor, chemotherapy
and radiation therapy were begun within 1 week postsurgery. Both the
baby and mother survived, and as of the 1-year follow-up examination,
there was no evidence of disease in the mother. This is only the second
report of a metastatic choriocarcinoma associated with a simultaneous
viable intrauterine pregnancy, and the only case in which surgical
removal of a brain metastasis was required. Coordinated
multidisciplinary treatment of mother and fetus by members of the
neurosurgery, medical oncology, neonatology, and obstetrics services
facilitated a good outcome in this case.
4
UI - 11704157
AU - Hammond CB
TI -
False positive hCG.
SO - Obstet Gynecol 2001 Nov;98(5 Pt 1):719-20
5
UI - 11876401
AU - Uzunlar AK; Yilmaz F; Bayhan G; Akkus Z
TI -
Expressions of p53, proliferating cell nuclear antigen, and Ki-67 in
gestational trophoblastic diseases.
SO - Eur J Gynaecol Oncol 2002;23(1):79-83
AD - Department of Pathology, The Medical Faculty of Dicle University,
Diyarbakir, Turkey.
OBJECTIVE: This study was done to determine whether the expressions of
p53, PCNA, and Ki-67 could differentiate spontaneous abortions with
hydropic changes from gestational trophoblastic diseases. MATERIALS AND
METHODS: Twenty partial hydatidiform moles, 21 complete hydatidiform
moles, nine invasive hydatidiform moles, three choriocarcinomas and 19
first trimester hydropic spontaneous abortions were evaluated by means
of immunohistochemical methods with antibodies to p53, PCNA, and Ki-67
in this study. RESULTS: The Ki-67, PCNA, and p53 immunoreactivity was
significantly higher in the gestational trophoblastic disease group than
in the spontaneous abortion group with hydropic changes. None of the
three parameters provided reliable discrimination among gestational
trophoblastic disease subgroups. CONCLUSION: Our findings suggest that
expressions of Ki-67, proliferating cell nuclear antigen and p53 can be
used to differentiate between spontaneous abortion with hydropic changes
and gestational trophoblastic disease when all three markers are used
together.
6
UI - 12214462
AU - Shimizu T; Yaegashi N
TI -
[Gestational trophoblastic tumors and recent clinical information]
SO - Gan To Kagaku Ryoho 2002 Aug;29(8):1363-70
AD - Dept. of Obstetrics and Gynecology, Tohoku University School of
Medicine.
Recent clinical advances in the field of gestational trophoblastic
diseases are described. WHO modified its risk factor scoring system.
This change was proposed to combine both the basic FIGO anatomic staging
with the modified WHO risk factor scoring system. Patients who score as
low-risk are treated with single agent chemotherapy, such as
methotrexate (MTX), and patients refractory to MTX are treated with a
combination chemotherapy, EMA/CO. Patients who score as high-risk are
treated with EMA/CO, and patients refractory to the first line
chemotherapy may be successfully treated with EP/EMA. Recent
epidemiological data showed that women with complete hydatidiform moles
could anticipate normal reproduction in the future. Studies found that
pregnancies after treatment of molar pregnancy resulted in 69%
full-term, live births; 8% premature deliveries; 1% ectopic pregnancies,
and 0.5% stillbirths. First-trimester spontaneous abortions occurred in
17% of pregnancies, and major and minor malformations were detected in
0.4% of infants. Patients with hydatidiform mole were at increased risk
of developing molar pregnancy in subsequent conceptions. After having
one molar pregnancy, the risk of having molar disease in a future
gestation was about 1%. The risk of persistent gestational trophoblastic
tumors was increased by long-term oral contraceptive use before
conception. In a large, multicenter, case-control study, the risk was
shown to be increased in women who had ever used oral contraceptives,
but was highest for women taking oral contraceptives during the cycle in
which they became pregnant. Partial hydatidiform moles were never
previously proven to transform into choriocarcinoma; however, a recent
study with molecular techniques clearly showed that partial moles could
transform into choriocarcinoma. All patients with suspected partial
moles should be reviewed centrally and require hCG follow-up.
7
UI - 12209690
AU - Matsui H; Suzuka K; Iitsuka Y; Yamazawa K; Tanaka N; Mitsuhashi A; Seki
TI -
K; Sekiya S
Salvage combination chemotherapy with 5-fluorouracil and actinomycin D
for patients with refractory, high-risk gestational trophoblastic
tumors.
SO - Cancer 2002 Sep 1;95(5):1051-4
AD - Department of Obstetrics and Gynecology, Chiba University School of
Medicine, Chiba, Japan. hmatsui@med.m.chiba.u.ac.jp
BACKGROUND: The objective of this study was to evaluate the efficacy and
toxicity of a high-dose 5-fluorouracil and actinomycin D regimen (the FA
regimen) as salvage chemotherapy for patients with high-risk gestational
trophoblastic tumors (GTTs). METHODS: From 1985 to 1997, 10 patients
with refractory, high-risk GTTs were treated with the FA regimen at
Chiba University Hospital. Of those 10 patients, 7 patients developed
drug resistance to methotrexate, etoposide, and actinomycin D
combination chemotherapy (the MEA regimen); 1 patient developed
recurrent disease after receiving the MEA regimen; and 2 patients
developed recurrent disease after receiving combination chemotherapy
with etoposide, methotrexate, and actinomycin D alternating with
cyclophosphamide and vincristine (the EMA/CO regimen). The hematologic
toxicity of the FA regimen was graded at every chemotherapy course.
RESULTS: With the FA regimen, the survival rate was 80.0% (8 of 10
patients) for a mean follow-up of 10 years. Two patients died due to
multidrug resistance, and two patients subsequently developed recurrent
disease. The two patients with recurrent disease were successfully
salvaged again with the MEA regimen. The toxicity of the FA regimen was
evaluated in 78 cycles. Myelosuppression seemed to be the dose-limiting
toxicity, and the incidences of World Health Organization Grade 4
leukocytopenia and thrombocytopenia were 6.4% and 3.8%, respectively, of
78 cycles. CONCLUSIONS: Although etoposide-containing chemotherapy is
currently the most effective and well-tolerated regimen for patients
with high-risk GTTs, 20-30% of patients develop resistance to
etoposide-containing regimens. Salvage combination chemotherapy with FA
is effective for these patients with refractory disease, and the
toxicity is predictable and manageable. Copyright 2002 American Cancer
Society.
8
UI - 12060455
AU - Ramondetta LM; Silva EG; Levenback CF; Burke TW
TI -
Mixed choriocarcinoma in a postmenopausal patient.
SO - Int J Gynecol Cancer 2002 May-Jun;12(3):312-6
AD - Department of Gynecologic Oncology, The University of Texas MD Anderson
Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030, USA.
lramonde@mail.mdanderson.org
Gestational trophoblastic disease rarely presents in patients beyond the
reproductive years. To our knowledge, this is the first case of mixed
trophoblastic disease in a postmenopausal woman. We present here a case
of a 60-year-old woman with evidence of a pelvic mass and pulmonary
metastasis. Surgery revealed an 8 x 6 x 6 cm multinodular uterine tumor
involving the right adnexa. Histologic review was consistent with
choriocarcinoma with intermediate trophoblastic features. Postoperative
beta-hCG was 381 561 mIU/ml.We conclude that maintaining a high index of
suspicion facilitates the identification of postmenopausal patients with
metastatic gestational trophoblastic disease. This case reconfirms the
deceptive presentation of the "great masquerader".
9
UI - 12144689
AU - McNally OM; Tran M; Fortune D; Quinn MA
TI -
Successful treatment of mother and baby with metastatic choriocarcinoma.
SO - Int J Gynecol Cancer 2002 Jul-Aug;12(4):394-8
AD - Department of Gynae-oncology, Ward 43, Aberdeen Royal Infirmary,
Foresterhill, Aberdeen AB25 2ZN, Scotland.
The second case of successful management of a mother and neonate with
metastatic choriocarcinoma is described. A response to paclitaxel in the
face of platinum-refractor disease in the mother is also detailed. In a
woman with a history of gestational trophoblastic disease, a high index
of suspicion and thereby early diagnosis lead to prompt treatment in
both mother and neonate.
10
UI - 12213732
AU - Oldt RJ 3rd; Kurman RJ; Shih IeM
TI -
Molecular genetic analysis of placental site trophoblastic tumors and
epithelioid trophoblastic tumors confirms their trophoblastic origin.
SO - Am J Pathol 2002 Sep;161(3):1033-7
AD - Department of Pathology, The Johns Hopkins University School of
Medicine, Baltimore, Maryland 21231, USA.
Trophoblastic tumors represent a unique group of human neoplasms because
they are derived from fetal tissue. Except for choriocarcinoma, the
neoplasms that develop from human trophoblast are poorly characterized.
Placental site trophoblastic tumors and epithelioid trophoblastic tumors
are thought to arise from intermediate (extravillous) trophoblasts based
on histopathological studies, but direct molecular evidence of a
trophoblastic origin has not been established. In this study, we
performed molecular analysis in an attempt to confirm their presumable
trophoblastic origin. We demonstrated that such tumors contain a
Y-chromosomal locus and/or new (paternal) alleles not present in
adjacent normal uterine tissue in all 31 informative cases. Loss of
heterozygosity was found in 60% of tumors and all 42 tumors assessed
contained wild-type K-ras. All of the trophoblastic tumors were
heterozygous in at least 1 of 10 single-nucleotide polymorphism markers
studied in contrast to homozygosity in all 10 single-nucleotide
polymorphism markers in most complete hydatidiform moles indicating that
these tumors are not related to complete hydatidiform moles. This study
provides the first molecular evidence that placental site trophoblastic
tumors and epithelioid trophoblastic tumors are of fetal (trophoblastic)
origin.
11
UI - 12232933
AU - Gokula RM; Falconer HG; Smith FO
TI -
Persistent gestational trophoblastic disease presenting as left
hemiparesis in a Jamaican teenager.
SO - West Indian Med J 2002 Jun;51(2):116-8
AD - Mandeville Public Hospital, Mandeville, Manchester, Jamaica.
rgokula@hotmail.com
A 19-year-old woman, who delivered a macerated stillborn at 32 weeks'
gestation and had persistent postpartum vaginal bleeding, presented with
a left hemiparesis three and a half months after delivery. A clinical
diagnosis of persistent gestational trophoblastic disease (GTD) was
made, based on quantitative serum beta-hCG of more than 200,000 IU/ml,
cannon ball metastases on chest X-ray and two ring enhancing lesions,
metastases, in the right parietal lobe on Computed Axial Tomography
(CAT) scan of the brain. Despite combination chemotherapy, with
methotrexate, cyclophosphamide and actinomycin D, her condition worsened
and she died.
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