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PubMed1993

Malignant trophoblastic tumors: immunohistochemical and flow cytometric comparison of choriocarcinoma and placental site trophoblastic tumors.

We performed an immunohistochemical and flow cytometric study of the formalin-fixed, paraffin-embedded tissues of eight recent gestational choriocarcinomas (CCs) and three placental-site trophoblastic tumors (PSTTs). The follow-up period ranged from 1 to 144 months (mean, 74.3 months). In the CCs, which consisted predominantly of cytotrophoblasts and syncytiotrophoblasts intermingled with small amounts of intermediate trophoblasts, cytotrophoblasts were occasionally positive for beta-subunit human chorionic gonadotropin (HCG) and syncytiotrophoblasts contained abundant HCG. Some intermediate trophoblasts were positive for HCG and many were positive for human placental lactogen. In the three PSTTs, which were characterized by a monomorphic proliferation of intermediate trophoblasts, the tumor cells were positive for human placental lactogen and placental alkaline phosphatase. The tumors of two patients, including one fatal case, contained more human placental lactogen-positive cells than HCG-positive cells, while the tumor of the remaining patient, who had high serum HCG levels, showed a reversed staining pattern resembling that of CC; this patient has been alive without disease for 9 years. One CC patient and one PSTT patient died of multiple lung metastases, despite hysterectomy and multiagent chemotherapy. All CCs and PSTTs had an exclusively diploid DNA content, and there was no correlation among histopathologic and immunohistochemical features, DNA ploidy, S-phase fraction, and clinical outcome for patients with these tumors. These results suggest that there is a PSTT that immunohistochemically resembles CC and that flow cytometric and immunohistochemical analysis may not be effective tools to predict the biologic behavior of malignant trophoblastic tumors.

Adult↗

PubMed1990

Placental site trophoblastic tumor: with features between an exaggerated placental site reaction and a placental site trophoblastic tumor.

Chorionic villi, whose presence in cases of trophoblastic disease is normally used to exclude both a choriocarcinoma and placental site trophoblastic tumor (PSTT), were present in the initial uterine curettage specimen of a trophoblastic tumor. The lesion shared morphologic features of both an exaggerated placental site reaction and a PSTT. There was infiltration of the posterior wall of the uterus by small clusters and isolated cells which had a prominent affinity for vessels and resembled a usual placental bed reaction. There was, however, deep involvement of myometrium with extension to the cervix, and the condition persisted for 5 months after uterine evacuation. Because different treatment is entailed, identification of this lesion as a tumor of nonvillous trophoblast is also of great importance in a region where the more usual forms of trophoblastic disease represent a declining but not infrequent event. When products of gestation are examined, the possibility of a PSTT should be considered and the clinician alerted if there is a suggestion of excessive intermediate trophoblastic activity, regardless of the presence of chorionic villi. While this may result in the unnecessary followup of some cases, it would permit, with the aid of serial beta-hCG and HPL levels, the earlier detection of PSTTs.

Adult↗

PubMed1998

Immunohistochemical analysis of cell cycle regulatory gene products in normal trophoblast and placental site trophoblastic tumor.

Intermediate trophoblast (IT) rarely gives rise to a placental site trophoblastic tumor (PSTT) To examine the different growth mechanisms present in normal and neoplastic IT, the expression of cell cycle regulatory molecules was compared at normal implantation sites and in PSTTs. Normal implantation sites in early gestation (19 patients) and PSTTs (6 patients) were immunohistochemically studied using antibodies against cytokeratin, human chorionic gonadotropin, and human placental lactogen to identify IT, and antibodies against Ki-67, cyclins (A, B, D1, and E), cyclin-dependent kinases (cdks), and p53 to investigate the proliferative activity of the trophoblast. Marked proliferative activity was observed in the trophoblast of the cell columns. Normal IT exhibited a very low labeling index for Ki-67, with negative expression for cdks and cyclins, except for cyclins B and E. The tumor cells of PSTT exhibited a high labeling index for Ki-67 with positive expression for all the cyclins and cdks examined. Expression of p53 was identified in tumor cells of PSTTs and the distribution of p53-positive cells correlated topographically with that of the cyclin A-positive cells. The transformed IT of PSTT has high proliferative activity with an abnormal expression of cell cycle regulatory molecules, which is not observed in normal IT.

Adult↗

PubMed2000

Etoposide and cisplatin/etoposide, methotrexate, and actinomycin D (EMA) chemotherapy for patients with high-risk gestational trophoblastic tumors refractory to EMA/cyclophosphamide and vincristine chemotherapy and patients presenting with metastatic placental site trophoblastic tumors.

PURPOSE: To evaluate the results of etoposide, cisplatin/etoposide, methotrexate, and actinomycin D (EP/EMA) chemotherapy in patients with gestational trophoblastic tumors (GTTs), who have relapsed after or who have become refractory to EMA/cyclophosphamide and vincristine (CO) chemotherapy, and in patients presenting with metastatic placental site trophoblastic tumors (PSTTs). PATIENTS AND METHODS: We have treated a total of 34 patients with GTT and eight patients with metastatic PSTT with the EP/EMA chemotherapy schedule. RESULTS: Twenty-two patients received EP/EMA because of apparent drug resistance to EMA/CO, and because the human chorionic gonadotropin (hCG) was near normal, they were not assessable for response. Twenty-one of these patients (95%) are alive and in remission. In the group where the hCG was high enough to confirm a response (greater than one log fall in hCG) to EP/EMA, all 12 patients responded and nine of these patients (75%) are alive and in remission. We have treated three patients with PSTT where the interval from antecedent pregnancy was less than 2 years, and all patients (100%) are alive and in remission. We have treated five patients where the interval from antecedent pregnancy was greater than 2 years and one fifth (20%) remain in remission. The survival for patients with GTT is 30 (88%) out of 34 patients and four (50%) out of eight patients for PSTT, giving an overall survival for these two cohorts of 34 (81%) out of 42 patients. The toxicity of this schedule is significant, with grade 3 or 4 toxicity (National Cancer Institute common toxicity criteria) recorded in hemoglobin (21%), WBC (68%), and platelets (40%). The role of surgery in this group of patients is important and contributed to sustained remission in five patients (23%) and possibly helped an additional seven patients (32%). CONCLUSION: EP/EMA is an effective but moderately toxic regimen for patients with high-risk GTT who become refractory to or relapse from EMA/CO chemotherapy. Also, EP/EMA clearly has activity in patients with metastatic PSTT.

Adolescent↗

PubMed1988

[Characteristics of the production of chorionic gonadotropin by the cells of trophoblastic tumors (immunohistochemical research)].

An immunohistochemical investigation of chorionic gonadotropin (CGT) in normal placental, hydatidiform mole and choriocarcinoma tissues was undertaken. Cyto- and syncytiotrophoblast both were shown to produce the hormone in normal and tumor trophoblast; the rate of synthesis increased in proportion to the degree of cell elements differentiation, except for very large elements of syncytiotrophoblast with numerous pycnotic nuclei which were found to contain either only traces of response to CGT or none at all. The percentage of syncytiotrophoblast--produced hormone progressively increased in the succession of the placenta--hydatidiform mole--choriocarcinoma. No significant difference in the levels of immunohistochemically--identified hormone was found in the hydatidiform mole and choriocarcinoma.

Choriocarcinoma↗

PubMed2004

Cystic trophoblastic tumor: a nonaggressive lesion in postchemotherapy resections of patients with testicular germ cell tumors.

Cystic trophoblastic tumor (CTT) is an uncommon lesion that is usually seen after chemotherapy in patients with testicular germ cell tumors. Its clinical significance has not been well studied. We identified 17 patients with CTT in retroperitoneal lymph node dissections (RPLNDs) after cisplatin-based chemotherapy for testicular germ cell tumors. None had other forms of persistent germ cell tumor except for teratoma, and no patient received additional chemotherapy after RPLND. At the time of RPLND, 7 patients were known to have had normal serum levels of beta-subunit of human chorionic gonadotropin (beta-hCG), whereas 5 had relatively mild elevations (1.6-165 mIU/mL, median, 8.0 mIU/mL). The CTTs consisted of circumscribed, small cysts, usually multifocal, lined by mostly mononucleated trophoblast cells with abundant eosinophilic cytoplasm, often with smudged nuclei and showing only infrequent mitotic figures. Although the epithelial lining was often stratified to several layers in thickness or formed intracystic papillary tufts, solid proliferations of trophoblast cells within the stroma were absent, as were clearly biphasic admixtures of mononucleated and multinucleated trophoblast cells. The cysts were either empty or contained fibrinoid material and were set in a hypocellular, fibrous stroma with adjacent teratoma. Stains for hCG highlighted rare cells. On follow-up of 15 patients, 11 were disease free (mean, 80 months). Three recurred with serum alpha-fetoprotein elevations at 25, 31, and 107 months, respectively, and one with beta-hCG elevation at 2 months. The latter patient, however, also had unresected mediastinal tumor postchemotherapy. We conclude that the finding of CTT in postchemotherapy resections does not warrant additional chemotherapy. Its clinical significance appears similar to that of residual teratoma.

Adolescent↗

PubMed1999

Oral contraceptive use and risk of gestational trophoblastic tumors.

BACKGROUND: Gestational trophoblastic disease refers to a spectrum of rare benign and malignant gynecologic disorders whose pathogenesis is not well understood. Recent studies from China and the United States have raised the hypothesis that long-term use of oral contraceptives before conception may increase the risk of gestational trophoblastic tumors. A multicenter case-control study of gestational trophoblastic tumors was undertaken to test this hypothesis. METHODS: Telephone interviews were conducted with 235 case patients, including 50 with gestational choriocarcinoma, and 413 control subjects matched on recentness of pregnancy, age at pregnancy, and area of residence. Relative risks (odds ratios) were computed by conditional logistic regression. Reported P values are two-sided. RESULTS: The relative risk estimate for ever having used oral contraceptives before the index pregnancy was 1.9 (95% confidence interval [CI] = 1.2-3.0), and the risk increased with duration of use (P for trend = .05). The estimate was highest for women who used oral contraceptives during the cycle in which they became pregnant (relative risk = 4.0; 95% CI=1.6-10), but there was no consistent pattern according to the time interval since last use. Separate analyses of choriocarcinoma and persistent mole yielded similar results, i.e., the relative risk estimates for oral contraceptive use were 2.2 (95% CI=0.8-6.4) and 1.8 (95% CI=1.0-3.0), respectively. Control for the number of sexual partners, which was independently associated with risk (P for trend = .05), did not materially change the results. CONCLUSIONS: This study, the largest to date, indicates that long duration of oral contraceptive use before conception increases the risk of gestational trophoblastic tumors. These findings may provide clues to the pathogenesis of this rare disease. Changes in use of oral contraceptives are not warranted, however, because the incidence attributable to oral contraceptive use is very low.

Adult↗

PubMed1978

A new placental protein test for the presence and identification of trophoblastic tumors.

Trophoblast-specific beta1-glycoprotein (TSG) is detected in serum of patients with trophoblastic and nontrophoblastic tumors by means of immunodiffusion in agar (IDF), immunoradioautography in agar (IRA), and double-antibody radioimmunoassay (RIA), The identification of TSG is carried out by monospecific rabbit antisera. By IRA, TSG was found in serum of patients with trophoblastic tumors both before treatment (82.4%) and after surgery and/or chemotherapy (37.2%). All so-called falsepositives were associated with teratocarcinoma of the testicle. By means of RIA, TSG was also discovered in serum of patients with a variety of malignancies. In total, the TSG level was elevated in 15% of 114 cases of nontrophoblastic malignancies; as a rule, from 3 to 12 ng/ml. TSG was not detected in normal adult blood sera and in different pathological conditions.

Female↗

PubMed1988

Clinical experience with placental site trophoblastic tumors at the New England Trophoblastic Disease Center.

From 1982-1986, seven patients with pathologically confirmed placental site trophoblastic tumors underwent treatment at the New England Trophoblastic Disease Center. All seven patients presented with nonmetastatic disease; the presenting symptom was vaginal bleeding in six patients and amenorrhea in one patient. Mitotic counts of the tumor may vary among endometrial curettings, hysterectomy specimens, and metastatic lesions. When placental site trophoblastic tumor is diagnosed on endometrial curettage, a thorough metastatic workup should be undertaken. Because of this tumor's poor response to chemotherapy, a diagnosis of nonmetastatic placental site trophoblastic tumor should be followed by prompt hysterectomy.

Adult↗

PubMed2005

Placental site trophoblastic tumor of the mediastinum.

Choriocarcinoma has been described as the most frequent subtype of mediastinal germ cell tumors showing trophoblastic differentiation. We report a unique case of a placental site trophoblastic tumor, which developed in the mediastinum of a 14-year-old boy 2 years after the resection of a mature teratoma. The recurrent tumor was composed of a grossly hemorrhagic and necrotic mass. Histologically, diffusely infiltrating large polygonal cells with focal nodular growth and a teratomatous part containing mature intestinal, respiratory, and squamous epithelium with adjacent cutaneous adnexal structures were found. The typical morphologic features included vessel wall infiltration by the neoplastic cells with fibrinoid deposits and geographic necroses within the tumor masses. Characteristic diffuse positivity for melanoma cell adhesion molecule and human leucocyte antigen G was found on immunohistochemical investigation, confirming the diagnosis of placental site trophoblastic tumor. The patient died 1 year later after polychemotherapy. The outcome of this rare tumor is similar to the reported poor clinical outcome in patients with mediastinal choriocarcinomas.

Adolescent↗

PubMed1985

Malignant placental site trophoblastic tumor.

Placental site trophoblastic tumor is a rare variant of trophoblastic disease. The malignant form of this disease with metastasis and death is even more infrequent, as is evident from only five cases in the literature. A 30-year-old black woman who died from this disease is presented. Patients with metastases are at extremely high risk with no reported survivors and must be treated aggressively with chemotherapy and cytoreductive surgery. This type of trophoblastic tumor apparently exhibits a different biologic behavior as compared with choriocarcinoma.

Adult↗

PubMed2005

Placental site trophoblastic tumor.

Placental site trophoblastic tumor is very rare. It is a gestational trophoblastic neoplasm which follows normal or molar pregnancy. It is usually confined to uterus & 15-20% behave in a malignant fashion. Clinically patients present with abnormal excessive bleeding or amenorrhoea. Though several trophoblastic lesions & tumors enter in the differential diagnosis, microscopically the diagnosis is usually straightforward in hysterectomy specimens. Hysterectomy is the treatment with or without chemotherapy. Progress after surgery should be monitored by placental lactogenic hormone.

Adult↗

PubMed2002

Advances in the understanding of placental site trophoblastic tumor.

Placental site trophoblastic tumor (PSTT) is the least common form of gestational trophoblastic disease. The tumor represents a neoplastic transformation of intermediate trophoblastic cells that normally play a critical role in implantation. PSTT can occur after a normal pregnancy, spontaneous abortion, termination of pregnancy, ectopic pregnancy or molar pregnancy. It displays a wide spectrum of behavior, and when metastatic, can be difficult to control even with surgery and chemotherapy. Because of PSTT's rarity, limited information is known about its natural history. Several recent studies have indicated that mitotic index is an important prognostic indicator. Advances in chemotherapeutic regimens have also improved clinical response in metastatic disease.

Cell Transformation, Neoplastic↗

PubMed2005

Activation of mitogen-activated protein kinase is required for migration and invasion of placental site trophoblastic tumor.

Placental site trophoblastic tumor (PSTT) is a gestational neoplasm derived from the extravillous (intermediate) trophoblast of the implantation site. PSTT is characterized by a highly invasive phenotype, but the molecular mechanisms are poorly understood. In this report, we demonstrate that PSTTs expressed the activated (phosphorylated) form of mitogen-activated protein kinase (MAPK) in 84% of cases, whereas the normal extravillous trophoblastic cells did not. To characterize the role of MAPK activation in PSTT, we established the first PSTT cell culture, IST-2, from a surgically resected PSTT. IST-2 cells expressed HLA-G and Mel-CAM but not E-cadherin, an immunophenotype characteristic of PSTT. IST-2 cells were highly motile and invasive in culture as compared to choriocarcinoma JEG-3 cells and normal extravillous trophoblastic cells. Based on wound assay, time-lapse videomicroscopy for cell tracking, and invasion chamber assays, we found that the motility and invasion of IST-2 cells were significantly reduced (P<0.01) after treatment with the MEK inhibitors CI-1040 and PD 59089, which prevent activation of MAPK. In contrast, neither compound had any effect on normal extravillous trophoblastic cells or JEG-3 cells. In conclusion, our findings demonstrate a functional role of MAPK activation in the motility and invasion of PSTT.

Benzamides↗

PubMed2000

[Pathology of gestational trophoblastic tumors].

Gestational trophoblastic tumours result from an abnormal proliferation of different types of trophoblasts. The morphological pattern, together with the immunohistochemical aspect, the cytogenetic data and the clinical profile, helps identify each pathological entity. Hydatiform moles represent malformed placentas caused by genetic aberrations of the villous trophoblast. A complete hydatiform mole displays an hydropic degeneration of all the chorionic villi with a more or less marked proliferation of trophoblasts. A partial hydatiform mole is made up of molar vesicles interspersed with normal chorionic villi. In an invasive hydatiform mole or chorioma destruens, molar vesicles penetrate the myometrium giving rise to a mass distorting the uterine wall. A choriocarcinoma is a malignant proliferation of atypical villous trophoblasts without villi formation. Necrosis, haemorrhage, vascular invasion and distant metastases strongly compromise its outcome. A trophoblastic implantation site tumor, clearly less frequent, results from a proliferation of extravillous trophoblasts, particular for their secretion of human placental lactogen hormone (hPL). This tumour, exceptionally malignant, should be differentiated from the exaggerated placental site and its variants. Except for the placental site trophoblastic tumour, and whatever the outcome (benign or malignant), all gestational trophoblastic tumours secrete the beta-subunit of the chorionic gonadotropic hormone (beta-hCG) more or less abundantly. The serum or urinary level of this unit is proportional to the tumour volume and represents a fundamental basis for the follow-up of these tumours. Multidisciplinary care of high-risk cases allows us to cure the disease, and helps the patient recover her reproductive uterine function.

Chorionic Gonadotropin, beta Subunit, Human↗

PubMed1987

[Trophoblastic tumor of placental location or trophoblastic pseudotumor. Apropos of 2 cases. Review of the literature].

Two cases of trophoblastic tumor of placental site are reported, less than 30 such lesions being listed in the published literature. Identification of this tumor from among other trophoblastic lesions is facilitated by immunohistochemical and electron microscopy technics, and demonstration of histoprognostic and biologic criteria improves assessment of evolutory potential of this type of tumor and allows adaptation of therapy. Treatment at the localized stage requires early diagnosis and wide surgical excision, results of chemotherapy in metastatic forms being, inversely than with choriocarcinoma, very deceiving.

Adult↗

PubMed1999

Failure of high-dose chemotherapy with peripheral blood stem cell support for refractory placental site trophoblastic tumor.

Placental site trophoblastic tumor (PSTT) is a rare form of gestational trophoblastic disease. The metastatic and refractory cases have a very poor prognosis. To our knowledge, this is the first report of the application of high-dose chemotherapy with autologous peripheral blood stem cell transplantation (PBSCT) for the treatment of refractory metastatic PSTT. A 36-year-old woman had a metastatic PSTT refractory to several lines of chemotherapy. She was treated with high dose of carboplatin and etoposide with autologous PBSCT. She showed only a temporary response to high-dose chemotherapy with PBSCT support and died of disease.

Adult↗

PubMed2001

Spontaneous uterine perforation mimicking ectopic pregnancy as the initial presentation of placental site trophoblastic tumor.

Placental site trophoblastic tumor (PSTT) is a rare form of gestational trophoblastic disease (GTD), with only 100 cases reported in the literature. Irregular vaginal bleeding has been reported to be the most common presenting symptom, however, spontaneous uterine perforation, mimicking ectopic pregnancy, as the initial presentation is extremely rare, and has not yet been reported in the Chinese literature. Herein, we report a 26-year-old female with PSTT complicating with uterine perforation that mimicked ectopic pregnancy as the initial presentation. She received wide excision of the uterine perforation margin only and now remains disease-free, 2 years after the operation. Reviewing the literature, while most cases of PSTT behave a benign fashion, some exhibit malignant behavior; surgery remains the mainstay of therapy. For patients whose disease is limited to the uterus, simple total abdominal hysterectomy is the treatment of choice. For patients with extensive or metastatic disease, cytoreductive surgery (total abdominal hysterectomy and resection of extrauterine tumor load) combined with chemotherapy should be applied. Etoposide, methotrexate, actinomycin D, cyclophosphamide, and vincristine (EMA/CO) chemotherapy appears superior to other available chemotherapeutic regimens in the treatment

Adult↗