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At least 19 recordsLinked to original sources
PubMedDate not supplied

Gestational trophoblastic neoplasms.

Gestational trophoblastic neoplasms have evolved from one of the most rapidly fatal malignancies to potentially one of the most curable, but these diseases have devastating emotional effects on the victims. Etiology, epidemiology, pathophysiology, diagnosis, and medical treatment are reviewed. Numerous nursing implications are discussed using crisis theory. A nursing care plan, based on nursing diagnosis, is outlined with specific nursing actions defined.

Chorionic Gonadotropin↗
PubMed1992

Pulmonary disease in gestational trophoblastic neoplasms.

Gestational trophoblastic neoplasms can present as pulmonary nodules without significant disease of the reproductive organs. This article describes a case of metastatic gestational trophoblastic disease to the lungs. This entity must be considered in the differential diagnosis in any female of reproductive age who presents with multiple pulmonary nodules. Thoracotomy has a limited role in the initial evaluation of patients with this disease. However, it may be needed in patients who have evidence of persistent pulmonary disease, despite appropriate therapy.

Adult↗
PubMed1992

The expression of human chorionic gonadotropin/human luteinizing hormone receptors in human gestational trophoblastic neoplasms.

Normal human placental trophoblasts have recently been shown to contain receptors for hCG/hLH. The present studies investigated the expression of these receptors in hyperplastic and anaplastic trophoblasts in gestational trophoblastic neoplasms. The results demonstrated that both hydatidiform moles and choriocarcinomas contained receptor messenger RNA (mRNA) and receptor protein. A variety of nontrophoblast tumors, on the other hand, contained neither receptor mRNA nor receptor protein. Choriocarcinomas contained more receptor mRNA and receptor protein than hydatidiform moles which in turn contained more than normal human placenta. Midluteal phase human corpus luteum contained more receptor mRNA than normal human placenta and about the same as choriocarcinomas. The hyperplastic and anaplastic trophoblasts in hydatidiform moles and choriocarcinomas contained more receptor immunostaining than the normal trophoblasts in the same tissue or those from normal placentas from about the same gestational age. The receptor immunostaining increased as the degree of trophoblast hyperplasia increased in hydatidiform moles. Anaplastic trophoblasts of choriocarcinomas contained a similar amount of receptor immunostaining as severely hyperplastic trophoblasts of hydatidiform moles. Invading anaplastic trophoblasts of choriocarcinoma contained greater amount of receptor immunostaining than the surrounding endometrial stromal and myometrial smooth muscle cells. In summary, this is the first study to our knowledge demonstrating the expression of hCG/hLH receptor gene in gestational trophoblastic neoplasms. The increased receptor expression in these neoplasms suggests that hCG, via its receptors, could play a fundamental and previously unsuspected autocrine role in the regulation of trophoblast transformation, growth, invasion, and high hCG secretion.

Adenocarcinoma↗
PubMed1977

Gestational trophoblastic neoplasms: morphologic considerations.

Abnormal trophoblastic proliferation is the hallmark of a spectrum of lesions constituting the gestational trophoblastic neoplasms. Rapid proliferation, infiltration, vascular invasion, hematogenous dissemination, and spontaneous regression are features of both normal and neoplastic trophoblast. Trophoblastic hyperplasia without hydrops, hydatidiform mole, invasive mole, and gestational choriocarcinoma are related lesions, characterized by increasingly aberrant trophoblastic growth and worsening prognosis, if untreated. Difficulties in diagnosis may arise with respect to the normal early implantation site, the hydropic abortus, and postgestational, involuting, residual trophoblast. Histologic grading or hydatidiform moles is relevant to their prognosis and biologic behavior. Trophoblastic neoplasia may begin at any stage of pregnancy or puerperally with immediate or late and local or distant manifestations in the mother or the child. Cognizance of the capricius potential behavior of trophoblast permits successful management of its proliferative lesions, monitored by serial measurement of gonadotropin secretion.

Choriocarcinoma↗
PubMed1976

Methotrexate with citrovorum factor rescue for nonmetastatic gestational trophoblastic neoplasms.

Fifteen patients with nonmetastatic gestational trophoblastic neoplasms were treated primarily with methotrexate and citrovorum factor. Complete and sustained remission was achieved in 14 of the 15 patients. Response to treatment was determined solely on the basis of serial serum human chorionic gonadotropin levels as measured by the beta subunit radioimmunoassay. All patients developed nonmetastatic gestational trophoblastic neoplasms following evacuation of a molar pregnancy. The known histologic diagnosis in all cases was hydatidiform mole. No significant toxicity was encountered despite careful monitoring of marrow, hepatic, renal, neurologic, and mucocutaneous parameters. Up to January 31, 1976, duration of remission ranged from 2 to 14 months.

Adolescent↗
PubMed1978

Methotrexate with citrovorum factor rescue for gestational trophoblastic neoplasms.

Thirty-five patients with nometastatic gestational trophoblastic neoplasms and 3 patients with metastatic gestational trophoblastic neoplasms were treated primarily with methotrexate and citrovorum factor rescue. The antecedent pregnancy was molar in all patients. The known histologic diagnosis in 34 patients was hydatdiform mole and choriocarcinoma in 3. Up to March 1977, the duration of remissions ranged from 1 to 21 months. Complete and sustained remission was achieved in 91% of patients with nonmetastatic disease and in 2 of the 3 patients with metastases, without evidence of marrow or hepatic and with substantially reduced epithelial toxicity. Response to treatment and the number of courses required to achieve remission were determined solely on the basis of the human chorionic gonadotropin response as measured by the beta subunit radioimmunoassay.

Adolescent↗
PubMed1995

[Clinical analysis of 6 cases of gestational trophoblastic neoplasms complicated by cardiotoxicity after chemotherapies].

Gestational trophoblastic neoplasm treated by large dosage of 5-fluorouracil and actinomycin could cause cardiotoxicity. In 6 cases of gestational trophoblastic neoplasms admitted to our hospital from March to December 1993, cardiotoxicity was found to have occurred after chemotherapies in 10/21 courses. There were 2 cases with heart failures, 4 cases with palpitation and 4 cases with feelings of oppression and (or) chest pains. In 7 cases the electrocardiogram (EKG) findings were abnormal (70.0%) and in 5 cases there were increased sera glutamic oxalacetic transaminase enzyme (AST). 90.0% of these complications were brought under control after decreasing the dosages and changing the methods of administration. If the proper managements were not given on time, patient may even expire. So attention should be paid to this complication. It is suggested that attention should be paid to patients' subjective symptoms, and proper surveillance by EKG and serum AST determinations should be conducted to minimize deaths due to chemotherapeutic complications.

Adult↗
PubMed1988

Immunohistochemistry of germ cell and trophoblastic neoplasms.

The immunoprofiles of 121 germ cell and trophoblastic neoplasms were defined, using a battery of antibodies against cytokeratin (CK), vimentin (VIM), epithelial membrane antigen (EMA), placental alkaline phosphatase (PLAP), S-100 protein, leukocyte common antigen (LCA), UCHL-1, LN-2, carcinoembryonic antigen (CEA), neuron-specific enolase (NSE), chromogranin A, Leu-7, alpha-fetoprotein (AFP), alpha-1-antitrypsin (AAT), and the beta subunit of human chorionic gonadotropin (BHCG). In addition to 85 neoplasms of testicular origin, the cases included eight ovarian germ cell tumors and 28 extragonadal neoplasms. All tissues had been subjected to formalin fixation and paraffin embedding. Similar immunoreactivity patterns were seen in gonadal and extragonadal neoplasms, gestational and nongestational choriocarcinomas, components of mixed germ cell tumors and their pure counterparts, and metastatic and primary lesions. Placental alkaline phosphatase was a sensitive marker of germ cell differentiation, and expression of this marker in the absence of EMA appeared to be a staining pattern unique to germ cell tumors. Both LCA and S100 were absent in neoplastic germ cells, and thus were useful in differentiating these tumors from malignant lymphoma and malignant melanoma, respectively. Cytokeratin was helpful in distinguishing seminomas/dysgerminomas from nonseminomatous germ cell tumors, although 10% of seminomas showed focal or diffuse cytokeratin reactivity. Finally, 75% of all germ cell neoplasms displayed NSE, calling the specificity of this determinant into question.

Alkaline Phosphatase↗
PubMed1977

Worldwide controversies in gestational trophoblastic neoplasms.

This article reviews worldwide controversies concerning gestational trophoblastic neoplasms (hydatidiform mole, invasive mole, and choriocarcinoma). The epidemiology, endocrinology, histopathologic grading, classification, diagnosis, treatment, management and follow-up (including chemotherapy, irradiation, and immunotherapy) of gestational trophoblastic neoplasms - particularly molar pregnancies - are discussed; and ways to help create a standardized classification system and provide optimal treatment for each type of patient are suggested.

Chorionic Gonadotropin↗
PubMed1994

Genetic origin of malignant trophoblastic neoplasms.

The genetic origin of three trophoblastic neoplasms (two choriocarcinomas and a placental site trophoblast tumor (PSTT)] was determined by analysis of the restriction fragment length polymorphism (RFLP) pattern. One choriocarcinoma, which was believed not illogically to have developed from an antecedent complete mole, contained both paternal and material RFLP alleles and thus was probably the product of a normal fertilization. The other choriocarcinoma was not of gestational origin but had RFLPs homozygous at some loci and heterozygous at others, compatible with the parthenogenic origin of this tumor from a germ cell after meiosis I. The PSTT required amplification of DNA sequences by polymerase chain reaction (PCR) because of the small amount of tumor material available. This tumor contained RFLP alleles from both parents and appeared to have resulted from a previous unrecognized (and abnormal) pregnancy.

Adult↗
PubMed1994

[Expression of human chorionic gonadotropin, human placental lactogen and pregnancy-specific 1-glycoprotein in malignant trophoblastic neoplasms].

The expression of placental hormones in 91 malignant trophoblastic neoplasms was studied immunohistochemically using a panel of antibodies against hCG, human placental lactogen (hPL) and pregnancy-specific 1-glycoprotein (SP). The results indicated that the expression of hCG in invasive moles was weaker than that in choriocarcinoma, but the expression of hPL and SP1 was stronger than those in choriocarcinoma. The expression of hPL and SP1 in the metastatic tumors of invasive moles was weaker than the expression at in the primary tumors, but the secretory capacity of hCG in metastatic choriocarcinomas was stronger than that in the primary neoplasms. In this study, the qualities of expression of the placental hormones in invasive moles and choriocarcinomas corresponded to the degree of tumor malignancy, the biological behaviour and the grading of trophoblastic cell differentiation. We believe that the detection of hCG, hPL and SP1, in malignant trophoblastic neoplasms was of value for establishing tumor diagnosis and typing and for judgement on prognosis.

Biomarkers, Tumor↗
PubMed1991

Successful treatment of refractory gestational trophoblastic neoplasm with high-dose etoposide and cyclophosphamide.

A patient with gestational trophoblastic neoplasm failed treatment with several standard chemotherapy regimens and had progressive disease with development of lung and brain metastases and a rising HCG level. Following resection of the metastases and whole-brain radiotherapy she was treated with high-dose etoposide and cyclophosphamide. She promptly attained a complete remission and remains free of disease 15 months after completion of therapy. This regimen, although initially developed for leukemia and lymphoma treatment, has potential as a therapy for refractory gestational trophoblastic neoplasm because it delivers high doses of agents very active in this disease.

Adolescent↗
PubMed1995

Malignant trophoblastic neoplasms with different modes of origin.

The genetic origin of 24 trophoblastic neoplasms was determined using PCR polymorphisms. Based on pregnancy history, these tumors included nine postmolar trophoblastic tumors, 12 tumors preceded by live birth or abortion, and three nongestational tumors. Androgenetic origin was defined in eight post-molar trophoblastic tumors, and the remaining one might have arisen from a normal fertilization. Six tumors retained genetic features carried by the homozygous complete mole. Two tumors showed PCR polymorphism compatible with that of the heterozygous complete mole. All 12 tumors in the second class had alleles of both paternal and maternal contribution. However, discordance of sex between the antecedent pregnancy product and the tumor was recognized in three choriocarcinomas. The absence of paternal contribution suggested a parthenogenetic origin of three nongestational choriocarcinomas. The findings that PCR polymorphisms were either homozygous in certain loci or heterozygous in others may mean that the tumor was derived from a germ cell after meiosis I. As a result, at least three subtypes with different modes of origin were demonstrated in the 24 trophoblastic tumors. These findings underscore the importance of precise genetic marker analyses in a large series to clearly identify clinical and biologic characteristics of each subset of tumors.

Base Sequence↗
PubMed2000

Expression of CDKI p27Kip1 in trophoblastic neoplasm.

OBJECTIVE: To evaluate the role of p27Kip1 in tumorigenesis and the development of trophoblastic cell disease. METHODS: Using immunohistochemistry, the expression of p27-protein was investigated in 10 normal chorionic villi in the first trimester of pregnancy, 15 complete hydatidiform moles (HM), 7 invasive moles (IM) and 7 choriocarcinomas (CC). RESULTS: In all cases, immunohistochemical staining localized p27-protein in the plasma. Decreased expression of p27Kip1 was observed in malignant trophoblastic neoplasms with a positive rate of 21.43%, which is significantly less than that in normal chorionic villi (80%) and in complete HM (73.33%) (P < 0.05). The positive rate of p27Kip1 in those complete HM with large uterine size for gestational age was lower than that in those with normal or small uterus (42.86% vs 100%, P < 0.05). CONCLUSION: p27Kip1 may be involved in the tumorigenesis of gestational trophoblastic neoplasm as a negative regulator of the cell cycle. The expression level of p27Kip1 in trophoblastic cells may be a prognostic factor for complete HM.

Cell Cycle Proteins↗
PubMed1979

Methotrexate with citrovorum factor rescue for nonmetastatic gestational trophoblastic neoplasms.

Fifty-one patients with nonmetastatic gestational trophoblastic neoplasms (NMGTN) were treated with either 4 or 6 mg/kg methotrexate (MTX) and citrovorum factor (CF) rescue to determine if the higher dosage could reduce the number of courses of chemotherapy required to achieve remission. Thirty-six of 41 patients treated with 4 mg/kg MTX achieved complete remission with 1 course of chemotherapy. Increasing the initial dose of MTX to 6 mg/kg in 10 patients did not reduce the need for subsequent courses of chemotherapy but did increase associated toxicity. The rate of fall in the human chorionic gonadotropin (hCG) titer following the initial course of MTX-CF was found to be an accurate predictor of therapeutic response. The need for further chemotherapy may be anticipated if the hCG titer has not fallen by 1 log within 18 days.

Adolescent↗
PubMed2001

Genetic origin of malignant trophoblastic neoplasms analyzed by sequence tag site polymorphic markers.

OBJECTIVE: To study the causative conception of malignant gestational trophoblastic neoplasms (GTNs), we analyzed malignant GTNs by microsatellite PCR markers. METHOD: DNAs extracted from 12 malignant GTNs were subjected to PCR for five different chromosomal locations. RESULT: Of the 7 cases after a complete mole (CM), 5 were derived from androgenesis, but the remaining 2 were from normal fertilization. Of the 5 cases after nonmolar pregnancies, 2 placental site trophoblastic tumors had alleles from both parents. Of the other 3 choriocarcinomas, 1 was from normal fertilization after spontaneous abortion but 2 originated from androgenesis, suggesting that 1 was from a CM prior to the antecedent abortion, transforming after a long interval. CONCLUSION: By combining the previous cases with these, our analysis of 39 cases demonstrated that trophoblastic neoplasms can arise from at least three different modes of origin (androgenesis, normal fertilization, and parthenogenesis), and antecedent pregnancy is not always identical to the causative conception. Placental site trophoblastic tumors might have different machinery for carcinogenesis because of the predominance of paternal and maternal contributions. In addition, a long dormancy of trophoblasts before malignant transformation, especially for those originating from normal fertilization, was also suggested.

Adult↗
PubMed1988

Update in cancer chemotherapy: genitourinary tract cancer, Part 7: Gestational trophoblastic neoplasms.

Part 7 of an update of the state of the art of cancer chemotherapy of the genitourinary tract is directed to the treatment of gestational trophoblastic neoplasms. Chemotherapy is the cornerstone of treatment for gestational trophoblastic neoplasms, as these tumors are generally highly curable with chemotherapy.In early stage disease, 40 percent of cases are cured with hysterectomy. In low-risk cases, single-agent methotrexate or dactinomycin provides cure rates of over 90 percent. In high-risk disease sequential methotrexate/dactinomycin, methotrexate plus dactinomycin plus cyclophosphamide or chlorambucil, or methotrexate plus 6-mercaptopurine, or a combination protocol consisting of cyclophosphamide, hydroxyurea, dactinomycin, methotrexate, vincristine (VCR), folinic acid, and doxorubicin (CHAMOCA) produce complete remission rates in 70 to 80 percent of patients. Newer studies are under way with etoposide (VP16), cisplatin, and investigational agents to determine whether better chemotherapy regimens can be developed.

Antineoplastic Combined Chemotherapy Protocols↗