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At least 127 records · Page 7Linked to original sources

PubMed2001

Placental site trophoblastic tumor: a 17-year experience at the New England Trophoblastic Disease Center.

OBJECTIVE: We reviewed cases of placental site trophoblastic tumors from the New England Trophoblastic Disease Center (NETDC) database from 1982-1999 in an effort to identify prognostic factors for recurrent disease. METHODS: A chart review was performed utilizing patients identified from the NETDC database. Data obtained included patient age at diagnosis, antecedent pregnancy, duration and extent of disease, presenting symptoms, pre- and posttreatment hCG levels, diagnostic and therapeutic procedures, treatment and outcome of patients. Statistical analysis was performed using Student's t test and chi(2) test when appropriate. RESULTS: Thirteen patients were identified. All ultimately underwent hysterectomy although initial treatment of 1 patient was uterine resection. There were 5 recurrences (43%)--3 among the 9 patients who had no metastases on presentation (33%) and 2 of 3 patients who presented with metastases (66%). The 5 patients who recurred were among 8 who had received peri- or postoperative chemotherapy (62.5%). Treatment of recurrences included continued or alternate chemotherapy, radiotherapy, and/or excision of locally recurrent disease. Follow up time averaged 56.2 months (range 12-182 months). One of the 4 patients receiving chemotherapy < or =1 week after hysterectomy recurred, whereas all 4 patients who received chemotherapy 3 weeks or more after hysterectomy recurred. Uterine tumor volume was significantly greater, 154.1 cm(3), in patients with initial metastases versus 42.3 cm(3) in patients without initial metastases (P = 0.04). Mitotic index (P = 0.04) was significantly increased in patients who developed recurrent disease. CONCLUSION: High mitotic index appears to be an adverse prognostic indicator for recurrence. Hysterectomy remains the mainstay of treatment. Chemotherapy is indicated for patients with metastases and may be indicated when the mitotic index is >5 mitoses/10 HPF. Radiation treatment may play a role in recurrent disease but must be evaluated on a case-by-case basis.

Adult↗

PubMed2004

Binding of galectin-1 (gal-1) on trophoblast cells and inhibition of hormone production of trophoblast tumor cells in vitro by gal-1.

Galectin-1 (gal-1), a member of the mammalian beta-galactoside-binding proteins, recognizes preferentially Galbeta1-4GlcNAc sequences of oligosaccharides associated with several cell surface glycoconjugates. As demonstrated histochemically, the lectin recognizes appropriate glycoepitopes on the syncytiotrophoblast and on chorionic carcinoma cells (BeWo). Freshly isolated trophoblast cells and trophoblast tumor cells Jeg3 did not bind gal-1. BeWo cells in contrast to Jeg3 form a syncytium in vitro and synthesize progesterone as well as hCG. BeWo cells were used as an approach to study the effects of gal-1 on hormone production. The lectin decreased cellular hCG and progesterone production as well as hCGbeta gene transcription as measured by real-time RT-PCR. Gal-1 mediated inhibition of cellular progesterone production was reduced in the presence of a Thomsen-Friedenreich (TF)-polyacrylamide conjugate. Inhibition of cellular hCG and progesterone production was also induced by anti-TF monoclonal antibodies. The results demonstrate that ligation of Galbeta1-4GlcNAc and Galbeta1-3GalNAc (TF) epitopes on BeWo cells may have regulatory effects on hCG and progesterone production.

Acrylic Resins↗

PubMed1985

Placental-site trophoblastic tumor (trophoblastic pseudotumor): case report demonstrating failure of chemotherapy, surgery, and radiotherapy to control metastatic disease.

A case of metastatic placental-site trophoblastic tumor (trophoblastic pseudotumor) is presented and compared to four previously reported cases. Chemotherapy with MAC (methotrexate, dactinomycin, cyclophosphamide), aggressive surgical debulking, and radiotherapy were ineffective in producing disease regression. Only two of the four similar cases in the literature showed short responses (4-7 months) to several different aggressive multiagent chemotherapy regimens. Optimal therapeutic outcome is likely to result from an early diagnosis and aggressive surgical treatment of localized tumor.

Adult↗

PubMed2003

Apoptosis of extravillous trophoblast cells limits the trophoblast invasion in uterine but not in tubal pregnancy during first trimester.

During the first trimester of pregnancy extravillous trophoblast cells (EVT) invade the maternal decidua. Invasion normally is reduced from the second trimester onwards and stops in the inner third of the myometrium. By contrast, in extrauterine tubal pregnancy, trophoblast invasion may even penetrate the tubal wall, which ultimately leads to the rupture of the fallopian tube. Induction of apoptosis of EVT cells, by maternal immune competent cells, may be an important mechanism to limit EVT invasion in uterine pregnancy. Tissue specimens from first and second trimester uterine pregnancy and first trimester tubal pregnancy were analyzed for apoptosis by TUNEL- and M30-staining. By immunohistochemical double labelling, maternal leukocyte subtypes were co-localized to apoptotic cells and in this context, the number of CD56(+)NK cells was analyzed. Our data show that apoptosis is confined to the decidua basalis. Most apoptotic cells are single cytokeratin-positive epithelial cells residing in the stromal compartment. Consequently these cells can only be EVT cells. Maternal leukocytes are not apoptotic. They are located in close contact to apoptotic cells. The number of apoptotic cells in the second trimester (1.8+/-0.7 per cent) is reduced compared to first trimester (5.6+/-0.7 per cent) of uterine pregnancy. In parallel, the number of NK cells declines from first (24.4+/-2.9) to second (12.4+/-1.8) trimester. Furthermore, apoptosis is significantly reduced in ectopic (0.9+/-0.3 per cent) compared to eutopic first trimester pregnancies. Consequently, we suggest that in first trimester uterine pregnancy, induction of EVT cell apoptosis by the maternal immune system is one mechanism to limit EVT invasion. During the second trimester, in parallel to declining numbers of NK cells, the mechanism changes. However, in tubal pregnancy due to differing immunological microenvironments at the ectopic implantation site, apoptosis induction fails, which deleteriously may result in uncontrolled invasion and penetration of the tubal wall.

Apoptosis↗

PubMed2003

Hypoxia alters expression and function of syncytin and its receptor during trophoblast cell fusion of human placental BeWo cells: implications for impaired trophoblast syncytialisation in pre-eclampsia.

The fundamental process of placental trophoblast cell fusion (syncytiotrophoblast formation or syncytialisation) which is a characteristic of this tissue is poorly understood. Pre-eclampsia is associated with placental hypoxia and suppressed syncytiotrophoblast formation. We therefore have studied the effect of low-oxygen tensions on the rate of cell fusion, relative abundance of mRNAs encoding syncytin and its receptor, amino acid transport system B(0), which are thought to be involved in trophoblast cell fusion (as well as the activity of amino acid transport through this system) in a cell model of syncytialisation (BeWo cells following forskolin treatment). Forskolin-induced cell fusion (determined by a quantitative flow cytometry assay) was reversibly suppressed in 2% oxygen compared to 20% oxygen. This was associated with suppressed secretion of human chorionic gonadotropin. Forskolin stimulated relatively less syncytin mRNA (determined by reverse transcription-polymerase chain reaction) in 2% than in 20% oxygen and there was no stimulation after 48 h in 2% oxygen. There was a spontaneous, time-dependent increase of amino acid transporter B(0) mRNA in vehicle, which was suppressed by 2% oxygen and by forskolin treatment in 20% oxygen. Forskolin-induced changes in amino acid transport system B(0) function were not seen in cells cultured for 48 h in 2% oxygen. These observations suggest that under conditions of low ambient oxygen, dysregulation of expression of syncytin and of its receptor may suppress the normal process of cell fusion necessary for syncytiotrophoblast formation and contributes to syncytiotrophoblast abnormalities characteristic of pre-eclampsia.

Alanine↗

PubMed1996

[Benign placental trophoblast nodule. Case report with overview of proliferative diseases of the intermediate stage trophoblast].

This report reviews proliferative diseases of intermediate trophoblast cells and summarises clinical findings and pathohistological and immunohistochemical features of a placental site nodule. This recently described entity is an endometrial or endocervical benign proliferation of intermediate trophoblast cells occurring after intrauterine gestation. Patients usually present with a history of abnormal vaginal bleeding and frequently cells that are present in their cervical smears are misinterpreted as squamous dysplasia. In such cases it is important to distinguish the placental site nodule from squamous lesions or decidual polyps; this is possible by means of immunohistochemistry.

Adult↗

PubMed1983

Placental site trophoblastic tumor (trophoblastic pseudotumor) of the uterus with metastases and fatal outcome. Clinical and autopsy observations of a case.

A 41-year-old woman who 5 years earlier had a hysterectomy for a placental site trophoblastic tumor (formerly called trophoblastic pseudotumor) was readmitted to the hospital with pelvic recurrence and multiple lung metastases. Despite an initial decrease in the size of the lung metastases and concomitant lowering of the serum values of human chorionic gonadotropin (beta-HCG) from 2,200 to 40 ng/ml, combined chemotherapy became ineffective. The patient died 4 months later with widespread metastases. The clinical course and the autopsy findings of this case are reported and compared with the two similar cases reported in the literature.

Adult↗

PubMed1981

Clinical studies on cell-mediated immunity in gestational trophoblastic disease: nonspecific cellular immunocompetence in patients with hydatid mole and trophoblastic neoplasia.

The nonspecific cell-mediated immunocompetence of 51 patients with gestational trophoblastic disease (GTD), including 16 patients with hydatid mole (HM), 24 with nonmetastatic trophoblastic neoplasia (NTN) and 15 with metastatic TN (MTN), was studied with the use of both in vitro and in vivo parameters of cell-mediated immunity (CMI) such as lymphocyte blastogenic response to phytohemagglutinin (PHA), subpopulation constitution, and delayed cutaneous hypersensitivity responses to 2,4-dinitrochlorobenzene (DNCB) and to purified protein derivative of tuberculin (PPD). The pretreatment cell-mediated immune status of patients with HM developing no malignant sequelae was shown to be essentially similar, in terms of both in vitro PHA and in vivo DNCB reactivities, to that of normal women and of patients with benign gynecological diseases. In patients with TN, however, there was a significant depression in the blastogenic lymphocyte response to PHA before evacuation of the mole, which was persistently demonstrated after uterine evacuation and more marked throughout the course of disease in patients with MTN, than in those with NTN, with a tendency to return to normal in remission. Moreover, patients with TN had a significant depletion of T lymphocytes as determined by rosette-forming cell procedures before treatment, which was most evident in patients with MTN. Plasma from the MTN patients was also shown to have an inhibitory effect on PHA responsiveness of lymphocytes from normal women. There was an increased incidence of impaired reactivity to DNCB in patients with TN (higher in MTN than in NTN), compared with HM and benign diseases, while no such difference in incidence was observed in response to PPD. On the basis of these findings, a preliminary characterization of altered immunocompetence in patients with TN and its mechanism are discussed.

Adult↗

PubMed1983

Plasma cholinesterase and trophoblastic disease. Gestational trophoblastic disease and reduced activity of plasma cholinesterase.

A case of prolonged action of suxamethonium in a patient with gestational trophoblastic disease is reported. Postoperatively the patient was found to have markedly reduced plasma cholinesterase activity (363 IU/litre) with a normal cholinesterase phenotype. Consequently plasma cholinesterase activity and phenotype were measured in six other patients with the condition and these results compared with those of 22 patients with normal first trimester pregnancies undergoing therapeutic abortion. Plasma cholinesterase phenotype was normal in all patients studied. The activity was significantly decreased (p less than 0.05) from the normal range (620-1370 IU/litre) in all patients with trophoblastic disease. In the 22 patients with normal pregnancies, 14 had activity values in the abnormal range (less than 620 IU/litre) while the mean cholinesterase activity of the group as a whole was significantly decreased (561.8 IU/litre, p less than 0.05) below the normal range. These results confirm the presence of a decrease in plasma cholinesterase activity in early pregnancy and provide new evidence for a decrease in activity in a pseudopregnancy state.

Adult↗

PubMed1994

EMACO in high risk gestational trophoblast disease--the Australian experience. Gestational Trophoblast Subcommittee, Clinical Oncological Society of Australia.

Sixty-five patients with high-risk trophoblast disease have been treated with the EMACO combination split regimen therapy in the 10 year period, 1981 to 1990. Four patients died but the remaining 61 (94%) remain free of disease up to 10 years later. Toxicity was manageable in most cases with minimal delay in treatment from myelosuppression. EMACO is a well tolerated regimen with a high cure rate in patients with high-risk gestational trophoblast disease (GTD).

Adolescent↗

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↗

PubMed1978

[Long-term cultures of trophoblast cells and mixed trophoblast cultures as a model for in-vitro studies (author's transl)].

Trophoblast cell-cultures provide a much promising model for qualitative and quantitative in-vitro-examinations of immunological, morphological and biochemical items. In the present paper an attempt has been made to analyze the light-microscopically identificable morphological modifications of the cultured cells under standardized culture-conditions in a temporary order. Furthermore, a number of single cases is presented in which mixed cultures of trophoblast cells with heterologous cells of embryonic origin and with cells derived from adult malignoma were tried.

Cells, Cultured↗

PubMed1989

[A comparative study of the main components of the nucleolus in different populations of rat trophoblast cells during differentiation. I. The nucleoli of the trophoblast cells in the labyrinth section of the placenta].

The nucleolus undergoes some steps of structural transformation during differentiation of the labyrinth trophoblast cells. Primarily (on day 13 of gestation) the nucleolar components become rather disjoined. The nucleolus is composed of a loose net of strands of granulofibrillar and dense fibrillar components bearing fibrillar centers (FCs). Strands are separated by large lacunae. This rare-occurring type of nucleoli is replaced on the next (14th) day by the nucleolonemal type and later--by the compact nucleolar type. FCs with dense fibrillar component strands become extended into the masses of granulofibrillar component. Such transformations of nucleolar structure seem to be an expression of a fast-proceeding differentiation of the labyrinth trophoblast cells.

Animals↗

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↗

PubMed1994

Subsequent pregnancy experience in patients with gestational trophoblastic disease. New England Trophoblastic Disease Center, 1965-1992.

We reviewed the subsequent pregnancy outcome in patients with partial mole, complete mole and persistent gestational trophoblastic tumor treated at the New England Trophoblastic Disease Center from June 1, 1965, to December 31, 1992. Such patients can be assured that they can anticipate a normal future reproductive outcome. However, when a patient has had a molar pregnancy, she is at increased risk (1%) of developing molar disease in a subsequent conception.

Female↗

PubMed1992

Inhibition of lymphocyte proliferation by bovine trophoblast protein-1 (type I trophoblast interferon) and bovine interferon-alpha I1.

Bovine trophoblast protein-1 (bTP-1) is a Type I interferon secreted by the bovine trophoblast from about Day 15 of pregnancy. It is not known whether bTP-1 has functional properties in common with other interferons. The aim of the present study was to determine whether bTP-1 inhibits proliferation of lymphocytes induced by mitogens, mixed lymphocyte cultures (MLC) and interleukin-2 (IL-2) and, if so, whether this activity is similar to that of a related interferon, bovine interferon-alpha I1 (bIFN-alpha I1). Stimulation of lymphocyte proliferation caused by phytohemagglutinin (PHA), concanavalin A (Con A) and pokeweed mitogen (PWM) was inhibited by bTP-1 and bIFN-alpha I1 without any reduction in cell viability. Maximum or near-maximum inhibition (less than 50%) was achieved at concentrations of 0.5-5.0 nM of bTP-1 and bIFN-alpha I1. Cells stimulated with PWM were less inhibited than cells stimulated with PHA and Con A. Both bTP-1 and bIFN-alpha I1 inhibited MLC to a greater degree than lectin-stimulated cells (maximum inhibition was 78% or greater). Also, bTP-1 and bIFN-alpha I1 slightly inhibited incorporation of [3H]thymidine ([3H]TdR) induced by the combination of phorbol ester, 12-O-tetradecanoylphorbol 13-acetate (TPA), and calcium ionophore A23187. Finally, bTP-1 and bIFN-alpha I1 had bimodal effects on incorporation of [3H]TdR by IL-2-induced lymphocytes. Incorporation of [3H]TdR was increased at 0.005 nM and 0.05 nM concentrations while higher concentrations caused a slight decrease in [3H]TdR incorporation. Results confirm that bTP-1 inhibits lymphocyte proliferation in a manner similar to that caused by the leukocyte-derived interferon, bIFN-alpha I1. Incomplete inhibition of mitogen-induced proliferation and differences in degree of inhibition between various stimulators suggest that bTP-1 and bIFN-alpha I1 preferentially inhibit certain lymphocyte subpopulations. Local inhibition of lymphocyte proliferation caused by bTP-1 may help protect the allogeneic conceptus from immune responses to fetal antigens or regulate the release of cytokines from endometrial lymphocytes.

Animals↗

PubMed1988

Ovine trophoblast protein-1 and bovine trophoblast protein-1 are present as specific components of uterine flushings of pregnant ewes and cows.

A rabbit antiserum raised against ovine trophoblast protein-1 (oTP-1) was used to stain Western blots of the protein components from the uterine flushings of pregnant ewes (n = 61), non-bred cyclic ewes (n = 22), bred-but-nonpregnant ewes (n = 36), pregnant cows (n = 34), and bred-but-nonpregnant cows (n = 15). Nonpregnant animals were defined as ones from which no embryo was recovered. Uterine flushings of pregnant ewes contained oTP-1 between Days 14 and 24 of pregnancy, but not at Day 12. All of the cyclic ewes and 34 of 36 bred ewes, judged as nonpregnant, tested negatively for the presence of oTP-1. With one exception, oTP-1 was not detected in the nongravid uterine horns of pregnant ewes in which the conceptus had been confined to one uterine horn. Bovine trophoblast protein-1 (bTP-1), which cross-reacts immunologically with oTP-1, was also detectable specifically in the uterine flushings of pregnant cows when anti-oTP-1 antiserum was used. The urine (n = 14) and certival mucus (n = 20) samples of all the pregnant ewes tested were free of any detectable oTP-1. Thus, a useful pregnancy test for ewes based on oTP-1 release into these fluids seems unlikely. Results of this study show that oTP-1 and bTP-1 are pregnancy-specific proteins that are secreted into the uterine lumen where they possibly exert a local response.

Animals↗

PubMed1991

Study and treatment of gestational trophoblastic diseases at the John I. Brewer Trophoblastic Disease Center, 1962-1990.

From 1962 through 1989, 5063 patients were referred to the John I. Brewer Trophoblastic Disease Center of the Northwestern University Medical School. Among these were 564 patients treated with chemotherapy for gestational trophoblastic tumors (choriocarcinoma and invasive mole). The overall cure rate was 94%, 100% for 323 patients without evidence of metastases and 85% for 241 patients with metastatic disease. Four factors were determined to significantly influence treatment response: (1) clinicopathologic diagnosis of choriocarcinoma, (2) metastases to sites other than the lung or vagina, (3) number of metastases, and (4) previous failed chemotherapy.

Antineoplastic Combined Chemotherapy Protocols↗