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At least 1,099 records · Page 61Linked to original sources
PubMed1991

Ovine trophoblast protein-one: evidence for possible glycosylation.

1. The polymerase chain reaction has been used to amplify specifically the cDNA coding for the secreted form of ovine trophoblast protein-one from a preparation of total cellular RNA extracted from sheep embryos removed from ewes 16 days after mating. 2. Cloning and sequencing of the amplified cDNA revealed two new sequence variants: SPW49 having 93% similarity with deduced amino acid sequences from published cDNA data, and SPW27 a variant coding for a deleted form of ovine trophoblast protein-one. 3. The gene for ovine trophoblast protein-one is intronless. 4. This study provides further evidence for the existence of an ovine trophoblast protein-one gene family. 5. Both variants contain a potential N-glycosylation site not apparent in published sequences for ovine trophoblast protein-one.

Amino Acid Sequence↗
PubMed1994

Improvement of attachment rate of bovine embryos after transfer with trophoblastic fragments.

Fragments of trophoblastic vesicles have been shown to improve embryo development when used in co-culture. We wished to investigate the effect of trophoblastic fragments on establishment of pregnancy after embryo transfer. Embryos (n=129) frozen by direct immersion in liquid nitrogen (Group 1), 82 embryos frozen by the slow freezing method (Group 2) and 55 fresh embryos stored at 20-22 degrees C for 21-22 h (Group 3) were transferred into recipient heifers. The embryos of each group were divided in 2 batches. Batch 1 embryos (control) were transferred without trophoblastic fragments, Batch 2 embryos of each group (experimental) were transferred in combination with frozen-thawed trophoblastic fragments at a rate of 5 to 7 fragments per embryo. The fragments were produced from 16-17 day bovine embryos frozen by vitrification. Two months following the embryo transfers it was established that the attachament rate for Batch 1 embryos in Groups 1, 2, 3 was 33%, 39% and 48%, respectively; for Batch 2 embryos in the same Groups the rate was 55%, 56% and 74%, respectively. We conclude that trophoblastic fragments promote embryo attachment, but their effect does not continue beyond the time of attachment.

Journal Article↗
PubMed1999

Pre-eclampsia: a mistake of trophoblastic cells for tumour cells?

Pre-eclampsia is a severe form of hypertension induced by pregnancy. In pre-eclampsia, there is deficient trophoblast invasion of the spiral arteries terminating in the placental bed. Perhaps some abnormality occurs in the immunosuppressive process as the maternal immune system encounters paternal antigens expressed by immunosuppressive decidual cells. This immunosuppressive abnormality might cause the deficient trophoblast invasion. Abnormal placentation might then lead to maternal endothelial cell damage by an ongoing process. There might be a recurring sequence of 4 steps: (1) The placenta releases trophoblastic cells with potentially cytotoxic characteristics. These circulating trophoblastic cells have an abnormal pattern of expression of integrins and perhaps other glycoproteins or proteins. (2) The circulating trophoblastic cells loosely bind to maternal endothelial cells, targeting them for anti-tumourigenesis. (3) The maternal immune system reacts against targeted maternal endothelial cells through anti-tumourigenic mechanisms. (4) Widespread maternal endothelial damage causes the characteristic kidney lesion called glomerula endotheliosis.

Cell Adhesion↗
PubMed1992

Genes for the trophoblast interferons and their distribution among mammals.

The trophoblast interferons (IFN), ovine and bovine trophoblast protein-1 (oTP-1 and bTP-1 respectively), possess many properties in common with other Type I IFN, including antiviral and antiproliferative activities. However, they differ from other IFN subtypes in terms of their specific pattern of expression and poor responsiveness to viral stimulation. We describe here data that suggest that the trophoblast IFN genes are also distinct from other Type I IFN genes with respect to species distribution, promoter organization and transcriptional regulation. These results have important implications in terms of trophoblast IFN gene evolution and add credence to the concept that the trophoblast IFN genes are a distinct IFN gene subtype well suited for their role in early pregnancy.

Animals↗
PubMed2003

Expression of IGR-IR and VEGF and trophoblastic proliferative activity in placentas from pregnancies complicated by IUGR.

Intrauterine growth retardation (IUGR) is recognized as an important cause of low birth weight and elective preterm delivery. IUGR is associated with multiple causative factors, including placental dysfunction. The aim of this prospective study was to investigate the role of trophoblastic proliferative activity and type I insuline-like growth factor receptor (IGF-IR) and vascular endothelial growth factor (VEGF) expressions in the pathogenesis of IUGR. Immunohistochemistry using VEGF, IGF-IR, and Ki-67 antibodies was performed on formalin-fixed placental tissues of third-trimester pregnancies complicated by IUGR (n = 19) and pregnancies with appropriately grown fetuses (n = 27). In addition, histopathological examination of the placentas was performed, and histological findings were categorized into three groups: utero-placental vascular pathologies (UPVP), coagulation-related pathologies, and chronic inflammation. Statistical analysis revealed that villous trophoblastic IGF-IR immunostaining was significantly weaker in placentas with IUGR (p < 0.001), whereas trophoblastic Ki-67 proliferative index and VEGF immunoscoring did not show any significant difference. Histologically, UPVP and chronic inflammation were significant findings in placentas with IUGR (p = 0.04 and p = 0.04, respectively). In addition, placentas were significantly smaller in the IUGR group (p < 0.001). We conclude that villous trophoblastic IGF-IR expression may play a significant role in the pathogenesis of IUGR, and histopathological examination of placentas in pregnancies complicated by IUGR may yield significant findings. In contrast, based on our findings, trophoblastic proliferation and VEGF expression are unlikely to be significant parameters in the pathogenesis of IUGR.

Adult↗
PubMed2004

The human chorionic gonadotropin molecule from patients with trophoblastic diseases has a high thyrotropic activity but is less active in the ovary.

To examine the pathogenesis of hyperthyroidism in women with trophoblastic diseases, the biological activity of human chorionic gonadotropin (hCG) molecules in women with normal pregnancy (n = 85) and in women with trophoblastic diseases (vesicular mole, n = 30; and choriocarcinoma, n = 12) was compared. Hyperthyroidism (thyroid stimulating hormone (TSH) < 0.3 mIU/l) was observed more frequently in women with trophoblastic diseases. All the sera were then subjected to Chinese hamster ovary cells transfected with the human TSH receptor (CHO-hTSHr cells) and cAMP production was compared. Sera from the women with choriocarcinoma showed the highest cAMP production. Interestingly, significant correlation between serum hCG level and cAMP production in CHO-hTSHr cells was observed only in women with trophoblastic disease. All the sera were then applied to CHO cells transfected with hCG/luteinizing hormone (LH) receptor (CHO-hCG/LHr cells). In contrast to the findings with the TSH receptor, sera from the women with normal pregnancy showed the highest cAMP production in these cells. Correlation between serum hCG level and cAMP production in CHO-hCG/LHr cells was significant only in normal pregnancy. These results indicate that the hCG molecule from women with trophoblastic diseases displays enhanced thyrotropic activity.

Adolescent↗
PubMed1985

Progesterone and prostanoid production by bovine binucleate trophoblastic cells.

A procedure for preparing highly enriched suspensions of bovine binucleate trophoblastic cells was developed and data showing that these cells produce progesterone, prostacyclin (PGI2), and prostaglandin E2 (PGE2) were obtained. Approximately 200 X 10(6) enzymatically dissociated cells from bovine cotyledons were applied to the surface of a density gradient of 2% to 4% Ficoll-400 using the Wescor CELSEP sedimentation chamber. After 90-120 min of sedimentation at unit gravity, fractions containing binucleate trophoblastic cells were obtained and washed in HEPES-buffered Medium 199. Preparations of 90% to 100% binucleate trophoblastic cells were obtained routinely; viability was 50% to 80%. After incubation at 37 degrees C, concentrations (ng/10(5) cells) of progesterone were greater in those fractions containing binucleate cells than in those containing primarily smaller, mononucleate cells. Total progesterone secreted (mean +/- SEM) after 4 h by 1 X 10(5), 2 X 10(5), 4 X 10(5), 8 X 10(5), and 1.6 X 10(6) binucleate cells was 0.27 +/- 0.03, 1.01 +/- 0.09, 4.02 +/- 0.37, 10.31 +/- 0.92, and 20.96 +/- 2.23 ng, respectively (r = 0.997). Addition of 10% fetal bovine serum (FBS) or normal anestrous cow serum increased (P less than 0.05) production of progesterone by binucleate trophoblastic cells. Luteinizing hormone, follicle-stimulating hormone, prolactin, thyrotropin, and 8-bromo-adenosine 3',5'-cyclic monophosphate had no effect. Binucleate trophoblastic cells also produced PGI2 in relation to number of cells incubated (r = 0.996). Time courses for production of PGI2, PGE2, and progesterone were similar. Aspirin inhibited production of PGI2 and PGE2 by about 50% at a dose of 100 microM; FBS stimulated production of both prostanoids.

6-Ketoprostaglandin F1 alpha↗
PubMed2006

Expression of the high-mobility group protein HMGI(Y) in gestational trophoblastic diseases.

The high-mobility group protein HMGI(Y) is a member of a family of nonhistone chromosomal proteins, which have been implicated in the regulation of inducible gene transcription, integration of retroviruses into chromosomes, and induction of neoplastic transformation and metastatic progression in cancer cells. The human trophoblast is a tissue that shares proliferation capacity and invasiveness with neoplastic tissues, but in which these processes are tightly regulated. Recently we could show that HMGI(Y) is expressed in the normal human placenta, where it is localized in the nuclei of villous cytotrophoblast, in the anchoring villi at the implantation site and in extravillous (intermediate) trophoblast invading the maternal decidua. In contrast, the majority of the nuclei of the villous syncytiotrophoblast, a terminally differentiated tissue, was negative. The purpose of this study was to investigate the expression pattern of HMGI(Y) in gestational trophoblastic diseases (GTD), which has not been studied so far. To analyze the expression of HMGI(Y), we performed immunohistochemistry on a total of 29 cases of GTD, including 21 hydatidiform moles and 8 choriocarcinomas. Hydatidiform moles showed a positivity for HMGI(Y) in villous cytotrophoblast and in areas of the trophoblast proliferations on the villous surface; villous syncytiotrophoblast was negative. The choriocarcinomas showed strong immunoreactivity in all cases. The expression pattern of HMGI(Y) in gestational trophoblastic diseases indicates that it might play a role in the pathogenesis of GTD and might be potentially useful as an additional diagnostic marker for such lesions.

Adult↗
PubMed2004

Persistent tubal pregnancy presenting with delayed hemorrhage from a second implantation of trophoblast on the ovary: a case report.

BACKGROUND: The use of conservative surgical techniques to treat ectopic pregnancies has been reported to increase the rate of incomplete trophoblastic tissue removal and subsequent regrowth. CASE: A persistent ectopic pregnancy occurred in a woman previously treated with laparoscopic linear salpingostomy for an ampullary ectopic pregnancy. Repeat laparoscopy was performed, and bleeding from an ovarian implantation site was treated with resection of the trophoblastic site and electrocautery. A repeat linear salpingostomy was also performed at the site of the prior salpingostomy, where trophoblastic tissue also persisted. CONCLUSION: This is the first known case of hemorrhage from the probable secondary ovarian implantation of persistent trophoblastic tissue. A repeat conservative surgical procedure to treat persistent ectopic pregnancies and maintain potential fertility is advocated. This case also serves as a reminder to diligently examine all areas of the pelvis for the possible secondary implantation of persistent trophoblastic tissue should reoperation be necessary.

Adult↗
PubMed1994

Relaxation of imprinting in trophoblastic disease.

Genomic imprinting--the uniparental-dependent transmittance of a genetic trait--has been accepted in recent years as a major mechanism in mammalian genetics. We studied the expression of the H19 gene, a parentally imprinted (maternally expressed) gene, by in situ hybridization in human placenta and trophoblastic disease. Expression was found to be abundant, in a decreasing order, in the intermediate trophoblast (villous and interstitial), the cytotrophoblast, and the syncytiotrophoblast. The villous stroma was also prominently labeled. Partial hydatidiform mole showed a similar pattern of expression as normal placenta. As expected, complete hydatidiform mole, whose genome consists of two haploid sets of paternal origin, was not labeled in the villous stroma and surrounding trophoblastic layer. However, some of the large mononuclear cells in the proliferating groups sprouting from the villous surface were strongly labeled. Prominent expression of H19 was found in placental site trophoblastic tumor and gestational choriocarcinoma. The phenomenon of emergence of expression of alleles subject to repression according to their gamete of origin is termed relaxation of imprinting, and is considered to be relevant to tumorigenesis. We suggest that the expression of the maternally expressed H19 gene in the androgenetic tissue of complete hydatidiform mole represents relaxation of imprinting and may be associated with its malignant potential.

Choriocarcinoma↗
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↗
PubMed2004

Advances in the clinical laboratory detection of gestational trophoblastic disease.

BACKGROUND: Gestational trophoblastic disease (GTD) consists of a spectrum of disorders that are characterized by an abnormal proliferation of trophoblastic tissue. Gestational trophoblastic neoplasia (GTN) refers to a subset of GTD with a persistently elevated serum hCG in the absence of a normal pregnancy and with a history of normal or abnormal pregnancy. Although previously a lethal disease, GTN is considered today the most curable gynecologic cancer. However, a delay in the diagnosis may increase the patient's risk of developing malignant GTN, and therefore the prompt identification of GTN is important. SERUM MARKERS: hCG test is essential for detection of GTN. It has emerged that there are problems with hCG tests. In addition to regular hCG, at least five major variants of hCG are present in serum samples. False-positive hCG (phantom hCG) can occur in the absence of GTN. Low-level real hCG may occasionally persist in the absence of clinical evidence of pregnancy or GTD. Alternatively, low-level real hCG may be due to pituitary hCG. Other placental hormones, human placental lactogen (hPL), inhibin and activin, and progesterone have also been evaluated as tumor markers for GTD. CONCLUSION: hCG has high diagnostic sensitivity, approaching 100% sensitivity, for managing the treatment of GTN and for detecting recurrences of disease. It is recommended to use hCG test that recognizes all forms of the hCG molecule. In cases where low-level hCG persists, it must be differentiated whether it is real or false. Real-hCG may be due to quiescent gestational trophoblastic disease or pituitary hCG. It has not yet been established whether measurement of markers other than hCG (hPL, inhibin, activin, and progesterone) is useful in the detection and follow-up of GTD.

Activins↗
PubMed2003

Placental site trophoblastic tumour.

Placental site trophoblastic tumour (PSTT) is a very rare and unique form of gestational trophoblastic disease (GTD). This tumour represents a neoplastic transformation of intermediate trophoblastic cells that normally play a critical role in implantation. PSTT can occur after a normal pregnancy, abortion, term delivery, ectopic pregnancy or molar pregnancy. It displays a wide clinical spectrum, and when metastatic, can be difficult to control even with surgery and chemotherapy. Unlike other forms of GTD, PSTT is characterized by low beta-hCG levels because it is a neoplastic proliferation of intermediate trophoblastic cells. Expression, however, of human placental lactogen (hPL) is increased on histologic section as well as in the serum. The most common presenting symptoms of PSTT are vaginal bleeding and amenorrhoea. Diagnosis is confirmed by dilatation and curettage (D and E) and hysterectomy but meticulous evaluation of metastasis is mandatory. Most cases are confined to the uterus but pelvic involvement, lung and other organ metastasis has been reported. Unlike other forms of GTD, the WHO prognostic score is of little help. For the PSTT patient, surgery is the primary treatment of choice. For patients desiring future childbearing, D and C and adjuvant chemotherapy is an option. Because these tumours tend to be less sensitive than other types of GTD to chemotherapy, the most successful regimen to date has been with EMA/CO or EMA/EP. Good prognosis is anticipated in cases localized to the uterus, and when the interval between antecedent pregnancy and treatment is less than 2 years. In cases with distant metastasis or delayed treatment, the outcome is dismal. Advances in chemotherapeutic regimens have improved clinical reponse in metastatic disease.

Antineoplastic Agents↗
PubMed1996

Major basic protein as a marker of malignant potential in trophoblastic neoplasia.

OBJECTIVE: We tested whether serum pregnancy-associated major basic protein levels distinguish between benign and malignant trophoblastic disease. STUDY DESIGN: We compared serum pregnancy-associated major basic protein levels in seven patient groups: nonpregnant and pregnant controls, partial moles, complete moles, persistent moles, placental-site trophoblastic tumors, and choriocarcinoma. RESULTS: The results showed that patients with partial and complete moles had elevated serum pregnancy-associated major basic protein levels comparable to normal pregnancy. In contrast, patients with persistent mole, placental-site trophoblastic tumors and choriocarcinoma had low median serum levels comparable to those of the nonpregnant controls. Significant differences were shown between the complete and persistent mole groups (p = 0.0001) and between the complete mole group and the choriocarcinoma group (p = 0.0001); however, persistent moles were indistinguishable from choriocarcinoma (p = 0.2010). CONCLUSION: Serum pregnancy-associated major basic protein levels thus distinguish between benign disorders, such as pregnancy and partial and complete moles, and trophoblastic tumors, such as persistent moles and choriocarcinoma. The absence of elevated serum levels of pregnancy-associated major basic protein may be useful clinically to indicate a more aggressive or frankly malignant tumor.

Biomarkers, Tumor↗
PubMed2005

Gestational trophoblastic diseases: recent advances in histopathologic diagnosis and related genetic aspects.

Gestational trophoblastic disease refers to a spectrum of proliferative disorders of the placental trophoblast, with a wide range of histologic appearances and clinical behaviors. This review discusses the more recent developments in the diagnosis of these entities. Changes in criteria for the histologic diagnosis of these lesions due to earlier clinical diagnosis are reviewed, and the ability to make more accurate diagnoses due to the introduction of newer antibodies such as p57 is highlighted. A discussion of epithelioid trophoblastic tumor, a newly introduced tumor subtype, with its differential diagnosis from placental-site trophoblastic tumor and squamous cell carcinoma is also presented. Last, a brief discussion on the role of genetic studies and the future direction of research in elucidating the nature of this intriguing group of lesions is presented.

Carcinoma, Squamous Cell↗
PubMed1998

Review: analogies between trophoblastic and malignant cells.

PROBLEM: The question of how trophoblastic and malignant cells evade immunologic recognition and rejection by their host was studied. METHOD OF STUDY: A literature review was conducted. RESULTS: Trophoblastic and malignant cells share a number of similarities. These include a lack of major histocompatibility complex antigen expression, resistance to lysis by natural killer cells, T-helper cell-2 (TH2)-biased response, prostaglandin E production, and response to transforming growth factor beta. In addition, the analogies between trophoblastic and malignant cells extend into immunotherapy in which anti-idiotype therapy has a viable role in the prevention of pregnancy loss and the treatment of cancer. CONCLUSIONS: Trophoblastic and malignant cells use a number of similar mechanisms to resist rejection by their host. By using similar strategies these cells are able to successfully co-exist in an immunologically hostile environment.

Female↗
PubMed2005

[Etopside, methotrexate, kengshengmycin/etopside, cisplatin chemotherapy for chemorefractory gestational trophoblastic tumour].

OBJECTIVE: To evaluate the results of etopside, methotrexate, kengshengmycin/etopside, cisplatin (EMA/EP) chemotherapy in patients with chemorefractory gestational trophoblastic tumour. METHODS: Fifteen patients with chemorefractory gestational trophoblastic tumour were treated by EMA/EP chemotherapy schedule. RESULTS: Twelve of the fifteen cases were choriocarcinoma, and the other three were metastatic placental site trophoblastic tumour (PSTT). International Federation of Gynecology and Obstetrics (FIGO), 2 cases stage I, 10 cases stage III, 3 cases stage IV. Eight cases had FIGO score of 7 to 12, the score of the other 7 cases was over 12. Fifteen patients received a total of 93 cycles of the study regimen. The median number of courses for each patient was 6.2. Eleven cases (73%) achieved a complete remission while 3 patients (20%) had a partial remission, 1 case (7%) showed nonresponse. The main complications for EMA/EP chemotherapy were myelosuppression and gastrointestinal symptoms. CONCLUSIONS: The EMA/EP regimen is an effective treatment for chemorefractory gestational trophoblastic tumour, and the chemotherapeutic results can be further improved while combined with surgery and arterial infusion chemotherapy in the selected patients. Meanwhile, EMA/EP regimen should be considered in the primary management of patients with metastatic PSTT.

Adult↗
PubMed1991

Pathology of trophoblast.

In summary, recent light microscopic studies, complemented by immunocytochemical and cytogenetic techniques, have demonstrated profound differences in the etiology, morphology, and clinical behavior of various forms of GTD. In addition, in vitro studies combined with immunohistochemical and ultrastructural analysis of normal trophoblast have provided new insight into the factors that coordinate the interactions of trophoblastic and maternal cells at the implantation site and have elucidated some of the mechanisms that regulate normal trophoblastic invasion. Analysis of the studies of normal and neoplastic trophoblast suggests that each of the specific forms of GTD is related to discrete pathologic aberrations occurring at different stages of gametogenesis and placentation. The results of these studies are examined in light of what is known about the pathobiology of GTD and are correlated with the histologic classification of GTD developed by the International Society of Gynecological Pathologists under the auspices of the World Health Organization.

Cell Differentiation↗