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Comparative studies of three enzymes in hydatidiform mole and normal placenta.January 1976 (has links)
Thesis (M. Phil.)--Chinese University of Hong Kong, 1976. / Bibliography: leaves 82-91.
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Fractionation of human chorionic gonadotrophin from hydatidiform mole.January 1973 (has links)
by Pui-Kwong Chan. / Thesis -- The Chinese University of Hong Kong. / Bibliography: leaves 139-145.
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Further studies of human chorionic gonadotropin in hydatidiform mole.January 1975 (has links)
Kwok-pui Fung. / Thesis (M.Ph.)--Chinese University of Hong Kong, 1975. / Bibliography: leaves 122-131.
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Studies on the urinary and trophoblastic chorionic gonadotropins from patients with hydatidiform mole.January 1977 (has links)
Thesis (M.Ph.)--Chinese University of Hong Kong. / Bibliography: leaves 87-96.
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An Unusual Clinical Course after Mole Evacuation: A Case ReportTOMODA, YUTAKA, SAKAIDA, HIROSHI, GOTO, SETSUKO, NOMURA, SEIJI, NAKANISHI, TORU, OKAMOTO, TOMOMITSU 03 1900 (has links)
No description available.
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Extent of DNA methylation in biparental hydatidiform moles and functional consequences of NALP7 mutationsDjuric, Ugljesa. January 2006 (has links)
Hydatidiform mole (HM) is an abnormal human pregnancy characterized by cystic degeneration of chorionic villi and absence of embryo. It has been correctly proposed that deregulation of imprinted genes, expressed in a parent-of-origin specific pattern, leads to this pathology due to the fact that biparental and androgenetic HMs are indistinguishable at the phenotypic level. To determine the extent of the abnormal DNA methylation in two biparental moles from a family with a mutation in NALP7, we assessed long interspersed nuclear elements (LINEs), inactive X-linked genes and three tumour suppressor genes and demonstrated their normal levels of methylation. Since the identification of the NALP7 as the causative gene of recurrent HMs, the role of inflammation and immunity has come into light as a possible cause of this disease. Due to the known role of NALP7 in cytokine processing, we addressed the ability of the patients' peripheral blood mononuclear cells (PBMCs) to secrete cytokines in response to stimulation with various antigenic molecules. We found a reduced level of IL-1beta and TNF-alpha secretion by the patients' PBMCs suggesting that abnormal processing of several cytokines may underlie this disease.
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Molecular alterations of urinary HCG from hydatidiform mole /Napaporn Kukiatinant, Thanit Kusamran, January 1984 (has links) (PDF)
Thesis (M.Sc. (Biochemistry))--Mahidol University, 1984.
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Partial purification of hCG and analysis of protein components in vesicular fluid of molar placenta /Sarintip Rajatasriprasert, Thanit Kusamran, January 1982 (has links) (PDF)
Thesis (M.Sc (Biochemistry))--Mahidol University, 1982.
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Extent of DNA methylation in biparental hydatidiform moles and functional consequences of NALP7 mutationsDjuric, Ugljesa January 2006 (has links)
No description available.
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Rôle de l’EG-VEGF (Endocrine Gland Derived-Vascular Endothelial Growth Factor) dans le développement et la progression tumorale placentaire : cas du choriocarcinome / Role of EG-VEGF (Endocrine Gland-Derived Vascular Endothelial Growth Factor) in placental tumor development and progression : case of choriocarcinomaTraboulsi, Wael 12 December 2016 (has links)
Le choriocarcinome est une tumeur trophoblastique hautement maligne qui se développe souvent suite à des grossesses molaires dénommées moles hydatiformes (MH). La progression d’une MH vers un choriocarcinome reste à ce jour non caractérisée. L’implication de facteurs angiogéniques dans ce processus a été proposée. Nous avons étudié le rôle d'un nouveau facteur angiogénique spécifique du placenta, l’EG-VEGF (Endocrine Gland-Derived Endothelial Growth Factor) dans la pathogenèse du choriocarcinome. EG-VEGF agit via deux récepteurs (RCPG), PROKR-1 et PROKR-2. Trois approches ont été utilisées pour vérifier cette hypothèse. Une approche clinique, utilisant des échantillons placentaires et des sera collectés chez des patientes MH (n = 38) et avec choriocarcinome (n = 3) et chez des femmes normales (n = 18), tous prélevés au cours du premier trimestre de la grossesse. Une approche in vitro, utilisant les cellules JEG3, lignée humaine de cellules de choriocarcinome et des cellules trophoblastiques normales du premier trimestre (CTN). Une approche in vivo qui a visé à développer un modèle animal du choriocarcinome qui a servi à l’étude de la progression du choriocarcinome. Les niveaux circulants d’EG-VEGF étaient significativement plus élevés dans les MH et le choriocarcinome comparés aux niveaux chez les patientes normales. Au niveau placentaire, à la fois les niveaux d’expression de l’EG-VEGF et ses récepteurs ont été augmentés. Dans les cellules JEG3, EG-VEGF augmente i) l'expression de PROKR-1 et PROKR-2, ii). La migration, l'invasion, la prolifération et la formation de sphéroïdes dans des systèmes de culture 2 et 3D. Ces effets étaient significativement diminués en présence des antagonistes des deux récepteurs, iii) la phosphorylation de diverses protéines impliquées dans la progression tumorale, ainsi que la sécrétion de MMP-2 et MMP-9. Le modèle de choriocarcinome a été développé par injection de cellules JEG3 en orthotopie dans le placenta de la souris SCID (brevet en cours). En 12 jours, les souris gestantes injectées ont développés un choriocarcinome qui a métastasé dans différents organes. L'injection des antagonistes des récepteurs de l’EG-VEGF réduit significativement le développement et la progression de la tumeur. Par ailleurs, nous avons caractérisé le mécanisme par lequel EG-VEGF contribuerait à la progression tumorale. Ce mécanisme implique le clivage de la protéine de la jonction endothéliale, la VE-Cadhérine, suite à sa phosphorylation sur tyrosine 685 par l’EG-VEGF. Au total, mon projet de thèse i) démontre l’implication directe de l’EG-VEGF dans le développement et la progression du choriocarcinome ii) élucide le mécanisme de cette progression et iii) propose une piste thérapeutique via l’antagonisation de ses récepteurs. / Choriocarcinoma is a highly malignant trophoblastic tumor that often develop from molar pregnancies also called hydatidiform mole (HM). Nevertheless, HM progression towards choriocarcinoma remains uncharacterized. Involvement of angiogenic factors in this process is proposed. Here, we investigated the role of a new placental angiogenic factor, EG-VEGF (Endocrine Gland-Derived Endothelial Growth Factor) in choricarcinoma pathogenesis. EG-VEGF acts via two GPCR receptors PROKR-1 and PROKR-2. Three approaches were used to verify this hypothesis. A clinical approach using sera and placental samples collected from HM (n=38) and Choriocarcinoma patients (n=3) and from normal pregnant women (n=18); all collected during the first trimester of pregnancy. An In vitro approach using JEG3 cells, a human choriocarcinoma cell line and normal first trimester trophoblast cells (NTC). An in vivo approach that aimed at developing an animal model of choriocarcinoma in which therapeutic agents have been tested. Circulating EG-VEGF levels were significantly higher in HM and choriocarcinoma compared to normal patients. Placental EG-VEGF, PROKR1 and PROKR2 expression exhibited the same pattern. In JEG3 cells, EG-VEGF increased i) the expression of PROKR-1 and PROKR-2, ii). Their migration, proliferation invasion and spheroid formation using both 2 and 3D culture systems. These effects were abolished using PROKR1 and PROKR2 antagonists, iii) phosphorylation of different proteins involved in tumor progression as well as secretion of MMP-2 and MMP-9. Choriocarcinoma model has been developed by injection of JEG3 cells orthotopically within the placenta of SCID mice (Patent in progress). Within 12 days, injected gravid mice developed a choricarcinoma that metastasis in multiple organs. Importantly, injection of EG-VEGF receptors antagonists significantly reduced tumor development and its progression. Also, we have characterized the mechanism by which EG-VEGF contributes to tumor progression. This mechanism involves the cleavage of the key junctional protein, the VE-cadherin, following its phosphorylation at the tyrosine 685, by EG-VEGF. In total my thesis project i) demonstrated the direct involvement of the EG-VEGF in the development and progression of choriocarcinoma ii) elucidated the mechanism of this progression and iii) proposes a potential therapeutic for choriocarcinoma through the antagonisation of its receptors.
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