Disease relevance of Hydatidiform Mole

• Nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase activity in hydatidiform mole tissue and choriocarcinoma cells [1].
• To assess the role that Ras-GAP plays in the development of trophoblastic tumors, we performed immunohistochemical analyses with anti RasGAP antibodies of normal placentas, hydatidiform moles, invasive moles, and malignant choriocarcinomas [2].
• PAI-1 antigen levels also were increased, and PAI-2 levels were decreased in placenta from women with molar pregnancies compared with placenta obtained by spontaneous abortion [3].
• Formalin-fixed, paraffin-embedded tissues from three normal term placentas, 13 hydatidiform moles (HM), five choriocarcinomas (CC) (three gestational, one testicular, one mediastinal), and five placental site trophoblastic tumors (PSTT) were immunolabeled with antibodies to the alpha-subunit of inhibin, hPL, and beta-hCG [4].
• The relationship between expression of c-ras, c-erbB-2, nm23, and p53 gene products and development of trophoblastic tumor and their predictive significance for the malignant transformation of complete hydatidiform mole [5].

High impact information on Hydatidiform Mole

• Mutations in NALP7 cause recurrent hydatidiform moles and reproductive wastage in humans [6].
• Letter: Ectopic gestation and hydatidiform mole in clomiphene-induced pregnancies [7].
• Linkage of two human pregnancy-specific beta 1-glycoprotein genes: one is associated with hydatidiform mole [8].
• Two cases of complete hydatidiform mole which progressed to choriocarcinoma show high levels of expression of both H19 and IGF2 [9].
• To evaluate the possible role of prostaglandin catabolism in neoplastic cells, we measured nicotinamide adenine dinucleotide-dependent 15-hydroxyprostaglandin dehydrogenase activity in hydatidiform mole tissue and in choriocarcinoma cells maintained in monolayer culture [1].

Chemical compound and disease context of Hydatidiform Mole

• CS did not respond at all to arginine infusion both in normal pregnancy and molar pregnancy [10].
• Evidence for the existence of an androgen binding protein in hydatidiform mole vesicles [11].
• Various aspects of thyroid hormone economy were examined in 15 patients with molar pregnancy and in 5 patients with choriocarcinoma [12].
• None of the patients with molar pregnancy was clinically thyrotoxic, though serum thyroxine (T4) was increased in 13 and free T4 concentrations were above normal in four of ten in whom measurements were made [12].
• Unresponsiveness to exogenous thyrotropin-releasing hormone (TRH) was observed in 5 patients with molar pregnancy whose serum total T4 and T3 levels were increased [12].

Biological context of Hydatidiform Mole

• Significant increases in plasma PAI-1 and decreases in plasma PAI-2 levels were observed in molar pregnancies when compared with the levels in normal pregnant women of similar gestational age [3].
• Only one case of hydatidiform mole was found to have a missense point mutation (codon 295, CCT-->CTT, i.e. proline to leucine) of the p53 gene [13].
• First-trimester serum levels of the beta-subunit of human chorionic gonadotropin in a tubal molar pregnancy [14].
• PTEN promoter methylation and protein expression in normal early placentas and hydatidiform moles [15].
• Localization of telomerase hTERT protein and survivin in placenta: relation to placental development and hydatidiform mole [16].

Anatomical context of Hydatidiform Mole

• Likewise, high expression levels of PAR1 and PAR3 were observed in the cytotrophoblast cells of complete hydatidiform mole as compared to minimal levels in normal age-matched placenta [17].
• The implications of altered Fas/FasL status of decidual T-cell subsets in hydatidiform mole are also discussed [18].
• This study was designed to characterize and quantitate Fas/FasL expression by decidual leukocytes in complete and partial hydatidiform mole compared with that in normal early pregnancy using single and double immunohistochemical labeling (i.e., avidin-biotin-peroxidase and avidin-biotin-alkaline phosphatase) [18].
• In contrast, p57KIP2 expression in cytotrophoblast and villous mesenchyme was absent or markedly decreased in 58 of 59 complete hydatidiform moles [19].
• M-CSF promotes the growth of early gestation chorionic cells, hydatidiform mole cells, and a human term placenta cell line (tPA30-1) [20].

Gene context of Hydatidiform Mole

• Further, although low hCS-L RNA levels (< 1%) were found in term placenta and two of the hydatidiform moles, hCS-L transcripts represented 11% of the total hGH/hCS RNA in a third hydatidiform mole [21].
• Expression of telomerase subunits and localization of telomerase activation in hydatidiform mole [22].
• AIMS: To assess the proliferative activity of gestational trophoblastic disease (GTD) using one of the novel proliferation markers (MCM7) and to determine its prognostic value in hydatidiform mole (HM) [23].
• MATERIALS AND METHODS: Twenty partial hydatidiform moles, 21 complete hydatidiform moles, nine invasive hydatidiform moles, three choriocarcinomas and 19 first trimester hydropic spontaneous abortions were evaluated by means of immunohistochemical methods with antibodies to p53, PCNA, and Ki-67 in this study [24].
• In situ hybridization revealed an increase in PAI-1 but not PAI-2 mRNAs in placenta from molar pregnancies in comparison with placenta from abortions [3].

Analytical, diagnostic and therapeutic context of Hydatidiform Mole

• The need for chemotherapy for trophoblastic tumour after evacuation of a hydatidiform mole was found to be significantly increased in patients taking oral contraceptives before normal human chorionic gonadotrophin (HCG) values were obtained [25].
• Serum human chorionic somatomammotropin (hCS) was measured in 35 patients with intact unaborted hydatidiform mole by a rapid radioimmunoassay using 70% dioxane in water to separate the bound from unbound fraction [26].
• A semi-quantitative assessment of the receptor was estimated in villous IT within cell columns in normal and molar pregnancies but, in conclusion, quantitative evaluation of uPAR cannot be used to predict development of post-molar persistent trophoblastic disease (PTD) [27].
• STUDY DESIGN: We examined 5 complete hydatidiform mole specimens and 5 partial hydatidiform mole specimens to determine whether HLA-G is expressed by immunohistochemistry and by RNA in situ hybridization analysis [28].
• This study investigates the extent of apoptosis in complete hydatidiform mole (CHM), using an in situ 3'-end DNA labelling (TUNEL) technique on formalin-fixed and paraffin-embedded sections [29].

References