Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027960 (mole)
 21,279 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The galactose alpha 1-3 galactose (Gal alpha 1-3 Gal) residue is a carbohydrate widely distributed in many non-human mammals. Since Gal alpha 1-3 Gal residues are described on the cell surface of tumor cells, we have examined the possibility of their expression on human trophoblastic cells at different stages of placental implantation and in various pregnancy-associated conditions. Using immunohistochemical methods, Gal alpha 1-3 Gal was demonstrated on interstitial and vascular trophoblast during pregnancy. For villous trophoblast, the staining disappeared in second trimester pregnancies. The density of staining for Gal alpha 1-3 Gal was increased in highly invasive trophoblast (mole and choriocarcinoma) and decreased in poorly invasive specimens (spontaneous abortion, XO monosomia). No cells displaying Gal alpha 1-3 Gal at their surface were identified in some segments of spiral arteries from pre-eclamptic women. The anti-Gal antibody titer increased in the first trimester of pregnancy and in the sera of pre-eclamptic and eclamptic patients. These findings suggest that Gal alpha 1-3 Gal residues could be considered as markers for trophoblast invasive capacity and that the binding of maternal anti-Gal antibodies to the trophoblast could contribute to limit trophoblastic invasion and thus participate to the immunological control of implantation.
Placenta
PMID:Galactose alpha 1-3 galactose and anti-alpha galactose antibody in normal and pathological pregnancies. 147 Jun 7

A new method of DNA analysis has been used for the determination of androgenesis as a cause of complete hydatidiform mole. This method, using a minisatellite core probe, requires only a small amount of DNA and detects the restriction fragment length polymorphisms (RFLPs) due to allelic differences in the number of tandem repeats containing the core sequence. Southern blot hybridization showed an individual-specific DNA fingerprint, and each polymorphic band in molar tissues could be identified as being of paternal, but not maternal, origin. Some polymorphic bands of paternal DNA were not observed in molar tissues, indicating that endoreduplication of a normal haploid sperm or fertilization by dispermy to an anuclear oocyte with no effective genome could be the cause of complete hydatidiform mole. This method is sufficiently reliable and rapid that differential diagnosis could be made between complete hydatidiform mole, partial mole and hydropic change.
Placenta
PMID:A new approach using DNA fingerprinting for the determination of androgenesis as a cause of hydatidiform mole. 257 Nov 47

Complete hydatidiform moles may originate from either the fertilization of an empty egg by a haploid sperm followed by duplication (producing a monospermic, homozygous mole) or the fertilization of such an egg by two haploid sperms (producing a dispermic, heterozygous mole). This difference in the mechanism leading to the formation of complete moles raises the question of whether the risk of subsequent malignancy is influenced by the zygosity of the mole. We have compared the incidence of postmolar sequelae in patients with homozygous and heterozygous moles. Using chromosomal heteromorphisms, human lymphocyte antigen (HLA) and phosphoglucuromutase 1 (PGM1) polymorphisms, we established the androgenetic origin of complete mole in 84 of 91 cases. Homozygosity was confirmed in 51 moles, and we found ten heterozygous moles. Five of ten patients with heterozygous moles developed postmolar trophoblastic disease, whereas only two of the 51 patients with homozygous moles had postmolar trophoblastic disease (an additional five patients showed signs of degenerating residual trophoblasts). The XY sex chromosome constitution of the two in vitro choriocarcinoma cell lines examined here provides further evidence of the propensity to malignancy of heterozygous moles.
Placenta
PMID:The propensity to malignancy of dispermic heterozygous moles. 282 29

In an elective study of 163 hydatidiform moles 38 were classified as partial mole (PHM) and 125 as complete mole (CHM) on the basis of pathology. Genetic studies showed the PHM to be triploid with one maternal and two paternal chromosome sets. In all cases of PHM the molar pregnancy resolved spontaneously after evacuation. On the basis of genetic studies CHM which were diploid could be subdivided into two entities: homozygous androgenetic CHMs that were 46,XX, and heterozygous CHMs which were androgenetic and usually 46,XY. In informative cases in this series the frequency of heterozygous CHM was 10 per cent. Twenty-two (17.6 per cent) of all the patients with CHM required subsequent chemotherapy for post-mole trophoblastic tumour. Where patients with CHM could be classified as having homozygous or heterozygous CHM the requirement for treatment (17.8 per cent and 25 per cent, respectively) was not found to be significantly different in the two groups.
Placenta
PMID:Genetic studies in hydatidiform mole with clinical correlations. 347 66

The HLA and ABO systems were studied in patients with complete hydatidiform mole (CHM). The study confirmed that CHM can immunize the patient against paternally derived HLA-ABC antigens. In patients who required subsequent treatment for trophoblastic tumours the frequency of antibody detection was much higher (10/14) at the time of treatment than it had been at the time of evacuation (2/14). The source of immunogen was considered to be the stroma of the placental villi. It was demonstrated that in a series of 82 CHMs none of the 25 patients mated to a husband of the same ABO group as her own required treatment for postmole trophoblastic tumours. Among unlike matings 17 out of 57 of the patients required treatment. Thus it appears that trophoblastic proliferation after evacuation of mole is favoured by an ABO difference between maternal environment and the molar tissue.
Placenta
PMID:Immunogenicity of hydatidiform mole. 361 78

The genetic origin of hydatidiform moles was analysed utilizing HLA-DNA typing. Using HLA-DR type-specific oligonucleotide probes, the DRB types of seven moles were determined and compared with the parental DRB types to determine the paternal and/or maternal origin of the moles. In four cases, the molar tissues showed single DRB types of paternal origin, although in one, the molar DRB type was also possessed by the mother. These four moles were, therefore, considered to be androgenetic in origin. Chromosomal karyotyping was carried out for three of these cases and confirmed the DR-DNA typing results. Two moles demonstrated a DRB-type triplet, which strongly suggested triploidy. Although one mole showed a heterozygous DRB type, karyotyping indicated triploidy (69, XXX) and suggested that this mole was caused by dispermy-fertilization, in which both of the sperms had the same DRB type. Although the majority (about 80%) of partial hydatidiform moles have been reported to be triploid as a result of dispermy, four of the moles analysed in this study (cases 1, 2, 3 and 4), diagnosed as partial macroscopically and/or histopathologically, were found to be androgenetic in origin using karyotyping and DR-DNA typing. Therefore, HLA-DR DNA typing, combined in some cases with karyotyping, provides an accurate method for diagnosing androgenesis and triploidy in complete and partial hydatidiform moles.
Placenta 1994 Jul
PMID:Genetic analysis of hydatidiform moles utilizing the oligonucleotide-DNA typing of the HLA-DRB gene. 799 53

This study examines the proliferative activity of trophoblast in hydatidiform mole, non-molar hydropic abortion and non-molar spontaneous abortion. Nine cases of complete mole, 10 cases of partial mole, eight cases of non-molar hydropic abortion and six cases of non-hydropic second trimester abortion were examined by routine histopathology and the rate of cell proliferation was assessed by immunoreactivity for proliferating cell nuclear antigen (PCNA). Hydropic abortion showed a significantly lower PCNA index than complete mole and partial mole. There was no significant difference in PCNA index between partial mole and non-hydropic abortion. The trophoblast of partial hydatidiform mole demonstrates significant cell proliferation but this, although higher than that of hydropic abortion, is no higher than that of non-hydropic abortion of a similar gestational age. The role of partial mole as a precursor of persistent gestational trophoblastis disease remains unclear.
Placenta 1994 Jul
PMID:Comparison of villous trophoblast proliferation rate in hydatidiform mole and non-molar abortion by assessment of proliferating cell nuclear antigen expression. 799 54

Ras GTPase-activating protein (GAP), an important downregulator of Ras activity, has previously been shown to be abundant in human placenta. The expression of p120 and p100 isoforms of GAP in human normal chorionic villi (n=5) and hydatidiform mole (n=5) was investigated to clarify the involvement of Ras GAP in the growth of chorionic villi in the first trimester of pregnancy. Immunoblot analysis revealed that both p120- and p100-GAP isoforms were remarkably less expressed in mole villi than in normal chorionic villi. The expression of p100-GAP significantly reduced in comparison with that of pl20-GAP in mole villi. Northern blot analysis showed that the amount of GAP mRNA reduced in hydatidiform mole less than one-third of that in normal chorionic villi. The GAP activity, measured by the effect of tissue extract on the hydrolysis of Ras-bound GTP, was significantly lower in hydatidiform mole than in normal chorionic villi. These results suggest that Ras GAP may play an important role in the normal growth and differentiation of human chorionic villi in the first trimester.
Placenta
PMID:Expression of Ras GTPase-activating protein (GAP) in human normal chorionic villi and hydatidiform mole. 925 Jul 5

Six new cases of placental mesenchymal dysplasia are presented and the findings compared to those reported in 16 similar cases published in the literature. Mesenchymal dysplasia was suspected when a placental scan showed a partial mole with a fetus of normal size and normal karyotype. Three fetuses of this series and nine out of 18 cases from the literature review also presented with Beckwith-Wiedemann syndrome features. This placental anomaly is more commonly associated with a 46,XX karyotype. Comparable placental histopathological features in cases of mesenchymal dysplasia with or without congenital anomalies diagnostic of Beckwith-Wiedemann syndrome suggest that in some of these cases the overgrowth of specific fetal tissue is limited to the placenta and the fetus remains unaffected. Histological similarity between mesenchymal dysplasia and cellular chorioangioma suggests a common embryologic origin for both these placental abnormalities. Ultrasound/Doppler serial investigations indicate that the circulatory imbalance is due to hypovascularization of the dysplastic lobules, found in mesenchymal dysplasia. This induces the progressive aneurysmal and varicose dilatation of chorionic vessels, however, these anatomical transformations are not associated with a change in resistance to flow in both uterine and umbilical circulations nor with an excess of obstetrical complication when the fetus is anatomically normal.
Placenta 1997 Nov
PMID:Perinatal features associated with placental mesenchymal dysplasia. 936 6

The partial hydatidiform mole is a histopathologic entity characterized by focal trophoblastic hyperplasia with villous hydrops together with identifiable fetal tissue which was first described by Szulman and Surti in 1978. Since then major advances in molecular biology have shown that more than 90 per cent of partial moles are secondary to diandric triploidy and that this condition accounts for most cases of persistent trophoblastic disease after partial mole. Case series describing the prenatal diagnosis of triploid partial mole were reviewed and outcomes were analysed for all pregnancies, and compared to those of non-molar triploidy using the chi-square test. In more than 90 per cent of both types of triploidy, the fetus shows growth restriction and multiple structural anomalies. Oligohydramnios and abnormal placental Doppler indices are common in both types. In triploid partial mole, 82.1 per cent of fetuses present with symmetrical growth restriction, the maternal serum human chorionic gonadotropin (MShCG) level is increased in 80.8 per cent of the cases and 41.9 per cent of the women are at risk of pre-eclampsia. The triploid partial mole is a lethal fetal condition which is linked with gestational trophoblastic disorders. The typical placental molar features are not always pathognomonic of triploid partial mole and are less likely to be apparent on ultrasound in early pregnancy. The perinatal diagnosis of this condition relies upon mainly on MShCG level and cytogenetic results which have to be correlated with the histopathologic diagnosis. Women with this pregnancy complication should be offered immediate termination and a specific follow-up.
Placenta
PMID:Partial moles: from postnatal to prenatal diagnosis. 1041 2


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