Gestational Trophoblastic Disease

Cw, Elston

doi:10.1136/jcp.41.2.239-a

Cited by 7 publications

(6 citation statements)

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“…Because of ultrasonographic evaluation, Pridjian and Moawad [1] recommended its abandonment and in its place the use of the terms anembryonic gestation for the empty sac or molar pregnancy and first or second trimester intrauterine fetal death or loss. The classification of hydatidiform [7][8][9][10][11] Fetal Diagn Ther 1998; 13:187-191 Brajenović -Milić /Petrović /Krašević /Ristić/ Kapović moles into two clinical entities has been verified by both pathologists and cytogeneticists [2][3][4]. Complete hydatidiform moles have rapidly progressing hydatidiform changes involving all the placental villi, widespread and gross trophoblastic hyperplasia and the absence of an embryo [3].…”

Section: Introductionmentioning

confidence: 99%

Chromosomal Anomalies in Abnormal Human Pregnancies

Brajenović-Milić¹,

Petrović

Krašević³

et al. 1998

Fetal Diagn Ther

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Objective: The aim of this study was to describe the cytogenetic observations on abnormal human pregnancies (anembryonic pregnancy, early fetal loss, and hydatidiform moles), and to detect the most frequent or typical chromosomal aberration for anembryonic pregnancy and early fetal loss. Study Design: Abnormal pregnancies were divided into three clinical and morphological groups: (a) anembryonic pregnancy; (b) early fetal loss, and (c) hydatidiform mole. Of the 119 karyotyped tissue samples, 42 (35%) were from anembryonic pregnancies, 64 (54%) from early fetal losses, and 13 (11%) were from hydatidiform moles (6 complete and 7 partial moles). Long-term cultures of chorionic villi and GTG-banding techniques were used for chromosome analysis. Results and Conclusion: The overall frequency of chromosome anomalies among the 119 karyotyped spontaneous abortions was found to be 37.8%. Trisomy (double trisomy included) accounted for 35.6% of all aberrations, followed by polyploidy (33.3%), mosaicism (11.1%), tructural abnormalities (4.4%), and monosomy X (2.2%). Although the difference was not statistically significant, single trisomy was the predominant chromosome abnormality found in anembryonic pregnancies (64.3%) while in cases of early fetal loss, trisomy (double trisomy included) (38.9%) and triploidy (27.8%) were quite frequently present. The frequency of triploidy among all chromosomal abnormalities was 28.9%, and 53.8% of them were found in partial hydatidiform mole. The rest of them were almost exclusively found in early fetal losses. Complete hydatidiform moles (androgenetic in origin) were present in 13.3% of all aberrations, of which 83.3% had a 46,XX, and the rest of them had a 46,XY karyotype.

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Section: Introductionmentioning

confidence: 99%

Chromosomal Anomalies in Abnormal Human Pregnancies

Brajenović-Milić¹,

Petrović

Krašević³

et al. 1998

Fetal Diagn Ther

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“…GTD encompasses a spectrum of disorders that arise from placental trophoblastic tissue after abnormal fertilization (Mazur et al, 1994;Elston et al, 1995). GTD is classified into distinct groups including hydatidiform mole (HM), invasive mole, choriocarcinoma, placental site trophoblastic tumor and epithelioid trophoblastic tumour.…”

Section: Introductionmentioning

confidence: 99%

Detection of mitochondrial DNA mutations in gestational trophoblastic disease

et al. 2003

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Mitochondrial DNA (mtDNA) mutations have been implicated in a wide range of human disease. However, its role in gestational trophoblastic disease remains unclear. In this study, the entire mitochondrial genome of 10 hydatidiform moles (HM) and one choriocarcinoma were examined by automated DNA sequencing after amplification by polymerase chain reaction. MtDNA sequences obtained separately from disease tissues (HM and choriocarcinoma) and patients' tissues were compared. Of the 133 neutral sequence variants identified, 41 have not been reported to date. Large or small-scale deletion or insertion was not detected in any of the samples studied. A total of six (five in the D-loop and one in the 16S rRNA gene) somatic point mutations were detected in the choriocarcinoma sample, in contrast to none being detected in the HM samples. Somatic mtDNA instability was detected in the D-loop region in three cases of HM as well as in the choriocarcinoma sample. Somatic mtDNA instability appeared in the same nucleotide position, from 303 to 309, within the Conserved Sequence Block II resulting in alteration in length of the homopolymorphic C-tract, reflecting microsatellite instability. The results suggest that mtDNA instability may be an early event occurring at a premalignant stage. Occurrence of multiple somatic mtDNA mutations in choriocarcinoma suggests that mtDNA mutations might play an important role in the molecular pathogenesis of invasive gestational trophoblastic disease.

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“…3,4 The reported incidences of subsequent development into gestational trophoblastic neoplasia requiring chemotherapy following complete and partial moles were quite variable, affected by the referral patterns, diagnostic criteria, and criteria for post-evacuation chemotherapy. 1,2,5,6 However, it is generally believed that such a risk is much higher after a complete mole when compared with a partial mole. The incidences of post-evacuation gestational trophoblastic neoplasia ranged from 8 to 29% in a complete mole and 0.5-5.5% in a partial mole.…”

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confidence: 99%

“…The original pathology diagnoses were made between 1990 and 2000 based on histological criteria 1,2 after examination of hematoxylin and eosin (H&E) stained sections of each case. In all, 36 complete moles and nine partial moles were thus diagnosed.…”

Section: Patientsmentioning

confidence: 99%

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Analysis of gestational trophoblastic disease by genotyping and chromosome in situ hybridization

et al. 2003

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Hydatidiform mole is classified into partial and complete subtypes according to histopathological and genetic criteria. Distinction between the two by histology alone may be difficult. Genetically, a complete mole is diploid without maternal contribution, whereas a partial mole is triploid with a maternal chromosome complement. To assess the accuracy of histological diagnosis by correlating with the genetic composition, we performed fluorescent microsatellite genotyping to detect the presence or absence of maternal genome in a hydatidiform mole and carried out chromosome in situ hybridization to analyze the ploidy. For genotyping analysis, paraffin sections of 36 complete and nine partial moles, diagnosed according to histological criteria, were microdissected and DNA was separately extracted from the decidua and molar villi. Six pairs of primers that flank polymorphic microsatellite repeat sequences on five different chromosomes were used. In all, 34 cases, including 31 complete moles and three partial moles diagnosed histologically, showed no maternal contribution by genotyping; thus these could be genetically considered as complete mole. The other 11 cases (five complete moles and six partial moles previously diagnosed by histology) showed the presence of maternal contribution and were genetically diagnosed as partial moles. The genotyping results correlated with histological evaluation in 88% (37/45) of hydatidiform mole and correlated with chromosome in situ hybridization findings in all the cases, that is, triploid hydatidiform moles had maternal-derived alleles, while diploid hydatidiform moles were purely androgenetic. Compared with genetic diagnosis, histological evaluation was more reliable for the diagnosis of a complete mole (91%, 31/34) than that of a partial mole (55%, 6/11) (P ¼ 0.0033). Seven complete moles and three partial moles diagnosed genetically developed gestational trophoblastic neoplasia. To conclude, genotyping and chromosome in situ hybridization can provide reliable adjunct to histology for the classification of a hydatidiform mole, especially in cases with difficult histological evaluation and early gestational age. As a partial mole still carries a risk of developing gestational trophoblastic neoplasia, follow-up is considered necessary for both complete and partial moles.

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Gestational Trophoblastic Disease

Abstract: Despite, or paradoxically due to, its comparative rarity, there has been a spate of publications on the subject of trophoblastic

Cited by 7 publications

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Chromosomal Anomalies in Abnormal Human Pregnancies

Chromosomal Anomalies in Abnormal Human Pregnancies

Detection of mitochondrial DNA mutations in gestational trophoblastic disease

Analysis of gestational trophoblastic disease by genotyping and chromosome in situ hybridization

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