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PubMedDate not supplied

Epidemiological studies on disturbances of human fetal development in areas with various doses of natural background radiation. II. Relationship between incidences of hydatidiform mole, malignant hydatidiform mole, and chorionepithelioma and gonad dose equivalent rate of natural background radiation.

The relationships between gonad dose equivalent rates and incidences of chorionic disease (i.e., hydatidiform mole, malignant hydatidiform mole, and chorionepithelioma) were analyzed with Kendall's rank correlation and regression methods. Data used were from 11 prefectures of Japan with various dose rates of natural background ionizing radiation between the years 1974 to 1976. The results suggested an association of the incidence of chorionic disease with the radiation dose rate in the very low dose-rate range.

Adult↗
PubMed1996

p53 expression in placentas with hydropic change and hydatidiform moles.

Hydatidiform moles result from abnormal fertilization and have been divided into partial and complete forms based on morphologic, cytogenetic, and clinical features. Little is known about their pathogenesis or malignant transformation. We applied an immunohistochemical marker for the p53 tumor suppressor gene product to placentas with hydropic change and hydatidiform moles to determine whether abnormal p53 gene product accumulation occurs in molar gestations. Ploidy of these placentas was determined by flow cytometry and fluorescence in situ hybridization. The mean percentages of p53-positive cells was determined by counting 200 cytotrophoblastic and proliferating trophoblastic cells. The staining intensity was graded on a scale of 1+ (faint) to 3+ (strong). The mean percentage of p53-positive cells for the placentas were as follows: 8.9% +/- 10.5 for hydropic change; 28.0% +/- 13.2 for partial mole; and 41.0% +/- 19.6 for complete mole. There was a significant difference in p53 expression between hydropic change and partial mole (P = 0.05) and hydropic change and complete mole (P = 0.0008). Although there was a difference between partial mole and complete mole, this did not reach statistical significance (P = 0.15). Hydatidiform moles exhibited 2+ to 3+ staining intensity, whereas hydropic placentas exhibited weaker intensity (1-2+). The finding of p53 gene product overaccumulation in partial and complete moles suggests that p53 gene mutations or alternatively, post-transcriptional changes in the p53 gene product occur resulting in inactivation and stabilization of the protein. This may play a role in uncontrolled trophoblastic proliferation and neoplastic transformation.

Female↗
PubMed2006

Heterogeneity in the origin of recurrent complete hydatidiform moles: not all women with multiple molar pregnancies have biparental moles.

Hydatidiform moles of two women, each with three molar pregnancies, were examined in order to study their origin. Multiple recurrences have previously been associated with women who have biparental complete hydatidiform moles (CHM). However, all the moles examined in this study were androgenetic CHM (AnCHM), indicating that recurrent (>2) moles, particularly in the absence of a positive family history, may be androgenetic rather than biparental. These data suggest that some women have a specific liability for having AnCHM. Making the distinction between a biparental or an androgenetic origin of recurrent moles is of relevance for counselling and when considering therapeutic options. Therefore, we propose that all recurrent moles should be investigated using molecular techniques.

Adult↗
PubMed2006

[Genetic advances in hydatidiform mole].

Hydatidiform mole is the most common gestational trophoblastic disease and is characterized by gross trophoblastic hyperplasia resulting from abnormal fertilization of the oocyte. It is of great interest to researchers because of its propensity for local invasion and spreading. Using cytogenetic and molecular genetic techniques researchers have performed various studies on hydatidiform mole. There are advances in the understanding of karyotype, DNA ploidy, fertilization types, expression of imprinted genes, the differences between genetic classification and pathologic classification, and the correlation to its invasion and spreading.

Female↗
PubMed1999

Genetic mapping of a maternal locus responsible for familial hydatidiform moles.

Hydatidiform mole (HM) is the product of an aberrant human pregnancy in which there is an abnormal embryonic development and proliferation of placental villi. The incidence of HM varies between ethnic groups, and occurs in 1 in every 1500 pregnancies in the USA. All HM cases are sporadic, except for extremely rare familial cases. The exact mechanisms leading to molar pregnancies are unknown. We previously postulated that women with recurrent hydatidiform moles are homozygous for an autosomal recessive defective gene. To map this gene genetically, we initiated a genome-wide scan with highly polymorphic short tandem repeats in individuals from two families with recurrent HM. Here, we demonstrate that a defective maternal gene is responsible for recurrent HM. This gene resides on chromosome 19q13.3-13.4 in a 15.2 cM interval flanked by D19S924 and D19S890. The identification of a gene for HM adds new insights into the molecular genetics of early embryogenesis and may be relevant to the large number of patients with sporadic HM.

Chromosome Mapping↗
PubMed1978

The syndromes of hydatidiform mole. II. Morphologic evolution of the complete and partial mole.

Hydatidiform moles studied with respect to cytogenetics and morphologic constitution were divisible into two syndromes: (1) complete, classical mole giving a 46 XX karyotype and (2) partial mole with an ascertainable embryo/fetus, dead or alive, giving a triploid karyotype. The complete moles undergo early and total hydatidiform change from edema to central cistern formation, the embryos proper having perished before the establishment of a functioning circulation. Trophoblastic hyperplasia is conspicuous and the connection of this group to chorioncarcinoma is well established. In the partial moles there is a slow hydatidiform change that affects only some of the villi, but which seems to follow along the same lines as in complete moles. There is focal moderate trophoblastic hyperplasia, villous "trophoblastic inclusions" (that appear in triploids only), and maze-like central cisterns in the later cases. The partial mole, 46 XX, partakes of morphologic characteristics of both main syndromes and may represent an unusual syndrome of its own. The two main syndromes can now be distinguished morphologically and the question of the association of the partial mole with chorioncarcinoma has now to be further studied.

Female↗
PubMed1988

Diagnosis and management of the primary hydatidiform mole.

Hydatidiform mole may be categorized as either complete or partial on the basis of gross morphology, histology, and karyotype. The diagnosis, natural history, and management of patients with complete and partial moles are reviewed in detail. The controversy concerning chemoprophylaxis at the time of molar evacuation is also discussed. Furthermore, subsequent reproductive outcome in patients with both complete and partial moles is analyzed.

Combined Modality Therapy↗
PubMed1988

Trophoblastic disease: clinical pathology of hydatidiform moles.

Hydatidiform moles are divided into two syndromes: those of complete and partial moles. Both forms are genetically, morphologically, and clinically distinct. Choriocarcinoma can be associated with the complete mole that has not been described for the partial syndrome. Residual trophoblastic disease, on the contrary, can be found with either syndrome, the substrate being locally invasive (nonembolic) behaviour.

Female↗
PubMed1997

Hydatidiform mole.

Hydatidiform mole is a gestational trophoblastic disease that arises from fetal rather than maternal tissue and can become metastatic. Most signs and symptoms occur late in the first trimester and are often confused with symptoms of a normal pregnancy and, thus, are often disregarded. The two most important diagnostic tools to detect this disease are the ultrasound and the quantitative beta-human chorionic gonadotropin assay. Treatment includes dilation and evacuation of the uterus and strict follow-up of quantitative beta-human chorionic gonadotropin levels. It is also important that the patient be placed on a reliable form of birth control during her follow-up period.

Adolescent↗
PubMed1990

The risk factors in the development of persistent trophoblastic disease following hydatidiform mole.

Hydatidiform mole (HM) is not uncommon in our country. Its dangerous sequalae is the fatal persistent trophoblastic disease (PTD). The prognostic risk factors for the development of PTD were analyzed in 108 cases of HM treated in Ramathibodi Hospital from 1978 to 1986. Statistical univariate analysis was by calculation of relative risk (RR) and chi-square test. The incidence of PTD was 27.8 per cent. The significant risk factors were the presence of theca-lutein cyst, gestational age of less than 16 weeks, "large for date" uterus, and patients' age of 40 years or more. Their RR were 4.25, 3.11, 3.00 and 2.68 respectively. These findings were comparable with previous reports. The use of prophylactic chemotherapy in patients with these risk factors was suggested.

Adolescent↗
PubMed2002

The maternally transcribed gene p57(KIP2) (CDNK1C) is abnormally expressed in both androgenetic and biparental complete hydatidiform moles.

Hydatidiform mole (HM) is an abnormal gestation characterized by trophoblast hyperplasia and overgrowth of placental villi. The genetic basis in the vast majority of cases is an excess of paternal to maternal genomes, suggesting that global misexpression of imprinted genes is the common molecular mechanism underlying the genesis of this condition. Although most complete HM are androgenetic in origin, a rare, frequently familial, biparental variant has been described. Here we evaluate the expression of p57(KIP2), the product of CDKN1C, an imprinted, maternally expressed gene in a series of these rare, biparental complete HM (BiCHM). We observed dramatic underexpression of p57(KIP2) in BiCHM, identical to that seen in complete HM of androgenetic origin (AnCHM). The series included two sisters, both of whom had BiCHM. Genotyping of this family identified a 15 cM region of homozygosity for 19q13.3-13.4 similar to that found in three other families with recurrent BiCHM. These results demonstrate that BiCHM, like AnCHM, result from abnormal expression of imprinted genes. In addition we provide further evidence for a major control gene on 19q13.3-13.4 which regulates expression of imprinted genes on other chromosomes.

Chromosomes, Human, Pair 19↗
PubMed1981

[Pathogenesis and behavior of invasive mole without preceding hydatidiform mole (author's transl)].

From 89 cases of invasive mole, collected by our department since 1948, 12 (13.5%) cases without preceding hydatidiform mole (group A) were taken out, and their clinical data and histological observations were studied in comparison with those preceded by hydatidiform mole (group B) in the remaining 77 (86.5%), with the following results: 1. Invasive mole in group A was preceded by artificial or spontaneous abortion, but not by premature or normal delivery. 2. All of the 12 cases developed the invasive mole within 6 months. 3. Relation between the size of the focus and the latency period was not observed in either of the two groups. 4. The incidence of preoperative metastasis was somewhat lower in group A, but no difference was visible between the two groups in prognostic result. 5. As for histological findings, edematization and vesiculation of stroma of villi were observed in all the cases of group A, though with difference in grade from case to case. These findings as well as proliferation and intervascular penetration of villous cells were similar to those of group B.

Abortion, Induced↗
PubMed2003

Is genetic analysis useful in the routine management of hydatidiform mole?

Complete hydatidiform mole and partial hydatidiform mole are two abnormal conceptuses that may be identified by clinical, ultrasonographic, gross morphological, histological, and genetic characteristics. Among all these criteria, the specific diagnosis is generally confirmed only upon histological review. However, an accurate diagnosis based on morphological criteria is difficult and several studies have shown that misclassifications are frequent, even for experienced pathologists. An erroneous diagnosis may imply that women are either not enrolled in an adequate beta-hCG follow-up with the risk that hydatidiform mole (HM) progresses to choriocarcinoma, or are enrolled in an unnecessary follow-up. A reliable and complementary method to the pathologic interpretation is a genetic study of the conceptus to eliminate the diagnostic dilemma by distinguishing non-molar spontaneous abortions from HM and to define the type of HM. The aim of our study was to review the genetic basis of HM and discuss its relevance in the routine management of the disorder.

Diagnosis, Differential↗
PubMed2001

Expression of Fas/Fas ligand by decidual leukocytes in hydatidiform mole.

Complete hydatidiform moles are entirely paternally derived and, therefore, represent a complete intrauterine allograft that might be expected to provoke an altered maternal immune response compared with that of normal pregnancy. Uterine decidua contains a large leukocyte population, of which 10%-20% are T lymphocytes. Fas ligand (FasL) expression by placental trophoblast may induce apoptosis of Fas+ lymphocytes, thereby facilitating immune tolerance and survival of the molar trophoblast. Our previous studies have shown an increase in activated CD4+ decidual T cells in molar pregnancy compared with normal pregnancy. 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). A significant increase was found in Fas and FasL expression by decidual CD4+ T cells in complete (Fas+, P = 0.0106; FasL+, P = 0.0081) and partial (Fas+, P = 0.0131; FasL+, P = 0.0051) hydatidiform moles, as was a significant decrease in Fas expression by decidual CD8+ T cells in complete (P = 0.0137) and partial (P = 0.0202) hydatidiform mole compared with normal early pregnancy. The implications of altered Fas/FasL status of decidual T-cell subsets in hydatidiform mole are also discussed.

Antibodies, Monoclonal↗
PubMedDate not supplied

Association between Breus' mole and partial hydatidiform mole: chance or can hydropic villi precipitate placental massive subchorionic thrombosis?

Breus' mole (massive subchorionic hematoma) is a rare entity most often found in the placentae of macerated stillborn fetuses. Previously considered to represent a postmortem event, recent evidence suggests that it occurs prior to fetal demise. A 23-week gestation male neonate was delivered of a 23-year-old gravida 3, para 2 woman and survived for 49 min. An autopsy with chromosomal studies resulted in a diagnosis of triploidy. Placental examination showed the presence of both Breus' mole and also partial hydatidiform mole. DNA samples extracted from portions of the fresh hematoma and from the fetal spleen were compared using molecular techniques. PCR analysis showed the presence of Y chromosome specific DNA in the placental clot, but a semiquantitative Southern blot demonstrated that roughly 85% of the clot DNA was of maternal origin. These findings suggest that Breus' mole represents primarily maternal thrombosis rather than fetal hemorrhage. We hypothesize that the partial mole could have contributed to the formation of the Breus' mole as some of the hydropic villi may have focally obstructed the maternal venous return from the intervillus space causing sluggish flow and promoting thrombosis. A review of the literature on Breus' mole shows that the majority of reported cases have not included cytogenetic findings. However, several authors have reported an association with triploidy and other chromosomal anomalies characterized by scattered placental hydropic villi. Thus, we suggest that obstruction of maternal venous return by hydropic villi may have played a contributory role in some of these other reported cases.

Adult↗
PubMed1987

Immunocytochemical localization of chorionic gonadotropin, placental lactogen, and placental alkaline phosphatase in the diagnosis of complete and partial hydatidiform moles.

Complete hydatidiform moles (CHMs) and partial hydatidiform moles (PHMs) represent different clinicopathologic entities with characteristic morphologic and cytogenetic findings. In the absence of cytogenetic data, the histologic distinction between these lesions and abortuses showing hydropic swelling (AHS) may be difficult. An immunocytochemical study analyzing the distribution of human chorionic gonadotropin (hCG), human placental lactogen (hPL), and placental alkaline phosphatase (PlAP) in CHMs, PHMs, and AHS was undertaken to determine whether the expression of these trophoblastic proteins might assist in the differential diagnosis. A total of 24 CHMs, 22 PHMs, and 13 AHS were selected on the basis of established morphologic criteria. Thirty-four specimens of abortuses without hydropic swelling and normal placentas, ranging from 6 to 24 weeks gestational age, were similarly analyzed. The immunocytochemical localization of the three trophoblastic proteins, predominantly in syncytiotrophoblast (ST), was scored using a semiquantitative scoring system. In CHMs hCG is widely distributed and PlAP is patchily distributed in ST regardless of the gestational age, whereas hPL tends to increase with increasing gestational age. In contrast, in PHMs hPL is more widely distributed in ST compared with CHMs regardless of gestational age, while PlAP increases with increasing gestational age; in PHMs the distribution of hCG is markedly less than in CHMs except early in the first trimester when the staining patterns are similar. The different patterns of distribution of hCG, hPL, and PlAP may reflect differences in the pathobiology of trophoblast in CHMs and PHMs and appear to be useful in the differential diagnosis of these conditions.

Abortion, Spontaneous↗