Recurrent Placental Site Trophoblastic Tumor of the Uterus: Clinical, Pathologic, Ultrastructural, and DNA Fingerprint Study

Kudoh, Shoji; Kase, Hiroaki; Aoki, Y.; Yahata, Tetsuro; Tanaka, Kenichi; Motoyama, Teiichi; Dewa, Koji

doi:10.1006/gyno.1996.0016

Cited by 15 publications

(9 citation statements)

References 5 publications

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“…Of these, 18 had a female antecedent gestation by history, this was confirmed by DNA analysis in 4 cases (Fisher et al, 1992;Kodama et al, 1996;Lathrop et al, 1988). In one case, in which the preceding gestational event was a complete mole, the DNA analyses confirmed that the tumors harbored two X chromosomes (Fisher et al, 1992).…”

Section: Literature Reviewmentioning

confidence: 79%

“…All five cases of PSTT analyzed here showed an XX chromosomal composition, indicating the origin from an antecedent female conceptus or from an antecedent complete mole. Four other cases of PSTT in the literature had, by molecular analysis, an XmXp chromosomal composition (Fisher et al, 1992;Kodama et al, 1996;Lathrop et al, 1988). Overall, 89% of the 26 cases (23 of 26) showed a XX genomic makeup in PSTT either by history or genetic analysis (Table 1).…”

Section: Discussionmentioning

confidence: 95%

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Pathogenesis of Placental Site Trophoblastic Tumor May Require the Presence of a Paternally Derived X Chromosome

Hui

Parkash

Perkins

et al. 2000

Laboratory Investigation

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SUMMARY:Placental site trophoblastic tumor (PSTT) is a neoplastic proliferation of intermediate trophoblasts that invades the myometrium at the placental site after a pregnancy. Less than 100 cases have been reported. Information of the sex assignment of the antecedent gestation is available in 21 cases: 18 of these were female. To explore this interesting phenomenon, we have determined the sex chromosome composition of the tumor tissue preserved in paraffin blocks for five new cases of this condition. The last documented gestational event included a normal vaginal delivery of female infants in three cases, normal vaginal delivery of an infant of unknown sex in one case and a molar gestation in one case. Using the X-linked human androgen receptor (AR) gene as a polymorphic marker, we showed that in all five cases the tumor had a likely XX chromosomal composition; and in four cases it was possible to determine that one of the X chromosomes was of paternal origin. In one case, the paternal X chromosome showed no polymorphism to either maternal X chromosomes. In addition, sensitive semi-nested PCR failed to show a human Y chromosome element in any of the five cases of PSTT. Overall, of 21 cases from the literature and 5 cases of ours, 89% (23 of 26) showed an XX genomic composition in PSTT, either by history or genetic analysis. These results suggest that most PSTT were derived from the antecedent female conceptus and were likely to have possessed a functional paternal X chromosome. Methylation status analysis at the AR locus was performed in the three PSTT in which the paternal X chromosome was identifiable. In two cases, the paternal AR locus was hypomethylated while the corresponding maternal locus was hypermethylated. The methylation status of other loci was not investigated. Collectively, sex chromosome analysis of five cases of PSTT with literature support suggests a unique genetic basis for the development of PSTT that involves the paternal X chromosome. Although largely speculative, an active paternal X chromosome may be of importance in the pathogenesis of PSTT. (Lab Invest 2000, 80:965-972).D uring conception, tissue having paternallyderived genetic material is implanted in the female uterus. Rarely, this event leads to the development of a disease in the mother in the form of gestational trophoblastic disease (GTD). GTD includes some entities characterized by distinct unique genetic modes of pathogenesis which have been recognized for long time (Kajii and Ohama, 1977;Szulman, 1984): in complete hydatidiform moles, more than 90% of the proliferative trophoblasts have a 46, XX diploid pattern, all derived from the sperm (androgenesis). In partial moles, the karyotype is triploid in most cases (eg, 69, XXY), resulting from fertilization of an egg with one or two sperm. In fact, triploid gestations in which there is no duplication of the paternal chromosomes do not have trophoblastic hyperplasia and do not meet the histologic criteria of molar gestation (Jacobs et al, 1982). Therefore, duplication of the pat...

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Section: Literature Reviewmentioning

confidence: 79%

Section: Discussionmentioning

confidence: 95%

Pathogenesis of Placental Site Trophoblastic Tumor May Require the Presence of a Paternally Derived X Chromosome

Hui

Parkash

Perkins

et al. 2000

Laboratory Investigation

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“…The bilateral ovaries were preserved, since they appeared normal macroscopically. Histologic analysis showed proliferation of hPL-positive intermediate trophoblasts in which the mitotic count was extremely low (2/10 high-power fields), with vessel permeation in the uterine cervix and corpus, invading to the uterine serosa [4]. After the operation, serum ß-hCG and CTP-ß-hCG levels rapidly became normal.…”

Section: Case Reportmentioning

confidence: 95%

“…Previously, we reported this case of recurrent PSTT with low mitotic rate treated with an operation and multiagent chemotherapy [4]. Subsequently, the patient had refractory and metastatic tumors, underwent the other two operations, and received several lines of chemotherapy, including high dose chemotherapy with PBSCT and radiotherapy.…”

Section: Discussionmentioning

confidence: 99%

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Failure of High-Dose Chemotherapy with Peripheral Blood Stem Cell Support for Refractory Placental Site Trophoblastic Tumor

Aoki

Kudoh²,

Kurata³

et al. 1999

Gynecol Obstet Invest

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Placental site trophoblastic tumor (PSTT) is a rare form of gestational trophoblastic disease. The metastatic and refractory cases have a very poor prognosis. To our knowledge, this is the first report of the application of high-dose chemotherapy with autologous peripheral blood stem cell transplantation (PBSCT) for the treatment of refractory metastatic PSTT. A 36-year-old woman had a metastatic PSTT refractory to several lines of chemotherapy. She was treated with high dose of carboplatin and etoposide with autologous PBSCT. She showed only a temporary response to high-dose chemotherapy with PBSCT support and died of disease.

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Metastatic Placental Site Trophoblastic Tumor: Long-Term Remission in a Patient Treated with EMA/CO Chemotherapy

Swisher¹

1998

Gynecologic Oncology

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Recurrent Placental Site Trophoblastic Tumor of the Uterus: Clinical, Pathologic, Ultrastructural, and DNA Fingerprint Study

Cited by 15 publications

References 5 publications

Pathogenesis of Placental Site Trophoblastic Tumor May Require the Presence of a Paternally Derived X Chromosome

Pathogenesis of Placental Site Trophoblastic Tumor May Require the Presence of a Paternally Derived X Chromosome

Failure of High-Dose Chemotherapy with Peripheral Blood Stem Cell Support for Refractory Placental Site Trophoblastic Tumor

Metastatic Placental Site Trophoblastic Tumor: Long-Term Remission in a Patient Treated with EMA/CO Chemotherapy

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