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At least 19 recordsLinked to original sources
PubMed1995

Gonadoblastoma with dysgerminoma in one ovary and gonadoblastoma with dysgerminoma and yolk sac tumor in the contralateral ovary in a girl with 46XX karyotype.

A case of gonadoblastoma with dysgerminoma in the left ovary and gonadoblastoma with dysgerminoma and yolk sac tumor in the right of a 10-year-old girl is reported. Her karyotype was 46XX, normal female type. A case of a gonadoblastoma without a Y chromosome is very rare. Furthermore, the prognosis for gonadoblastoma accompanied by germ cell tumors other than dysgerminoma was very poor in the past, but the patient remains well 25 months after the first operation.

Child↗
PubMed1981

Dysgerminoma with syncytiotrophoblastic giant cells. A histologically and clinically distinctive subtype of dysgerminoma.

The clinical and pathological features of six dysgerminomas containing syncytiotrophoblastic giant cells were studied; these represented 3% of the dysgerminomas in the AFIP files. Syncytiotrophoblastic giant cells, the distinguishing histological feature, were present either in clusters or were distributed diffusely. Human chorionic gonadotropin was demonstrated immunocytochemically within the cytoplasm of the syncytiotrophoblastic giant cells in both of the two tumors tested for it. Serum or urine gonadotropin titers, measured in four patients, were elevated in three, and two of these were thought to have ectopic pregnancies. All of the dysgerminomas were Stage Ia, and the six patients were well 1-14 years after treatment.

Adnexa Uteri↗
PubMed2002

Dysgerminoma in a patient with a tumor of the neck. Empiric treatment of stage IV dysgerminoma.

The evolution of therapy for malignant ovarian germ cell tumors is one of the true success stories in oncology. Treatment outcome has improved greatly thanks to cisplatin-based combination chemotherapy. According to the well-established treatment guidelines for advanced cases, we treated a case of stage IV undifferentiated germ cell tumor in which we were able to preserve the patient's fertility. We concluded that the PEP regimen is an effective treatment for the patient with metastatic germ cell tumor.

Adult↗
PubMed2004

OCT4: a novel biomarker for dysgerminoma of the ovary.

The prognosis and therapy for dysgerminomas are different from those of other ovarian tumor types, making accurate diagnosis imperative for patient care. OCT4 (POU5F1) is a transcription factor involved in the regulation of pluripotency during embryonic development. It can be detected in both pluripotent cells and other early germ cells. This study examines the expression of OCT4 in both dysgerminoma and nondysgerminomatous neoplasms involving the ovary. Formalin-fixed, paraffin-embedded cell blocks of 33 cases of dysgerminoma including 2 cases of gonadoblastoma associated with dysgerminoma and 3 cases of metastatic dysgerminoma, and 111 cases of nondysgerminomatous neoplasms involving the ovary were stained using the antibody against OCT4. All cases of dysgerminomas and gonadoblastomas were positive for OCT4 with strong nuclear staining. More than 90% of dysgerminoma cells in each case showed diffuse strong nuclear staining. In addition, 3 metastatic dysgerminomas also showed uniform strong nuclear staining. All nondysgerminomatous tumors (mature teratoma, 14; yolk sac tumor, 4; Sertoli-Leydig cell tumor, 15; granulosa cell tumor, 22; Brenner tumor, 3; carcinoid tumor, 4; struma ovarii, 2; fibroma, 5; thecoma, 1; serous adenocarcinoma, 5; endometrioid adenocarcinoma, 4; small cell carcinoma, 6; stromal sarcoma, 1; malignant lymphoma, 6; metastatic malignant melanoma, 1; metastatic carcinoid, 2; metastatic small cell carcinoma, 1; and metastatic lobular carcinoma of the breast, 1) were negative for OCT4, except for some cases of clear cell adenocarcinoma of the ovary. Four of 14 clear cell adenocarcinomas showed focal positive nuclear immunoreactivity for OCT4. OCT4 is a sensitive and relatively specific biomarker for the detection of dysgerminoma. It may also be useful in the diagnosis of gonadoblastoma, which contains similar cells and may be associated with dysgerminoma. OCT4 may aid in the detection of small foci of metastatic dygerminoma in extraovarian sites and may also help distinguish dysgerminoma from other primary and metastatic tumors of the ovary.

Adenocarcinoma, Clear Cell↗
PubMed1992

Serum lactic dehydrogenase as a tumor marker in dysgerminoma.

Dysgerminoma is the most common malignant germ cell tumor in young women. The management of advanced-stage dysgerminoma challenges the gynecologic oncologist to achieve maximal survival, while maintaining childbearing potential. Radiation therapy has been extremely successful in curing dysgerminoma, but ovarian conservation is usually not possible. In contrast, various chemotherapeutic regimens have achieved high cure rates with continued ovarian function. Diagnosing recurrent dysgerminoma promptly so that salvage therapy can be initiated is important when conservative management has been employed. While alpha-fetoprotein and human chorionic gonadotropin have proven useful as tumor markers in some types of germ cell tumors, they have not been useful in patients with dysgerminoma. Serum lactic dehydrogenase (LDH) levels are known to be elevated in some patients with dysgerminoma. We treated a patient with Stage IIIC dysgerminoma whose initial serum LDH level was markedly elevated. After unilateral salpingo-oophorectomy with pelvic and paraaortic lymphadenectomy, followed by four cycles of VAC chemotherapy, her LDH level returned to normal. Her LDH level rose with disease recurrence and returned to normal again with salvage BEP chemotherapy. This is the first report to document the utility of serial LDH measurements in detecting disease recurrence in patients with ovarian dysgerminoma.

Abdominal Neoplasms↗
PubMed2006

Cytokeratin and CD30 expression in dysgerminoma.

Dysgerminoma is a malignant germ cell tumor of the ovary that shares morphological, immunophenotypic, and genetic features with its testicular counterpart, seminoma. Recent evidence supports the hypothesis that seminoma can differentiate into non-seminomatous germ cell tumor types. The progression of these tumors can be measured by their acquisition of the potential to express cytokeratin intermediate filaments, a characteristic specific to epithelial differentiation. Although testicular seminomas have been widely investigated, little is known about cytokeratin or E-cadherin expression in dysgerminomas. We investigated 26 formalin-fixed, paraffin-embedded ovarian dysgerminomas with immunohistochemical stains for CAM5.2, AE1/AE3, epithelial membrane antigen, cytokeratin 7, cytokeratin 20, high-molecular-weight keratin, and E-cadherin. In addition, we investigated the CD30 and vimentin immunoreactivity of these tumors. Immunoreactivity for CAM5.2 and for AE1/AE3 was present in more than 10% of neoplastic cells in 5 (19.2%) of 26 cases and in 2 (7.7%) of 26 cases, respectively. Cytokeratin 7 showed only focal positivity and never showed positive staining in greater than 10% of dysgerminoma cells. E-cadherin staining was positive in 2 cases showing weak membranous immunostaining in more than 10% of cells. Vimentin immunoreactivity was observed in only 2 dysgerminomas, both of which had less than 10% of the neoplastic cells staining. Cytokeratin 20, epithelial membrane antigen, high-molecular-weight keratin, and CD30 were consistently negative in all cases. Our study demonstrates that cytokeratin expression in dysgerminomas is not unusual and is consistent with the hypothesis that dysgerminomas have the capacity to differentiate along epithelial lines. Furthermore, the immunohistochemical staining patterns for cytokeratins, E-cadherin, and CD30 in dysgerminomas need to be considered when assessing differential diagnoses in difficult cases of primary ovarian tumors.

Adolescent↗
PubMed2004

c-KIT codon 816 mutation in a recurrent and metastatic dysgerminoma of a 14-year-old girl: case study.

Dysgerminomas are rare female germ-cell tumors that correspond histologically and immunohistochemically to seminomas. Analogous to seminomas, most dysgerminomas respond very well to cisplatin- or carboplatin-based chemotherapy and to radiotherapy. KIT tyrosine kinase is crucial for normal germ-cell development, and its expression is observed in the majority of seminomas and dysgerminomas. Recently, activating KIT mutations were described in a panel of male germ-cell tumors [5, 10]. All mutations were localized in exon 17, encoding the second tyrosine kinase domain. Because receptor tyrosine kinase KIT might also be involved in the pathogenesis of dysgerminomas, we studied the expression and mutational status of a pure dysgerminoma, which was sent to our department for diagnostic reasons. The tumor revealed an exon 17 D816 V mutation in the c-KIT gene and strong KIT expression was found immunohistochemically. Clinically, the tumor was highly aggressive and resistant to carboplatin-based chemotherapy. Our case raises the question of whether exon 17 c-KIT mutations might be involved in the pathogenesis of dysgerminoma and whether exon 17 KIT mutations may predict aggressive and chemotherapy-resistant behavior of dysgerminomas.

Adolescent↗
PubMed2004

Increased expression of 25-hydroxyvitamin D-1alpha-hydroxylase in dysgerminomas: a novel form of humoral hypercalcemia of malignancy.

Humoral hypercalcemia of malignancy (HHM) is a common paraneoplastic disorder usually associated with increased synthesis of parathyroid hormone-related peptide (PTHrP). Unlike non-cancer forms of hypercalcemia, HHM does not routinely involve increased circulating levels of the active form of vitamin D, 1,25-dihydroxyvitamin D3 (1,25(OH)2D3). Dysgerminomas are a notable exception to this rule, previous reports having described hypercalcemia with elevated serum 1,25(OH)2D3. To investigate the etiology of this form of HHM we have characterized expression and activity of the enzyme that catalyzes synthesis of 1,25(OH)2D3, 25-hydroxyvitamin D-1alpha-hydroxylase (1alpha-hydroxylase), in a collection of 12 dysgerminomas. RT-PCR analyses indicated that mRNA for 1alpha-hydroxylase was increased 222-fold in dysgerminomas compared to non-tumor ovarian tissue. Parallel enzyme assays in tissue homogenates showed that dysgerminomas produced fivefold higher levels of 1,25(OH)2D3 compared to normal ovarian tissue. Immunolocalization studies indicated that 1alpha-hydroxylase was expressed by both tumor cells and by macrophages within the inflammatory cell infiltrate associated with dysgerminomas. The immunological nature of the increased 1,25(OH)2D3 production observed in dysgerminomas was further emphasized by correlation between expression of 1alpha-hydroxylase and the endotoxin recognition factors CD14 and toll-like receptor 4 (TLR4). These data suggest that inflammatory mechanisms associated with dysgerminomas are the underlying cause of the increased expression and activity of 1alpha-hydroxylase associated with these tumors. We further postulate that this autocrine/paracrine action of 1alpha-hydroxylase may lead to increased circulating levels of 1,25(OH)2D3 and a form of HHM which is distinct from that seen with PTHrP-secreting tumors.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗
PubMed1995

Transformation of ovarian dysgerminoma to yolk sac tumor: evidence for a histogenetic continuum.

Dysgerminoma has traditionally been considered an end-stage neoplasm without potential for further differentiation. Although there have been several reports of transformation of testicular seminoma to yolk sac tumor, a similar event has not been previously reported in dysgerminoma of the ovary. Three cases of ovarian germ cell tumor (two pure dysgerminomas and one mixed germ cell tumor with dysgerminoma and yolk sac components) that revealed histologic changes compatible with early transformation to yolk sac tumor are described. In general, the areas of transformation were located at the periphery of the tumor lobules which otherwise had features of typical dysgerminoma. They were characterized by the presence of microcysts and small glandular structures, which though not readily identified on H&E became more evident with stains for keratins, alpha-fetoprotein, and blood group-related antigen. The small size and focal nature of change, and the apparent transition favor the interpretation that this change represents transformation rather than admixture of two germ cell components. The relationship of dysgerminoma to the solid variant of yolk sac tumor is discussed and an alternate histogenetic scheme in which dysgerminoma represents the stage of earliest differentiation from which other non dysgerminomatous tumors may arise is presented. Although previously proposed for testicular germ cell neoplasia, this scheme has not yet been applied to their ovarian counterparts.

Adolescent↗
PubMed2003

Genome profiles of bilateral dysgerminomas, a unilateral gonadoblastoma, and a metastasis from a 46, XY phenotypic female.

We present a case report of a 16-year-old, phenotypic female with bilateral dysgerminomas, a unilateral gonadoblastoma, and a peritoneal metastasis. The patient's constitutional karyotype was 46,XY. The chromosomal copy number, examined by the comparative genomic hybridization technique, showed 3 gains in the dysgerminoma of the right ovary, 6 gains in the dysgerminoma of the left ovary, and 2 gains and 1 loss in the gonadoblastoma of the left ovary. The metastasis showed 5 gains of which 4 were also observed in the dysgerminoma of the left ovary. The DNA ploidy classifications of the gonadoblastoma and the dysgerminoma in the right ovary were tetraploid, whereas the dysgerminoma in the left ovary and the metastasis were aneuploid. We therefore propose that the metastasis most probably developed from the dysgerminoma of the left ovary.

Adolescent↗
PubMed1990

Dysgerminoma. The Radiumhemmet series 1927-1984.

Dysgerminoma is a rare, highly radiosensitive, malignant germ cell tumor occurring in young females. At Radiumhemmet, Stockholm, Sweden, from 1927 to 1984, 60 patients with histologically confirmed pure dysgerminoma were treated. Primary treatment was surgery followed by radiotherapy. Recurrences were irradiated. The mean age was 23.2 years. Sixty-seven percent were in International Federation of Gynecology and Obstetrics (FIGO) Stage I, 6% Stage II, 22% Stage III, 3% Stage IV, and 2% were not staged. The median follow-up time was 19 years (range, 1-53). Generally, women with Stage IA disease had unilateral oophorectomy and unilateral external irradiation. Fourteen have borne 22 children after treatment. Seventeen women in the series have died, 11 from dysgerminoma. Actuarial survival, only counting deaths from dysgerminoma, was 83% at 5 years. No patient has died of dysgerminoma since 1963 when radiotherapy with megavoltage x-rays was introduced. The authors consider external irradiation to be an effective treatment as a complement to surgery in dysgerminoma of the ovary.

Adolescent↗
PubMed1999

Late relapse of ovarian dysgerminoma: case report and literature review.

Dysgerminoma of the ovary is a rare tumor. Ovarian dysgerminoma is chemosensitive and potentially curable even when in advanced stage. We report a case of intra-abdominal relapse of stage Ia ovarian dysgerminoma 20 years following initial surgery. The patient was treated with surgical resection followed by a full course of platinum-based chemotherapy. However, she had rapidly progressive disease and eventually died. To date, this is the latest reported case of relapse of ovarian dysgerminoma. This rare situation has been reported in patients with germ cell tumors of the testis, the male counterpart of ovarian germ cell tumors. Testis cancer patients with late relapse are rarely, if ever, curable by chemotherapy. A diagnosis of recurrent dysgerminoma should be considered in patients who have the appropriate findings with a history of dysgerminoma, even if remote. Patients with late recurrences of ovarian germ cell tumors may be less responsive to chemotherapy.

Adult↗
PubMed1995

Differentiation potential of ovarian dysgerminoma: an immunohistochemical study of 15 cases.

An immunohistochemical study of 15 ovarian formalin-fixed, paraffin-embedded dysgerminomas showed positive staining of tumor cells for vimentin in all cases. Ten dysgerminomas stained for cytokeratin 18. Desmin positivity of single tumor cells was detected in four dysgerminomas. Glial fibrillary acidic protein was present in two tumors. Prominent human beta chorionic gonadotropin staining was seen in one tumor. S-100 protein was found in two and carcinoembryonic antigen in one of the dysgerminomas. Placental alkaline phosphatase was present in 12 of the 15 tumors studied. The heterogeneity of the cytoskeletal profile and of other markers showed some similarities to our previously published results on testicular seminomas. Thus, in contrast to previous concepts, dysgerminoma, as is the case with its testicular counterpart the seminoma, appears to be capable of further differentiation, albeit at a primitive level. Our observations also may help to elucidate the relationship between dysgerminoma and other nondysgerminomatous ovarian germ cell tumors, and may be of help in the differential diagnosis with poorly differentiated carcinoma, ovarian lymphoma, or other germ cell tumors.

Biomarkers, Tumor↗
PubMed2006

Chromosome 12p abnormalities in dysgerminoma of the ovary: a FISH analysis.

Dysgerminoma is the most common malignant ovarian germ cell tumor and shares histological and immunophenotypical features with its testicular counterpart, seminoma. Chromosome 12p abnormalities are genetic hallmarks of testicular seminomas. Little is known about these genetic changes in dysgerminoma. We performed dual color fluorescence in situ hybridization (FISH) analyses with a centromeric alpha-satellite probe for chromosome 12 and a subtelomeric probe for 12p on paraffin-embedded tissue sections from 21 dysgerminomas and two gonadoblastomas. Chromosome 12p abnormalities were detected in 81% of dysgerminomas. In all, 57% of cases had only isochromosome 12p and 5% had only 12p overrepresentation. In all, 19% had both isochrome 12p and 12p overrepresentation. Gonadoblastomas were negative for isochromosome 12p or 12p overrepresentation. Chromosome 12p abnormalities are common in dysgerminoma of the ovary. FISH analyses for chromosome 12p abnormalities may be a useful diagnostic adjunct for confirming the diagnosis of dysgerminoma and for distinguishing it from nongerm cell malignancies that enter into the differential diagnosis.

Adolescent↗
PubMed2000

Pure dysgerminoma of the ovary: a review of 45 well staged cases.

PURPOSE: To evaluate the significance of meticulous surgical staging, and whether type of initial surgery or adjuvant therapy impacted on survival in cases of pure ovarian dysgerminoma. METHODS: Retrospective chart review of 45 patients treated for pure ovarian dysgerminoma at a single institute. Survival analysis with the Kaplan Meier and log rank test and the chi-square test for the comparison of categorical variables were used. RESULTS: Of the 45 patients subjected to a surgical staging procedure 30 (67%) had stage I disease, 2 (4%) had stage II, 9 (20%) had stage III, and 4 (9%) had stage IV pure ovarian dysgerminoma. Thirteen of these 45 patients were referred to have seemingly stage I disease. Restaging within 2 months proved stage IIIC disease in 3 (23%) of them. With a median follow-up of 61 months, the overall survival rate for ovarian dysgerminoma in this series was 84%. Significantly lower survival rates were found in patients with advanced stage (stage III-IV) ovarian dysgerminoma (53.9%), when compared with earlier stages (96.9%). Twenty-one patients with unilateral disease and fertility desire were treated with conservative surgery, 19 patients with nonconservative surgery, and in 5 suboptimal debulking could be carried out. As regards recurrence or survival rate, no significant difference was found between patients who were treated conservatively or nonconservatively, whether or not adjuvant chemotherapy or radiotherapy was given. Of the 21 patients treated with conservative surgery, 11 (52%) achieved one or more pregnancies. CONCLUSION: After careful surgical staging and confirming unilateral disease, conservative surgery, followed if necessary by adjuvant chemotherapy, seems to be the ideal treatment in cases of pure ovarian dysgerminoma.

Adolescent↗
PubMed2004

[Ovarian dysgerminoma in children and adolescents. Retrospective clinico-pathologic study].

BACKGROUND: To review the treatment strategy, follow up and outcome for all patients with pure ovarian dysgerminoma treated in childhood and adolescence. METHODS AND RESULTS: Twenty-one patients younger than 18 years were treated between 1979-2002 in Faculty Hospital Motol for newly diagnosed pure ovarian dysgerminoma. Patients were included into the cohort on the basis of revision of archival biopsy specimens deposited in Institute of Pathology and in Molecular Medicine tumor registry. The staging was reviewed retrospectively on the basis of surgical and pathological findings and on results of imaging investigations and outlined according to the TNM and International Federation of Gynecology and Obstetrics (FIGO) classification. The median age at the time of diagnosis was 12.5 years (range 6 years, 5 months--17 years, 11 months). There were ten FIGO stage IA tumors, one stage IB, two of stage IIC, one stage IIIB and seven IIIC tumors. All patients, except two girls with bilateral dysgerminoma, underwent unilateral adnexectomy or ovarectomy. Ten girls were treated postoperatively with chemotherapy, eight with chemotherapy and radiotherapy (eleven with cisplatine based chemotherapy). Three girls with dysgerminoma confined to the ovary (stage IA) have not received adjuvant chemotherapy. With a median follow up 7.1 years all girls remained continuously disease free. The 5-year overall and event free survival is 100%. Majority of patients does not have severe treatment sequelae, three pregnancies have occurred so far. CONCLUSIONS: Most patients with dysgerminoma, including those with metastases can expect cure when treated with conservative surgery and cisplatine based chemotherapy. Reduction of treatment toxicity and preservation of reproductive function is a main task. The girls with dysgerminoma confined to the ovary (stage IA) can be treated with fertility sparing surgery, other should be treated with cisplatine based chemotherapy.

Adolescent↗