Cases reported "Ovarian Neoplasms"

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1/14. Bilateral calcified ovarian fibromas in a patient with sotos syndrome.

    OBJECTIVE: To present a case of bilateral calcified ovarian fibromas in sotos syndrome (cerebral gigantism). DESIGN: Descriptive case study. SETTING: Mackay Memorial Hospital. PATIENT(S): A 26-year-old woman with sotos syndrome and bilateral solid adnexal masses on gynecologic ultrasound. INTERVENTION(S): Surgical removal of an 8 x 6 x 6 cm left ovarian fibroma and a 3 x 2 x 2 cm right ovarian fibroma. MAIN OUTCOME MEASURE(S): Ultrasound. RESULT(S): Histopathologic examination revealed bilateral ovarian fibromas with extensive foci of calcification and occasional ossification. CONCLUSION(S): The presence of bilateral calcified ovarian fibromas in this patient with sotos syndrome may reflect the effects of overgrowth in sotos syndrome on ovarian tumorigenesis or may be a coincidence.
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keywords = tumorigenesis
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2/14. Uterine tumor resembling ovarian sex cord tumor: report of a case with t(X;6)(p22.3;q23.1) and t(4;18)(q21.1;q21.3).

    Uterine tumor resembling ovarian sex cord tumor (UTROSCT) is a rare tumor of reproductive-age and postmenopausal women. We present the first case of UTROSCT with cytogenetic analysis. The tumor occurred in a 34-year-old woman who presented with menorrhagia and a uterine mass. Histologic examination showed tumor with features of sex cord-like epithelium and abundant fibromuscular stroma without an endometrial stromal sarcoma component. The tumor cells expressed cytokeratin, CD99, vimentin, desmin, smooth muscle actin, and estrogen and progesterone receptors. The majority of the cells analyzed by cytogenetic studies showed two balanced chromosomal translocations: t(X;6)(p22.3;q23.1) and t(4;18)(q21.1;q21.3). Several known tumor-related genes (bcl-2, MALT-1, FVT1, SCCA1, SCCA2, and DCC at 18q21; RAP1 at 4q21; and STL at 6q23) and a gonadal-development related gene (H-Y regulator gene at Xp22.3) are located at or near the translocation breakpoints. The tumor cells of sex cord-like elements were strongly and diffusely immunoreactive for bcl-2 antibody. These cytogenetic and immunohistochemical data may suggest potential molecular mechanisms of tumorigenesis of UTROSCT.
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keywords = tumorigenesis
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3/14. trisomy 12 and 4 in a thecoma of the ovary.

    cytogenetic analysis of short-term tissue culture from a thecoma of the ovary demonstrated the presence of trisomies of chromosomes 12 and 4 in all analyzed cells. Our finding confirms the consistency with which trisomy 12 is observed in benign sex cord/stromal tumors and suggests that trisomy 4 may be a second event in tumorigenesis of thecoma.
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keywords = tumorigenesis
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4/14. Genetic analysis of radiation-associated rectal cancer.

    Genetic aberrations in radiation-associated colorectal cancer have not been studied in detail. We analyzed genetic aberrations in five rectal cancers that developed long after radiotherapy had been performed for cervical cancer. microsatellite instability (MSI) in tumors was examined at five loci: D2S123, D3S966, TP53, DCC, and BAT26. mutation of simple repeat sequences within the hMSH3, BAX, and transforming growth factor beta type II receptor ( TGFBetaRII) genes was examined by polymerase chain reaction and single-strand conformation polymorphism (PCR-SSCP). mutation of p53 exons 5-8 was examined by PCR-SSP and direct sequencing. Mutations of the K- ras gene were analyzed by two-step PCR. No MSI was found in tumor specimens at any of the loci examined, and no mutations in the target genes were observed. K- ras mutation was detected in two carcinomas, but not in their irradiated normal mucosa, while p53 mutation was observed in another two carcinomas, but not in their irradiated normal mucosa. Our results suggest that the radiation-associated rectal carcinomas examined in this study did not develop through the mutator phenotype pathway; rather, tumorigenesis was probably mediated through the multistep carcinogenesis pathway.
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keywords = tumorigenesis
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5/14. Analysis of chromosome abnormalities by comparative genomic hybridization in malignant peripheral primitive neuroectodermal tumor of the ovary.

    OBJECTIVE: Malignant primitive neuroectodermal tumor (PNET) originating from the ovary rather than from the central nervous system is extremely rare. The aim of this study is to demonstrate the chromosomal abnormalities in a case of peripheral primitive neuroectodermal tumor (PPNET) arising from the ovary of a girl. methods: The 13-year-old girl underwent exploratory laparotomy because of a huge pelvic tumor in lower abdomen and pelvis. She underwent removal of ovaries, tubes, omentum, peritoneal nodules, and portion of urinary bladder. Tumor specimens were sent for pathology, short-term tissue culture, and for storage in deep freezer for laboratory studies. Immunohistochemical stainings of the tumor with antibodies against O-13 (MIC/CD99), NSE, GFAP, S-100, cytokeratin AE1/AE3, desmin, NF, and AFP were performed. Short-term cell culture of fresh tumor was done for analysis of chromosomal aberrations by the technique of comparative genomic hybridization (CGH). names of specific genes corresponding to the losses or gains on gene map loci were identified from OMIM (Online Mendelian Inheritance in Man) of the NCBI website,. The overexpressions of N-myc and EGFR as well as underexpressions of Rb and ARHI were detected by RT-PCR analysis. The patient expired 17 months later despite of chemotherapy, repeated surgery, and radiation therapy. RESULT: The histopathology of the specimens revealed malignant neuroectodermal tumor, involving ovaries, tubes, bladder, omentum, and peritoneum. Immunohistochemical stainings of PPNET of the ovary showed positive reaction for O-13 (MIC2/CD99) and NSE, but negative for GFAP, S-100, cytokeratin AE1/AE3, desmin, NF, and AFP. Analysis of CGH revealed multiple chromosomal abnormalities including losses of chromosomes in 1p, 1q, 4q, 6p, 6q, 7q, 8q, 13q, and 19q; as well as gains of chromosomes in 1q, 2p, 7p, 9q, 18q, and Xq. Losses of 13q14.1-q14.2, 1p31, and 4q34-q35 indicated that Rb gene, ARHI, and FAT were deleted. Gains of 2p24.1, 1q23, and 7p12.3-p12.1 demonstrated that N-myc oncogene, FASL, GITRL, and EGFR were amplified. RT-PCR analysis showed that N-myc and EGFR were overexpressed, while Rb and ARHI were underexpressed. CONCLUSIONS: This report is the first to show multiple chromosomal aberrations in PPENT arising from the ovary. The deletions of Rb, ARHI, and FAT, as well as amplification of N-myc, FASL, GITRL, and EGFR, may be the crucial factors for tumorigenesis and the aggressive biological behavior of PPNET.
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keywords = tumorigenesis
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6/14. Thyrotoxic adenoma followed by atypical hyperthyroidism due to struma ovarii: clinical and genetic studies.

    OBJECTIVE: Atypical forms of hyperthyroidism represent a diagnostic challenge for clinicians. struma ovarii is an ovarian teratoma and constitutes a rare cause of ectopic thyroidal hormonal production. We describe a case of struma ovarii that combined two different sources of hyperthyroidism in the same patient and report genetic studies in order to contribute a better understanding of the autonomy and tumorigenesis of the struma ovarii. CASE REPORT: A 73-year-old nulliparous woman presented a thyroid toxic adenoma that was successfully treated with 10 mCi radioiodine. Unexpectedly, a new onset of hyperthyroidism prompted us to look for a second etiology. A whole-body scan with (123)I detected a pelvic hyperfixation suggesting struma ovarii, and a thyroid differentiated left ovarian teratoma 3 cm in size was surgically removed. We screened for mutations of thyroid-stimulating hormone receptor and Gs-alpha protein genes, as these mutations are common in thyroid adenomas. We did not identify any mutations. Androgen receptor study demonstrated a monoclonal status. comparative genomic hybridization did not reveal any chromosomal abnormality. However, loss of heterozygosity analysis showed several structural abnormalities, compared with the majority of benign ovarian teratomas, which show a normal karyotype. CONCLUSIONS: This is the first well-documented report of thyrotoxic struma ovarii revealed after treatment of a single thyroid toxic adenoma. We have shown in this case that struma ovarii originates from a single germ cell, and, albeit benign, this tumor presents several chromosomal abnormalities. struma ovarii-induced hyperthyroidism is likely to be mediated by mechanisms different from those of the classical thyroid toxic adenoma.
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keywords = tumorigenesis
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7/14. Familial dysgerminoma associated with 46, XX pure gonadal dysgenesis.

    Although the occurrence of pure gonadal dysgenesis PGD is usually sporadic and nonfamilial, here we present 3 sisters with 46, XX PGD, who are born from a first cousin marriage. review of their family pedigree is compatible with autosomal recessive inheritance. Surprisingly, 2 of these sisters developed ovarian tumors. Both showed the pathological result of dysgerminoma with syncytiotrophoblastic giant cells. These 2 cases are examples of tumorigenesis in PGD without an identifiable y chromosome. Therefore, malignant degeneration of the streak gonads should be considered in the patients with 46, XX PGD.
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ranking = 1
keywords = tumorigenesis
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8/14. Epithelial ovarian carcinoma in patients with intersex disorders: the role of pituitary gonadotropins in ovarian tumorigenesis.

    The common epithelial tumors of the human ovary have rarely been found in the gonads of intersex patients with gonadal dysgenesis or true hermaphroditism. This report describes a patient with ovarian serous cystadenocarcinoma and mixed gonadal dysgenesis (45,X/46,XY) and reviews other reported cases. Intersex patients require early evaluation with treatment based on the karyotypic risk of malignant gonadal transformation. Epithelial ovarian tumors arising in dysgenetic gonads, which lack ova and are incapable of ovulating, provide a unique model for understanding the role of pituitary gonadotropins in ovarian epithelial tumorigenesis.
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ranking = 5
keywords = tumorigenesis
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9/14. Multifocal tumorigenesis in the upper female genital tract--implications for staging and management.

    A review of 128 cases of "primary" ovarian mullerian carcinoma treated at the King George V Memorial Hospital was undertaken to determine the relative frequency with which such tumors were associated with evidence of multifocal primary neoplasia. Of the 128 cases studied, 115 were invasive carcinomas and 13 were noninvasive or borderline ovarian tumors ("tumors of low malignant potential"). Eight of 10 borderline serous ovarian tumors (80%) and 37 of 75 invasive serous carcinomas (49%) exhibited evidence of independent primary neoplasia at more than one anatomical site in the biopsy material available for review. Many of these cases represented bilateral primary ovarian tumors, but autochthonous extraovarian neoplasia was also commonly encountered. A single borderline endometrioid ovarian tumor and six of 15 endometrioid carcinomas (40%) were associated with biopsy-proven multifocal primary tumorigenesis. These were predominantly neoplasms in one or both ovaries plus adenocarcinoma in the uterine corpus. Other histological types of malignant common epithelial tumors of the ovaries did not demonstrate any such tendency, highlighting major differences in pathogenesis between members of this loosely associated group of ovarian cancers. Our study suggests that gynecological endometrioid and serous malignancies are commonly multifocal and we feel this has significant implications for the way these neoplasms are staged and therefore treated.
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ranking = 5
keywords = tumorigenesis
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10/14. Adnexal tumor and a pigmented nevoid lesion in a benign cystic ovarian teratoma.

    We describe a case of an unusual adnexal lesion and concurrent collections of dendritic melanocytes of the type occurring in a blue nevus in a mature cystic teratoma of the ovary. To our knowledge, there have been no previous reports of benign skin adnexal tumors in an ovarian dermoid cyst. This rarity would indicate that the cutaneous adnexal tissue in a benign teratoma is not unduly prone to undergo further more-specialized secondary tumorigenesis. The combination of the three benign lesions is therefore probably purely coincidental.
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keywords = tumorigenesis
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