Cases reported "Carcinoma"

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1/75. Progression of a Nelson's adenoma to pituitary carcinoma; a case report and review of the literature.

    A 25-year-old woman developed Nelson's syndrome, 3 years after successful bilateral adrenalectomy for Cushing's disease. Despite pituitary surgery and radiotherapy the tumour showed invasive growth, leading to visual disturbance, paresis of the oculomotor nerve and, 34 years after adrenalectomy, to death by widespread purulent leptomeningitis. autopsy revealed a large adenohypophyseal carcinoma with a metastasis attached to the dura, both tumours showing immunocytochemical staining for ACTH and TSH. We review the literature on metastatic adenohypophyseal carcinoma in Cushing's disease and Nelson's syndrome and discuss the role of proliferation markers as indicators of malignant progression.
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2/75. The use of paclitaxel and cisplatin in a patient with epithelial ovarian cancer and human immunodeficiency virus.

    OBJECTIVE: Several spots exist of human immunodeficiency virus (hiv)-positive patients developing epithelial ovarian cancer. The optimal chemotherapeutic regimen has been unclear due to potential immunotoxicity from chemotherapy in these already immunocompromised patients. This is the first report of paclitaxel-based combination chemotherapy in an hiv-positive patient with ovarian cancer. METHOD: A 39-year-old woman with hiv was diagnosed with poorly differentiated serous carcinoma. She underwent optimal cytoreductive surgery and received six courses of paclitaxel and cisplatin. RESULTS: The patient experienced a complete clinical response to therapy with no adverse effect on surrogate markers for human immunodeficiency virus (CD4 count, beta2 microglobulin, neopterin, p24 antigen, and viral load). CONCLUSION: paclitaxel- and platinum-based chemotherapy, the standard of care for adjuvant chemotherapy in advanced ovarian carcinoma, is appropriate therapy for ovarian cancer patients with hiv. There is no evidence that the paclitaxel/cisplatin regimen is associated with progression of hiv or increased chemotherapy-associated morbidity.
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3/75. Sarcomatoid carcinoma of the prostate: progression from adenocarcinoma is associated with p53 over-expression.

    BACKGROUND: The pathogenesis of sarcomatoid metaplasia of prostatic adenocarcinoma is uncertain. The histologic features of sarcomatoid carcinoma arising in two patients with previously irradiated prostatic adenocarcinoma are reported and the relationship between prostatic adenocarcinoma and subsequent sarcomatoid carcinoma is investigated by immunohistochemical detection of epithelial and soft tissue tumor markers, and p53 protein. methods AND RESULTS: Two patients, aged 72 and 67 years, underwent localized radiotherapy for prostatic adenocarcinoma and re-presented with sarcomatoid carcinoma 41 months and 60 months later, respectively. In both cases the tumor consisted of anaplastic spindle cells with occasional osteoclast-like giant cells. The initial tumors showed immunohistochemical staining typical of prostatic adenocarcinoma with absence of expression of p53 protein. The subsequent sarcomatoid carcinomas were positive for vimentin and negative for epithelial cell markers. In both cases serial biopsies showed a temporal increase in tumor expression of p53 protein. CONCLUSIONS: The development of sarcomatoid carcinoma in prostatic adenocarcinoma is associated with progressive accumulation of p53. This is suggestive of increasing clonal dominance of dedifferentiated tumor cells carrying p53 mutations.
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4/75. Morphometric evaluation of paraneoplastic neuropathies associated with carcinomas, lymphomas, and dysproteinemias.

    Paraneoplastic peripheral neuropathies are caused by indirect effects of carcinomas, mainly small cell bronchogenic carcinomas, lymphoproliferative disorders (lymphomas, myelomas, polycythemia vera), and dysproteinemias (benign monoclonal paraproteinemia, Waldenstrom's macroglobulinemia) including cryoglobulinemias. Those associated with carcinomas are usually considered as severe, those associated with benign gammopathies (monoclonal gammopathies of unknown significance, MGUS) as mild, and those with cryoglobulinemias as of variable severity. In a larger series of 104 autopsy and biopsy cases, we noted a wide range of severity concerning various morphometric parameters of peripheral nerve fibers by evaluating sural nerves. There were no apparent morphometric differences between the groups of disorders. The most valuable parameter of optic-electronic evaluation and comparison turned out to be the myelin area expressed as a percentage of the endoneurial area because this measure comprises the relative number, size, and myelin thickness of the myelinated nerve fibers. In the 104 cases of the three disease groups, most of the cases (38 cases; 36.5%) showed a moderate reduction of the myelin sheath area per endoneurial area of sural nerves. This was followed by 34 cases (32.7%) with severe and very severe reduction. Twenty-nine cases (27.9%) presented with mild reduction. It is concluded that the severity of the neuropathy depends largely on the stage of the disease and the time of progression rather than on the type of the underlying disorder.
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5/75. Analysis of the genetic alterations in a case of juvenile multiple colon carcinoma with hypogammaglobulinemia.

    BACKGROUND: We have previously reported the clinical characterization of a case of juvenile multiple colorectal carcinoma with hypogammaglobulinemia. Several recent studies have determined that agammaglobulinemia was caused by the loss of Bruton's tyrosine kinase (Btk) function. However, any genetic alterations associated with carcinoma formation in individuals with this immunodeficient disease have not been reported. methods: dna from eight carcinoma tissues and nine adenoma tissues from this reported case were examined for mutations in p53 by single strand conformation polymorphism analysis, K-ras by mutant allele specific analysis, and replication error or loss of heterozygosity of the TP53 locus on chromosome #17. RESULTS: We found that p53 and K-ras were mutated in the carcinoma tissues. However, each tumor showed unequal and diverse results. CONCLUSIONS: The progression of individual tumor was not due to a common genetic event caused directly under the influence of the primary disease at the genetic level.
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6/75. Clinical management of a case of recurrent apocrine gland carcinoma of the scalp: efficacy of a chemotherapy schedule with methotrexate and bleomycin.

    Apocrine carcinoma of the skin is a rare tumor. Wide surgical excision with complete removal of the neoplasm is the standard therapy and this appears to offer the best chance of cure. radiotherapy may be used in case of local relapse or regional lymph node involvement. Systemic chemotherapy has not proved to be effective in the treatment of this tumor. We report on a 46-year-old woman with a recurrent apocrine carcinoma of the scalp that had previously been treated with surgery, radiotherapy and chemotherapy (Al-Saraff schedule). The patient was responsive to a second-line systemic chemotherapy regimen consisting of a weekly combination of methotrexate and bleomycin, and achieved long-term progression-free survival.
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7/75. Chromosomal imbalances in gastric cancer. Correlation with histologic subtypes and tumor progression.

    dna copy number changes were analyzed by comparative genomic hybridization (CGH) in 38 gastric carcinomas and correlated with tumor histologic type and progression. Gains of copy numbers were observed in all tumors, affecting all chromosomes except chromosome 16. The average number of copy number gains was 7 (range, 1-13), most frequently located on chromosomes 11, 12, 15, 17, and 20 in 45% to 97% of tumors. High-level amplifications were found on chromosomes 12, 15, 17, and 20; the latter was affected most frequently (66%). Loss of dna copy numbers was detected in 14 tumors affecting 7 chromosomes. No statistically significant differences in the frequency and pattern of chromosomal imbalances were observed in tumor histologic type (Lauren classification) and grade of differentiation, as well as the prognostic parameters depth of invasion (pT) and lymph node involvement (pN). Our results indicate that in gastric cancer there is no specific recurrent pattern of dna aberrations to be correlated with tumor histologic type or stage. However, CGH analysis could reveal new, recurrent genetic changes in gastric cancer affecting chromosomes sites that harbor genes known to participate in tumorigenesis and progression of several human malignant neoplasms.
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8/75. Chromosomal aberrations in pituitary carcinoma metastases.

    Four pituitary carcinoma metastases [two adrenocorticotropic hormone (ACTH) and prolactin cell tumors each] were studied by comparative genomic hybridization. Chromosomal gains were found in all four carcinoma metastases, but losses only in the two prolactin cell carcinoma metastases. overall, pituitary carcinoma metastases showed an average of 8.3 chromosomal imbalances per tumor (7 gains vs 1.3 losses), 10 in prolactin cell carcinoma metastases (7.5 gains vs 2.5 losses) and 6.5 in ACTH cell carcinoma metastases (6.5 gains vs 0 loss). The most common changes were gains of chromosome 5, 7p, and 14q (in three tumors each). High-level gains were found on 13q22-qter and 14q (two cases each) and on 1q, 3p, 7, 8, 9p, and 21q (one case each). To date, gains of chromosome 14q have not been reported among pituitary tumors. It remains to be shown whether gain of 14q is associated with malignant progression and metastatic dissemination of pituitary carcinomas.
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9/75. Paucicellular variant of anaplastic thyroid carcinoma: report of two cases.

    The paucicellular variant of anaplastic carcinoma is an infrequent type of thyroid tumor. It was described as a tumor characterized by very low cellularity and prominent fibrosis, probably secondary to extensive infarction. These features could lead to an erroneous diagnosis of Riedel's thyroiditis. In this paper, we report the clinical and pathological features of two new cases of this unusual entity. Tumor cells were negative for thyroglobulin immunostaining and positive for keratins and p53. Although the number of reported cases is small, the cumulative data on these two cases and the previously reported ones lead us to suggest that the paucicellular variant may occur in younger patients than the conventional anaplastic thyroid carcinoma and that the tumor may be associated with a less aggressive tendency to local progression and metastasis.
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10/75. Unusual case of metastatic thyroid nodule: nonpalpable breast mass as origin.

    OBJECTIVE: To document a case of thyroid cancer metastatic from the breast. methods: We present the clinical, laboratory, radiologic, and biopsy findings in our patient and review the related literature. RESULTS: A 47-year-old female patient was referred to our clinic because of dyspnea and generalized bone pain. physical examination revealed a diffusely enlarged nodular goiter, and fine-needle aspiration biopsy demonstrated intrathyroidal anaplastic cells. Total thyroidectomy was done, and the histopathologic diagnosis was anaplastic carcinoma. Unexpected rapid progression of the disease with cervical and intrathoracic lymphadenopathies and osteoblastic metastatic lesions without radioiodine uptake prompted us to attempt to rule out a primary nonthyroidal malignant lesion metastatic to the thyroid gland. The plasma level of CA 15-3 was profoundly increased (388 U/mL). Detailed reassessment of the patient disclosed a small mass in the right mammary gland with histopathologic features similar to those of the thyroidectomy material. Reevaluation of the thyroid specimens resulted in a final diagnosis of primary breast carcinoma in conjunction with metastatic carcinoma of the thyroid. CONCLUSION: Thorough systemic clinical assessment of a patient with a thyroid nodule and careful study of biopsy specimens should be done to ascertain whether the nodule is a primary or a metastatic lesion.
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