ABSTRACT
OBJECTIVE: To present a rare case of malignant struma ovarii (MSO) and synchronous thyroid cancer, review the medical literature, and present the latest trends in management. METHODS: The case of a woman with MSO and concomitant thyroid cancer is presented, including clinical presentation, treatment, and follow-up care. A search of the English-language literature was conducted using MEDLINE and Google Scholar data bases. RESULTS: We found 10 publications (one abstract) describing 10 patients with MSO and concomitant thyroid cancer. Six additional patients were reported by a study that analyzed the SEER (cancer registry) database. The median age of women was 42 years, with the majority of them presenting with abdominal symptoms. Histologically, most tumors were papillary carcinomas in both organs. In 5 patients, there was extrathyroidal tumor extension at time of surgery. CONCLUSION: MSO can occasionally coexist with highly aggressive eutopic thyroid cancer. Although this concurrence is even rarer than MSO, clinicians should routinely investigate for possible synchronous thyroid cancer in all cases of MSO and also consider aggressive postoperative treatment including thyroidectomy and radioiodine ablation therapy in cases of MSO.
ABSTRACT
BACKGROUND AND AIMS: Sweet's syndrome or acute febrile neutrophilic dermatosis is characterized by fever, leukocytosis and tender erythematous plaques, which show infiltration by mature neutrophils on histological examination. Pulmonary involvement is rare in Sweet's syndrome. METHOD: We describe the case of a 17-year-old man with a myelodysplastic syndrome following therapy for Hodgkin's lymphoma who developed Sweet's syndrome and cryptogenic organizing pneumonia. In addition, we conducted a review of the related English literature. RESULTS: Literature review yielded six similar reports of biopsy-proven cryptogenic organizing pneumonia associated with Sweet's syndrome. We present the clinical and laboratory characteristics, as well as the response to treatment, of all cases of cryptogenic organizing pneumonia reported in patients with Sweet's syndrome. CONCLUSIONS: Cryptogenic organizing pneumonia is a rare manifestation of Sweet's syndrome, which may be complicated by respiratory failure. Prompt treatment with corticosteroids usually leads to clinical and radiographic improvement.
Subject(s)
Adrenal Cortex Hormones/administration & dosage , Cryptogenic Organizing Pneumonia/diagnosis , Methylprednisolone/administration & dosage , Sweet Syndrome/diagnosis , Administration, Intravenous , Adolescent , Adrenal Cortex Hormones/therapeutic use , Cryptogenic Organizing Pneumonia/drug therapy , Cryptogenic Organizing Pneumonia/etiology , Hodgkin Disease/complications , Hodgkin Disease/drug therapy , Humans , Male , Methylprednisolone/therapeutic use , Myelodysplastic Syndromes/complications , Myelodysplastic Syndromes/drug therapy , Sweet Syndrome/drug therapy , Sweet Syndrome/etiology , Treatment OutcomeABSTRACT
The expression, cellular distribution, and subcellular sorting of the microtubule (MT)-nucleating γ-tubulin small complex (γTuSC) proteins, GCP2 and GCP3, were studied in human glioblastoma cell lines and in clinical tissue samples representing all histologic grades of adult diffuse astrocytic gliomas (n = 54). Quantitative real-time polymerase chain reaction revealed a significant increase in the expression of GCP2 and GCP3 transcripts in glioblastoma cells versus normal human astrocytes; these were associated with higher amounts of both γTuSC proteins. GCP2 and GCP3 were concentrated in the centrosomes in interphase glioblastoma cells, but punctate and diffuse localizations were also detected in the cytosol and nuclei/nucleoli. Nucleolar localization was fixation dependent. GCP2 and GCP3 formed complexes with γ-tubulin in the nucleoli as confirmed by reciprocal immunoprecipitation experiments and immunoelectron microscopy. GCP2 and GCP3 depletion caused accumulation of cells in G2/M and mitotic delay but did not affect nucleolar integrity. Overexpression of GCP2 antagonized the inhibitory effect of the CDK5 regulatory subunit-associated tumor suppressor protein 3 (C53) on DNA damage G2/M checkpoint activity. Tumor cell GCP2 and GCP3 immunoreactivity was significantly increased over that in normal brains in glioblastoma samples; it was also associated with microvascular proliferation. These findings suggest that γTuSC protein dysregulation in glioblastomas may be linked to altered transcriptional checkpoint activity or interaction with signaling pathways associated with a malignant phenotype.
