Biomedical subjects
Publications and source records attributed to Joachim Baehring.
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The emergence of temozolomide as an effective alkylating agent with little acute toxicity or cumulative myelosuppression has led to protracted courses of chemotherapy for many patients with gliomas. Secondary, or treatment-related, myelodysplasia (t-MDS) and acute myelogenous leukemia (t-AML) are life-threatening complications of alkylating chemotherapy and have been reported in patients with primary brain tumors. We describe a case of temozolomide-related t-MDS/AML and discuss the clinical features of this condition. Administration of an alkylating agent in patient populations with long median survivals must be undertaken with an understanding of the potential for this treatment complication.
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Amyloidoma can occur within the brain parenchyma. Periventricular amyloidomas developed in a man aged 69 years as gadolinium-enhancing lesions on magnetic resonance imaging. The lesions were composed of amyloid AL lambda with congophilia resistant to potassium permanganate. There was no evidence of systemic amyloidosis or an underlying inflammatory or neoplastic disorder.
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OBJECTIVE AND IMPORTANCE: We report a rare complication after resection of a recurrent intracranial nongerminomatous germ cell tumor in an adult. The growing teratoma syndrome, as originally described with pediatric germ cell neoplasms, represents tumor recurrence, often cystic, that sometimes is observed after partial response to multimodality therapy and despite decreasing tumor serum markers. The enlarging tumor consists of elements of a mature teratoma that presumably are refractory to chemotherapy or radiation. To our knowledge, this is only the third case of the growing teratoma syndrome in an adult patient with nongerminomatous germ cell tumor. CLINICAL PRESENTATION: A 26-year-old man had signs of recurrent obstructive hydrocephalus 6 months after multimodality treatment of a diencephalic yolk sac tumor and endoscopic third ventriculostomy. Imaging studies revealed large multilocular cystic masses originating from the tumor bed and partially obstructing the ventriculostomy. INTERVENTION: Near total tumor resection and fenestration was performed. Histopathological analysis demonstrated a mature teratoma. CONCLUSION: Surgical resection, if feasible, is the treatment of choice for the growing teratoma syndrome to establish the correct diagnosis and prevent complications.
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Women predisposed to hereditary nonpolyposis colorectal cancer are at high risk of developing endometrial carcinoma at a young age. Hereditary nonpolyposis colorectal cancer-associated endometrial carcinomas are of the endometrioid type, usually arise from complex atypical hyperplasia, and often show microsatellite instability. To identify occult hereditary nonpolyposis colorectal cancer individuals among endometrial carcinoma patients, we examined complex atypical hyperplasias and endometrial carcinomas of 60 women < or =50 years of age (mean age: 35.7 years) using microsatellite instability, immunohistochemistry, and DNA sequence analysis. Three patient groups were recruited: group 1, patients with complex atypical hyperplasia exclusively (n = 27); group 2, patients with complex atypical hyperplasia and synchronous or metachronous endometrial carcinoma (n = 15); group 3, patients with endometrial carcinoma only (n = 18). Overall, 13 of 33 endometrial carcinomas (39%) displayed high-level microsatellite instability. None of the complex atypical hyperplasias in group 1 had high-level microsatellite instability or loss of hMLH1/hMSH2 protein expression. In group 2 patients, 33% of complex atypical hyperplasias and 53% of endometrial carcinomas had high-level microsatellite instability. Loss of hMSH2 protein expression was found in six endometrial carcinoma patients, five of them with verified hMSH2 germline mutations, including four patients with high-level microsatellite instability in complex atypical hyperplasia. Among group 3 patients, 28% of endometrial carcinomas displayed high-level microsatellite instability; three of those five endometrial carcinomas were from patients with multiple extrauterine hereditary nonpolyposis colorectal cancer-associated tumors. We conclude that young women (< or =50 years of age) with concurrent complex atypical hyperplasia and multiple hereditary nonpolyposis colorectal cancer-associated carcinomas are at risk of developing high-level microsatellite instability endometrial carcinoma. Combined microsatellite instability and immunohistochemistry analysis allows the identification of a high proportion of hereditary nonpolyposis colorectal cancer patients among young women with endometrial carcinoma and complex atypical hyperplasia. All complex atypical hyperplasias with high-level microsatellite instability progressed to endometrial carcinoma. Only one third of the complex atypical hyperplasias with microsatellite stability progressed to high-level microsatellite instability endometrial carcinoma, while seven complex atypical hyperplasias progressed to microsatellite stability endometrial carcinoma. Microsatellite analysis of complex atypical hyperplasia in young patients may therefore be a useful prognostic marker for predicting possible progression to high-level microsatellite instability endometrial carcinomas.
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We present two cases of focal, tumefactive, masslike lesions of diffuse cerebral amyloid angiopathy (CAA) that presented as areas of increased signal intensity on long TR sequences without contrast enhancement or restricted diffusion. MR spectroscopy revealed normal metabolite ratios and unremarkable spectra. Pathologic tissue showed CAA and CAA with angitis of the CNS. Tumefactive CAA is a rare condition, and we describe its characteristics at MR spectroscopy and diffusion-weighted imaging.