Gamma-ray multiplicity distribution associated with massive transfer.
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Biomedical subjects
Publications and source records attributed to T Inamura.
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Deficient repair of nucleotide mismatches in the genome is considered a major factor in tumorigenesis. Such deficiency is evidenced by alterations in dinucleotide repeats of microsatellite sequences, specifically microsatellite instability (MSI) or replication errors. We investigated the frequency of MSI in human gliomas in terms of patient outcome. Frequency of MSI was estimated by examining five loci on chromosomes 2, 5, 10, 11, and 13 in 31 gliomas using high-resolution fluorescent microsatellite analysis. MSI was found at all loci in only 2 malignant gliomas (6.5%). MSI was detected at the D10S197 locus in 3 of 11 glioblastomas (27.2%) and 4 of 8 anaplastic astrocytomas (50%), while no MSI was detected in low-grade gliomas. Among patients with anaplastic astrocytoma, the 4 with MSI at D10S197 died from local recurrence less than 18 months after surgery, while 3 of the patients without MSI survived for more than 20 months. MSI at D10S197 may be a prognostic marker for patients with anaplastic astrocytomas.
PURPOSE: Central nervous system (CNS)-T cell lymphoproliferative disorder (T-LPD) developing during the course of chronic active Epstein-Barr virus (CAEBV) infection is reported. PATIENTS AND METHODS: CAEBV was diagnosed in a 14-month-old boy with fever, cytopenia, hepatosplenomegaly, and abnormal high titers of anti-Epstein-Barr virus (EBV) antibodies. At 8 years of age, he had a splenectomy because of progressive disease. RESULTS: After 27 months of clinical remission, muscle weakness and paresthesia developed. Magnetic resonance imaging of his brain showed spotty T2 prolongation in left parietal, bilateral frontal, and temporal white matter with meningeal enhancement. Brain biopsy revealed the cerebral infiltration of CD3+, CD4+, CD8-, CD45RO+, CD56-, and EBV-encoded RNA 1+ cells. CONCLUSIONS: The CNS involvement of EBV-associated T-LPD is a rare but serious complication in CAEBV without known underlying immunodeficiency.
An autopsy case of primary choroid plexus adenocarcinoma arising in a 40-year-old female, who was associated with a high serum level of a carbohydrate antigen 19-9 (CA19-9), is herein presented. After a subtotal removal of a tumor in the left lateral ventricle, the serum level of CA19-9 decreased rapidly, and immunohistochemical examinations of tumor tissue specimens obtained at surgery revealed intense reactivity for CA19-9. The present case may be the first example in which a primary choroid plexus carcinoma was shown to produce CA19-9.
BACKGROUND: Malignant glioma remains a fatal disease. Continuous or frequent low-dose (FLD) chemotherapy with nitrosoureas reportedly causes fewer side-effects than single-bolus therapy without decreasing the antitumour effects. MATERIALS AND METHODS: To study the effect of FLD treatment with nimustine (ACNU) in rats with glioma, we intracerebrally inoculated with C6 glioma cells. We began the ACNU treatment 5 or 8 days later (total dose, 25 or 40 mg/kg) i.p. as either one bolus or smaller doses spread over 5 days week. RESULTS: At a total dose of 25 mg/kg beginning at day 8, survival duration did not differ between untreated controls and the FLD group, while the bolus significantly prolonged survival; the FLD group showed some improvement beyond control survival at 40 mg/kg (each p <0.001). Beginning treatment after 5 rather than 8 days prolonged survival somewhat further. CONCLUSION: FLD treatment with ACNU is less effective against experimental glioma in rats than bolus treatment.
OBJECTIVE: We describe a 29-year-old man with gliosarcoma in the lateral ventricle. CASE: The patient presented with headache and impairment of consciousness. Computed tomography and magnetic resonance imaging localized the tumor to the right lateral ventricle and showed heterogeneous enhancement with administration of contrast agents. The tumor was partially removed via a transcallosal approach. Histologic examination disclosed gliosarcoma arising by malignant transformation of an ependymoma. POST-OPERATIVE COURSE: The patient died of tumor progression 78 days after admission, despite intensive radiotherapy and chemotherapy.