Meningiomas are one of the most frequently encountered brain tumors. They usually grow slowly with long asymptomatic phase and may remain silent until death. There are several issues about the treatment of meningioma. One is the treatment of asymptomaticm eningiomas. C linicalr eports revealed that only minorityo f them became symptomatic. As the operative morbidity of patients with asymptomatic meningiomas is not low, it is advisable to follow up the patients before treatment. The second is the treatment of aggressive meningiomas. Under the new WHO classification, t umors that are classified to atypical meningiomas have changed and increased. We have to reconsider the strategy to these tumors because the results of old clinical studies may not be applicable to them. However, we do not have effective methods to treat aggressive meningiomas other than surgery and radiation therapy, yet.

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Currently only microscopical examinations are insuffcient for histologic classification and grading of gliomas. In recognition of the emerging role of molecula dr iagnostic approaches to glioma classification g, enetic profiles have been emphasized, as in the distinct subtypes of glioma. Glioblastomas (WHO grade IV) may develop de novo (primary glioblastomas) or through progression from lower-grade astrocytomas (secondary glioblastomas), but bothg lioblastoma sshow similar histologica fleatures. In contrast, these subtypes of glioblastom caonstitute distinct disease entities that evolve through different genetic pathways, and are likely to differ in prognosis and response to therapy. Oligodendroglioma is recognized as a particular subtype of gliomas that shows remarkable response to chemotherapy m, aking their correct diagnosis important H. owever h, istologica dlifferentiatio onf oligodendrogliomas from diffuse astrocytoma could be highly subjective in cases without typical morphological features. Although primary central nervous system lymphoma (PCNSL) and non-CNS lymphoma also show similar histologica fleatures, it is very important to discriminate primary tumors or metastatic tumors. This article suggests that more biological and molecular approaches to brain tumor classification will provide improved means to type these tumors.

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Differentiation of brain tumors from other disease is usually possible from clinica al nd radiologica flindings. However, it sometimes becomes difficult because of atypical clinical course and radiological features that simulate brain tumors. We report three cases with lesions mimicking brain tumors out of 95 stereotactic biopsy cases. The first case was right thalamic infarction with progressing left hemiparesis. Magnetic resonance (MR)imaging showed a mass lesion with heterogeneous enhancement in the right thalamus simulating malignant glioma. The histologica slpecimen showed coagulative necrosis due to infarction. The second case was Balo's concentric sclerosis whose onset was generalized convulsion. MR imaging showed a ring-enhancing lesion in the left parietal lobe. A histologica dliagnosis of diffuse astrocytoma was made. Several days after the biopsy, the patient developed left visual disturbance and MR imaging showed contralateral new lesions. Reviewed histologica dliagnosis was a demyelinatin dgisease. The third case was myelinoclasti dciffuse sclerosis. MR imaging showed a diffuse lesion extending from corpus callosum to the bilateral frontal lobes with a left temporal small lesion. As a clinical diagnosis of a demyelinating disease was made, administration of high dose corticosteroid asnd plasma exchange were carried out. However t, he response was poor and multiple enhancing new lesions appeared on MR imaging S. tereotactic biopsie ws ere carried out twice and the histologica dliagnosis was a demyelinating disease. To avoid unnecessary invasive procedures, we should be aware of these cases mimicking brain tumor.

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We clinically experience the recurrence of astrocytoma after intensive medical treatment in many cases. We now present clinico-pathological study about cell kinetics of recurrent astrocytoma. In all examples of recurrence, the degree of histological malignancy is higher than in the examples of initial astrocytoma. The case in which the degree of histological malignancy is higher had the shorter period to a recurrence from the initial. In DNA-ploidy, diploid pattern was found in many cases at the time of a recurrence.

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Extensive resection of malignant gliomas without compromising neuronal function has been believed to prolong the survival of the patients. Among the therapeutic triad, radiation therapy has been shown to improve overall survival. Recent publication of a positive phase 3 trial comparing radiation therapy (RT) alone with RT and temozolomide chemotherapy in patients with glioblastomas introduced a new standard chemotherapy. Significan atdvantage was detected of the patients who have methylated MGMT promoter in the treatment of temozolomide. On the other hand, oligodendrogliomas with 1p/19q loss was reported to have good clinical course without PCV chemotherapy T. heses examples show that genomic analyses such as 1p/19qd eletion or MGMT status in glial tumors are necessary to predict sensitivity against chemotherapy.

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