Biomedical subjects

K Tokuda

Publications and source records attributed to K Tokuda.

At least 55 records · Page 3Linked to original sources

PubMed1992

Endo- and aminopeptidase activities of rat cathepsin H.

Employing soluble denatured protein substrates and their derivatives, the proteolytic activity of rat cathepsin H was investigated. The enzyme showed aminopeptidase activity which sequentially released amino acid from the N-terminal of the substrate. The aminopeptidase activity did not act on N alpha-acetylated peptides and showed moderate ionic-strength dependence when methionyl-methylcoumarylamide was employed as a substrate. These results indicate that the activity essentially requires an N-terminal free amino group of the substrate and recognizes it electrostatically to some extent. On the other hand, the enzyme was also indicated to exhibit endopeptidase activity by employing appropriate N alpha-acetylated peptide substrates. In contrast to the aminopeptidase activity, the endopeptidase activity showed rather strict specificity, preferring hydrophobic residues at P2 and P3 sites. Because of the broad specificity and high efficiency of the aminopeptidase activity, it was difficult to directly observe endopeptidase activity in the digestion of large peptide substrates with a free alpha-amino terminal. Thus, this is the first experimental evidence that indicates endopeptidase activity by assigning internal peptide bonds cleaved by this activity. From this data, we proposed a model of the binding site of this enzyme.

Amino Acid Sequence↗

PubMed1992

[Effect of pretreatment with N-methyl-N-nitrosourea or streptozotocin on the cytotoxicity and the induction of sister chromatid exchanges in human and rodent brain tumor cells treated with chloroethylnitrosourea].

Effects of pretreatment with N-methyl-N-nitrosourea (MNU) or streptozotocin (STZ) on cytotoxicity and induction of sister chromatid exchanges (SCE) in human and rodent brain tumor cells treated with 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) or 1-(2-chloroethyl)-1-nitrosourea (CNU) were investigated. 9L-2 and SF-188 cells were more resistant to the cytotoxic effects of chloroethylnitrosourea than 9L and SF-126 cells. SF-295 cells were more resistant to the cytotoxic effects than SF-126, but more sensitive than SF-188 cells. Pretreatment of 9L-2 cells with MNU or STZ resulted in a dose-dependent increase in cytotoxicity and SCE induction by BCNU. Treatment with 1mM MNU or 1.5mM STZ completely reversed the cellular resistance of 9L-2 cells to BCNU but did not potentiate either cytotoxicity or SCE induction in 9L cells. Pretreatment of SF-188 and SF-295 cells with MNU or STZ resulted in a dose-dependent increase in cytotoxicity and SCE induction by CNU. Treatment with 500 microM MNU or 1.5mM STZ for SF-188 cells, and with 250 microM MNU or 1.5mM STZ for SF-295 cells completely reversed the cellular resistance to CNU. These results are consistent with the hypothesis that pretreatment with MNU or STZ inhibits O6-alkylguanine-DNA-alkyltransferase (O6-AT) and inhibition of the enzyme allows the formation of DNA interstrand cross-links resulting in increase in cytotoxicity and induction of SCE in resistant cells treated with chloroethylnitrosourea. In this regard, O6-AT plays an important role in determining the cytotoxicity and induction of SCE by chloroethylnitrosourea in both rodent and human brain tumor cells.

Animals↗

PubMed1991

Genetic analysis of functional differences among distinct ferredoxins in Rhodobacter capsulatus.

Rhodobacter capsulatus has been known to possess two ferredoxins (I and II) with distinct physicochemical and structural properties: ferredoxin I is a 2[4Fe-4S] type and the other is a [3Fe-4S] [4Fe-4S] type. To analyze their possible functional differences, their genes (fdxN and fdxA) were cloned, sequenced, and subjected to interposon mutagenesis experiments. The former gene was adjacent to a gene encoding a chloroplast-type [2Fe-2S] ferredoxin (fdxC). Mutants with inactivated fdxN and/or fdxC were obtained, and they showed virtually no growth under nitrogen-fixing conditions. Complementation experiments confirmed that both fdxN and fdxC were required for nitrogen fixation. On the other hand, we have not been able to disrupt fdxA under the screening conditions surveyed, including conditions that do not require nitrogenase activity for growth, suggesting that ferredoxin II could have an unknown essential role(s). These indicate functional differences among multiple ferredoxins in one bacterium other than in cyanobacterial heterocysts and indispensability of certain ferredoxins in nitrogen fixation other than Rhizobium meliloti FdxN.

Amino Acid Sequence↗

PubMed1991

Rat cathepsin H-catalyzed transacylation: comparisons of the mechanism and the specificity with papain-superfamily proteases.

We found that rat cathepsin H showed strong transacylation activity under physiological conditions. It is a feature of cathepsin H to utilize amino acid amides not only as acyl-acceptors but also as acyl-donors in the reaction. The pH-dependence of the transacylation activity was distinct from those of other papain-superfamily proteases. The alkaline limb (pKapp = 7.5) could be regarded as the pKa of the alpha-amino group of the acyl-donor, which was also involved in the original amino-peptidase activity. The acidic limb (pKapp = 5.8) was suggested to be involved in the deacylation step, where amino acid amide attacked the acyl-intermediate as a nucleophile in place of water in the hydrolysis. Although the N alpha-deprotonated acyl-acceptor, which is supposed to govern the nucleophilic attack, has a small population in the acidic pH range (above pH5), the transacylation was detectable even at the acidic pH-range because of the high S1'-site binding ability and suitable nucleophilicity of the acyl-acceptor. In the transacylation between various amino acid amides, the S1 and S1' site appeared to prefer hydrophobic residues without and regardless of a branch at beta-carbon, respectively. From these results and the sequence homology in the papain superfamily, we concluded that the reaction was governed by the acyl-donor having a protonated amino group, the acyl-acceptor having a deprotonated amino group and the remarkable hydrophobic character (especially favoring tryptophan amide) of the S1' site, presumably reflecting the good conservation of Trp177 in papain-superfamily proteases.

Amino Acid Sequence↗

PubMed1991

Purification and characterization of aseanostatins: actinomycete-derived fatty acid inhibitors to myeloperoxidase release from human polymorphonuclear leukocytes.

We found inhibitors, designated aseanostatins P1 and P5, against myeloperoxidase (MPO) release from human polymorphonuclear leukocytes (PMN). Aseanostatins were extracted from an actinomycete isolated in Thailand and purified by a series of column chromatography of charcoal and silica gel, and HPLC. Physico-chemical characterization by gas liquid chromatography and GC-MS indicated that aseanostatins were fatty acids. The active forms of aseanostatins were recovered by hydrolyzing their methyl esters after HPLC. Two components P1 and P5 with the IC50 of 0.96 and 0.54 microgram/ml to the MPO release were obtained as pure forms, indicating aseanostatin P5 was higher activity than aseanostatin P1. The component P1 was identical with 12-methyltridecanoic acid and P5 was indistinguishable to 12-methyltetradecanoic acid (ante-i-15:0). Aseanostatin P5 (1 microgram/ml) did not inhibit beta-glucuronidase release, but O2- production a little. It has no effect on chemotaxis of PMN to fMet-Leu-Phe (10(-8)M), PMN adhesion or phosphorylation of a 64-kD protein in the PMN cell-lysate system.

Actinomycetales↗

PubMed1991

[Two autopsied cases of radiation-induced gliosarcoma].

Two autopsied cases of radiation induced gliosarcoma are presented in detail with a review of the literatures. Case 1 was that of a 36-year-old female who was found to have a metastatic choriocarcinoma in the right occipital lobe and received radiation therapy of 45 Gy. Four years later CT scan showed a new enhanced tumor in the cerebellum within the previously irradiated field. Total removal was performed and histological diagnosis of the tumor was a gliosarcoma. She died 12 months after the operation. Case 2 was that of a 63-year-old male who had a protoplasmic astrocytoma in the left temporal lobe and received radiation therapy of 60 Gy after surgery. The tumor recurred in the left temporal base after 9 years. Histological finding of the surgical specimens showed gliosarcoma. The patient died 2 months after he was operated on. The tumors had obviously two defined neoplastic components. One was gliomatous features with anaplastic glial cells which stained for glial fibrillary acidic protein. The other was malignant mesenchymal features with spindle shaped fibrosarcoma cells which contained numerous reticulin fibers. Postmortem examination revealed these similar features. Criteria for identifying a tumor as a radiation induced neoplasm have been proposed by Fajado. The main criterion is that the induced tumor should occur in the previously irradiated field. Secondly, it should appear after a latent period. Thirdly, the pathology should be different from the initial neoplasm. Our cases fulfil these criteria.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1990

[Combined postoperative radiotherapy and chemotherapy for malignant gliomas].

A retrospective analysis was performed on 70 patients with malignant supratentrial astrocytic gliomas (astrocytoma Grade III or glioblastoma multiforme) treated with radiotherapy combined with vincristine (VCR), ACNU and PS-K. From January 1979 through December 1983, 27 patients were treated with treatment protocol A (group A). Protocol A was as follows: (1) total dose of 50 to 65 Gy radiation was given after surgery; (2) radiation plus combination VCR (0.02 mg/kg IV on 1st and 29th day of radiation) and ACNU (2 mg/kg IV 24 hrs after VCR) (3) after synchronized radiotherapy, ACNU (2 mg/kg IV every 6 or 8 weeks) and PS-K (3 or 6 g PO every day). Other 43 patients were treated with treatment protocol B (group B) from January 1984 through June 1988. Protocol B was as follows: (1) radiation dose was same as protocol A; (2) radiation plus combination VCR (0.02 mg/kg IV one day before radiotherapy) and ACNU (2 mg/kg IV on 1st and 1 mg/kg IV on 7, 21, 35th day, 1 hour before radiotherapy) (3) maintenance chemotherapy was same as protocol A. The difference between protocol A and protocol B was based on treatment schedule of ACNU. The characteristics of all patients were studied and identified, mainly age, histologic type, initial performance status, extent of tumor resection, maintenance chemotherapy. The reduction rate of tumor volume was 46.7% in the A group and 49.9% in the B group (not significant). The survival rates at 1, 2 and 3 years after surgery were 74.1%, 55.6% and 51.9% respectively for A group, and 80.5%, 42.4%, and 42.4%, respectively for B group.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗

PubMed1990

Modification of tumor blood flow and enhancement of therapeutic effect of ACNU on experimental rat gliomas with angiotensin II.

Blood flow was measured in transplanted rat gliomas before and during a constant intravenous infusion of angiotensin II using hydrogen clearance methods. The brain tumor models were produced in syngeneic Wister-King-Aptekman male rats with stereotaxic inoculation of ethylnitrosourea-induced glioma cells (KEG-1). Induced hypertension up to 150 mmHg (mean arterial pressure) with the infusion of angiotensin II resulted in a significant increase of blood flow to tumor center compared to the normotensive state (p less than 0.001). Blood flow measured simultaneously in brain tissue of tumor-free contralateral hemisphere did not change. The therapeutic effect of administration of the simultaneous 1-(4-Amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea hydrochloride (ACNU) and angiotensin II was evaluated in four experimental groups with the tumor-bearing rats. Twelve days after tumor implantation, the rats were administered angiotensin II to increase the mean arterial blood pressure to 150 mmHg, followed by intravenous injection of ACNU injection. The increased blood pressure was steadily maintained for 20 minutes. The ACNU/induced hypertension group showed a median survival time of 27.0 days, which was significant longer (p less than 0.02) than that of an ACNU treatment group (22.0 days), a hypertension treatment group (19.0 days), or a no treatment group (18.5 days). The enhanced therapeutic effect can be attributed to improving chemotherapeutic drug delivery due to increased blood flow in the tumor.

Angiotensin II↗

PubMed1989

[Clinicopathologic investigation of 63 cases of pituitary adenoma--special reference to immunohistochemical study of hormone production].

We have referred 63 cases of pituitary adenoma during past 10 years at department pathology of Hokkaido University Hospital. The mean age at diagnosis was 38 years, with a range from 13 to 73 years. 35 patients complained of non-hormonal sign (head ache, disturbance of vision, disturbance of consciousness, fatigability), 32 patients presented with hormonal sign (acromegaly, troubles of menstruation, galactorrhoea, cushing syndrome) and 7 patients had both signs. Immunohistochemically, GH cell adenoma was 16 cases, Prolactine cell adenoma was 11 cases, ACTH cell adenoma was 4 cases, Non-functioning adenoma was 19 cases and Mixed type was 10 cases.

Adenoma↗

PubMed1989

Mammary gland growth and response to hormones in mastomys compared with mice.

Mammary gland growth with or without hormone manipulation was examined in virgin mastomys (Praomys (mastomys) natalensis) and compared with C3H/He mice having a low mammary tumor incidence. Mammary glands of mastomys consisted mostly of duct systems even at 720 days of age, whereas conspicuous formation of normal end-buds and preneoplastic hyperplastic alveolar nodules were seen in the glands of mice after 180 days of age. Mammary glands of mastomys showed a higher response to estrogen or progesterone rather than prolactin, which is much different from other rodents.

Age Factors↗

PubMed1988

Differences in DNA alkylation products formed in sensitive and resistant human glioma cells treated with N-(2-chloroethyl)-N-nitrosourea.

The distribution of alkylated deoxynucleosides and bases has been determined in the DNA of a sensitive and a resistant human glioma-derived cell line exposed to therapeutic levels of [3H]N-(2-chloroethyl)-N-nitrosourea in vitro. The resistant cell line is 5-fold less sensitive to the cytotoxic effects of N-(2-chloroethyl)-N-nitrosourea and 8-fold less sensitive to sister chromatid exchange than the sensitive cell line. In comparison with the sensitive cells, DNA from the resistant cells contains much less of the cross-link, 1-(3-deoxycytidyl),2-(1-deoxyguanosinyl)ethane. DNA from the resistant cells also contains significantly fewer minor base modifications. The decrease in 1-(3-deoxycytidyl),2-(1-deoxyguanosinyl)ethane cross-link formation is probably explained by the higher level of O6-alkyltransferase in the resistant cell line. The lower levels of other DNA modifications could be explained by the presence of higher levels of other DNA repair activities.

Alkylation↗

PubMed1988

Cytotoxicity and induction of sister chromatid exchanges in human and rodent brain tumor cells treated with alkylating chemotherapeutic agents.

Rodent (9L and 9L-2) and human (SF-126 and SF-188) brain tumor cells were treated with methylating, ethylating, and chloroethylating nitrosoureas. 9L-2 and SF-188 cells were 10-fold and 5.4-fold more resistant to the cytotoxic effects of 1-(2-chloroethyl)-1-nitrosourea (CNU) than were 9L and SF-126 cells. SF-188 cells were 2.5- to 3-fold more resistant to N-methyl-N-nitrosourea (MNU) and streptozotocin (STZ) than SF-126 cells. 9L-2 cells were slightly more resistant to the cytotoxic effects of STZ and MNU than were 9L cells, but the rodent cells were 5- to 15-fold more resistant to these agents than the human cells. There were only small differences in cytotoxicity among the four cell lines after treatment with N-ethyl-N-nitrosourea (ENU). SF-188 and 9L-2 cells were 7- to 8-fold more resistant to the induction of sister chromatid exchange (SCEs) by CNU than were SF-126 and 9L cells. SF-126 cells were 80-fold more sensitive to the induction of SCEs by both STZ and MNU than were SF-188 cells. Only small differences in SCE induction were observed in 9L and 9L-2 cells treated with MNU and STZ. After ENU treatment, SF-126, 9L, and 9L-2 cells showed similar levels of SCEs; SF-188 cells were more resistant to the induction of SCEs by ENU. Pretreatment of 9L-2 cells with MNU resulted in a dose-dependent increase in cytotoxicity and SCE induction by 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU). Treatment with 1 mM MNU completely reversed the cellular resistance of 9L-2 cells to BCNU but did not potentiate either cytotoxicity or SCE induction in 9L cells. These results suggest that O6-alkylguanine-DNA-alkyltransferase (O6-AT) plays an important role in determining the cytotoxicity of and the induction of SCEs by CNU in both rodent and human tumor cells. O6-AT may also influence the response of human cells to both the cytotoxic effects of and the induction of SCEs by MNU and STZ. In the rodent cells, however, biochemical mechanisms other than O6-AT appear to determine the cytotoxic response to these agents. O6-AT does not appear to influence the cytotoxicity of ENU in either human or rodent cells but may have a small effect on SCE induction in human cells.

Alkylating Agents↗

PubMed1988

The effects of human recombinant tumor necrosis factor on glioma-derived cell lines: cellular proliferation, cytotoxicity, morphological and radioreceptor studies.

To determine whether tumor necrosis factor is of potential value for the treatment of human malignant gliomas, we studied the effects of human recombinant tumor necrosis factor (rTNF-alpha) on the morphology, incorporation of tritiated thymidine, and proliferation of 5 established cell lines derived from human malignant gliomas and 3 normal human brain cell cultures. A radioreceptor analysis for rTNF-alpha was performed on all cell lines and cultures. Two of the 5 human glioma cell lines (SF-188 and U 343 MG-A) demonstrated a marked decrease (60% or less of untreated controls) in the uptake of tritiated thymidine when treated with rTNF-alpha at a concentration of 40 U/ml; rTNF-alpha at 100 U/ml had antiproliferative and cytotoxic effects on both cell lines. The growth and proliferation of cell lines SF-126 and U 251 MG were not affected by rTNF-alpha even at high concentrations (5,000 U/ml). The growth and proliferation of SF-539 were affected to an intermediate degree. A colony-forming efficiency assay corroborated the results of the proliferation studies: SF-126 was relatively resistant (surviving fraction of 0.9 at 500 U/ml) and SF-188 was relatively sensitive (surviving fraction of 0.08 at 500 U/ml) to the cytotoxic effects of rTNF-alpha. Time-sequence electron microscopy showed that rTNF-alpha at a concentration of 500 U/ml caused ultrastructural changes in SF-188, including increased intracytoplasmic vesiculation, swelling and degeneration of mitochondria, loss of cell:cell junctional complexes, and fragmentation of the plasma membrane. Studies with 125I-rTNF-alpha showed a variable degree of binding in all cell lines and cultures. SF-188, a highly sensitive cell line, demonstrated the strongest binding of 125I-rTNF-alpha (3,400 receptors/cell with high affinity; kd = 0.27 nM), while SF-126, a highly resistant cell line, had the weakest binding (809 receptors/cell; kd = 0.25 nM). We conclude that there is a spectrum of antiproliferative and cytotoxic activity among glioma-derived tumor cell lines exposed to rTNF-alpha. An increased number of rTNF-alpha receptors appears to be a necessary but insufficient condition to explain the antiproliferative effects observed in some glioma-derived cell lines.

Cell Division↗

PubMed1988

[A case of von Hippel-Lindau disease associated with bilateral renal cell carcinoma].

A case of von Hippel-Lindau disease associated with bilateral renal cell carcinoma is presented. A 27-year-old female noticed myodesopsia and underwent laser coagulation of right retinal hemangioma in 1973. In addition, cerebellar hemangioblastomas were removed in 1977, 1978, 1983 and 1987. The patient was referred to the department of urology for further examination of bilateral renal masses which were incidentally found on abdominal computed tomography (CT) and magnetic resonance-CT. Fine needle biopsy performed and microscopic examination revealed the presence of clear cell type renal cell carcinoma (grade 1). Renal arteriography demonstrated multiple neovascularity in the bilateral masses. Complete tumor excision was impossible to retain the minimum of renal function, the patient was conservatively subjected to a follow-up study.

Adult↗

PubMed1987

Glutathione and related enzymes in rat brain tumor cell resistance to 1,3-bis(2-chloroethyl)-1-nitrosourea and nitrogen mustard.

Reduced glutathione (GSH) and activities of several glutathione-related enzymes were measured in two 9L rat brain tumor cell lines with differing sensitivities to both 1,3-bis(2-chloroethyl)-1-nitrosourea (BCNU) and nitrogen mustard. GSH, measured by a specific high-performance liquid chromatographic method, was found to be approximately twice as high in 9L cells sensitive to BCNU but resistant to nitrogen mustard. The nitrogen mustard resistant cell line was also found to have 2.5-fold more bulk glutathione transferase activity and approximately 3-fold more gamma-glutamyl transpeptidase activity. Glutathione reductase activity, protein thiol, and total protein content were similar in the two cell lines. Pretreatment of 9L cells with 50 microM buthionine sulfoximine for 24 h to deplete GSH only slightly potentiated BCNU cytotoxicity in a clonogenic assay whereas that of nitrogen mustard was markedly potentiated in both cell lines. Similarly, buthionine sulfoximine pretreatment had little effect on the induction of sister chromatid exchanges by BCNU, but significantly increased the number of sister chromatid exchanges induced by nitrogen mustard in both cell lines. Depleting GSH also had no significant effect on the cytotoxicity of 1-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea and 1-(2-chloroethyl)-3-(trans-4-methylcyclohexyl)-1-nitrosourea to 9L cells. Pretreatment of 9L cells with 1 mM GSH significantly protected against nitrogen mustard cytotoxicity. Moreover, nitrogen mustard incubated with GSH and glutathione transferase was 4-fold less cytotoxic than nitrogen mustard incubated with GSH alone. Incubation of BCNU with GSH alone or with glutathione transferase had no effect on BCNU cytotoxicity. These results indicate that elevated GSH and glutathione transferase activity is one mechanism of cellular resistance to nitrogen mustard in the 9L cell line, but it does not correlate with resistance to BCNU or other clinically important nitrosoureas.

Animals↗

PubMed1987

Cytotoxicity and sister chromatid exchanges in 9L cells treated with monofunctional and bifunctional nitrogen mustards.

To investigate the role of DNA interstrand crosslink formation on cytotoxicity and the induction of sister chromatid exchanges (SCEs), we treated 9L cells with the bifunctional mustard bis(2-chloroethyl)methylamine (HN2), which can alkylate DNA and form DNA interstrand crosslinks, or with two monofunctional mustards, bis(ethyl)-2-chloroethylamine and bis(methyl)-2-chloroethylamine, which can only alkylate DNA. On a molar basis, HN2 was 900-2400 times more cytotoxic and 471-686 times more effective at inducing SCEs than the monofunctional mustards. HN2 induced high levels of DNA interstrand crosslinks in 9L cells; no interstrand crosslinks were detected in cells treated with the monofunctional mustards. Comparison of the alkylating activity of each of the mustards by 4-(p-nitrobenzyl)pyridine reactivity showed only a 4-fold difference, which is not sufficient to account for the large differences in cell survival and induction of SCEs. We conclude that the effectiveness of HN2 at inducing cytotoxicity and SCEs results from the formation of DNA interstrand crosslinks.

Alkylation↗

PubMed1986

[Experimental studies on induced hypertension chemotherapy of intracerebral inoculated gliomas in rats].

Blood flow of transplanted intracerebral rat gliomas was measured before and after a constant I.V. infusion of angiotensin II-induced arterial hypertension using hydrogen clearance method. The brain tumor model was produced in syngeneic Wistar-King-Aptekman male rats by stereotaxic inoculation of ethylnitrosourea-induced glioma cells (KEG-1). Induced hypertension by angiotensin II infusion resulted in a significant increase in tumor blood flow compared with control levels (P less than 0.001). In addition, the therapeutic effect of administration of 3-[(4-amino-2-methyl-5-pyrimidinyl) ethyl] -1-(2-chloroethyl)-1-nitrosourea (ACNU) during angiotensin II-induced hypertension was evaluated. At 12 days after implantation, tumor-bearing rats were administrated angiotensin II as the mean blood pressure reached 150 mmHg, followed by ACNU injection, maintained the same blood pressure for 20 minutes. ACNU with induced hypertension group showed a median survival time of 27.0 days, which was significantly (P less than 0.02) longer than that of ACNU alone (22.0 days). It is therefore suggested that chemotherapy with angiotensin II-induced hypertension has a enhancing effect on chemotherapy for improving the drug delivery to tumor tissue by a increased tumor blood flow.

Angiotensin II↗

PubMed1986

[Foramen magnum tumor--the diagnosis and surgical approach].

The seven cases of the foramen magnum tumors were presented with the clinical manifestations and surgical consideration. Early clinical symptoms of the cases with extramedullary lesions were suboccipital neck pain followed by dysesthesia, clumsiness of hand and weakness. On the other hand, early symptoms of the cases with intramedullary lesions were dysesthesia, often followed by swallowing difficulty or hoarsness, which may have some difference from the clinical course of the extramedullary tumor cases. CT scan was remarkably useful in the diagnosis of the foramen magnum tumor. Surgical treatment was done to 6 cases: Five of these cases were operated by suboccipital craniectomy, and one case with an anteriorly located meningioma in the foramen magnum region was operated by transoral approach. Total removal could be performed in the case without damage to the medulla or spinal cord. The surgical treatment was reviewed, and the approach appropriate to tumor location around the foramen magnum should be selected.

Adolescent↗