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Dive into the research topics where Kenji Tada is active.

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Featured researches published by Kenji Tada.


Neurosurgery | 2004

Correlation between promoter hypermethylation of the O6-methylguanine-deoxyribonucleic acid methyltransferase gene and prognosis in patients with high-grade astrocytic tumors treated with surgery, radiotherapy, and 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea-based chemotherapy.

Takanori Kamiryo; Kenji Tada; Shoji Shiraishi; Naoki Shinojima; Masato Kochi; Yukitaka Ushio

OBJECTIVEO6-Methylguanine-deoxyribonucleic acid methyltransferase (MGMT) is a deoxyribonucleic acid repair protein associated with the chemoresistance of chloroethylnitrosoureas. We investigated whether MGMT promoter hypermethylation is associated with prognosis in patients with high-grade astrocytic tumors treated uniformly with surgery, radiotherapy, and 1-(4-amino-2-methyl-5-pyrimidinyl)methyl-3-(2-chloroethyl)-3-nitrosourea (ACNU)-based chemotherapy. METHODSUsing the methylation-specific polymerase chain reaction, we assayed promoter hypermethylation of the MGMT gene in tumor deoxyribonucleic acid from 116 adult patients with supratentorial high-grade astrocytic tumors (42 anaplastic astrocytomas [AAs] and 74 glioblastomas multiforme [GBMs]). The Cox proportional hazards model was used in forward stepwise regression to assess the relative role of prognostic factors (i.e., age at surgery, sex, Karnofsky Performance Scale score, extent of surgical resection, methylation status of the MGMT promoter, and association between MGMT promoter methylation and survival). RESULTSMGMT promoter hypermethylation was confirmed in 19 (45.2%) of 42 AA patients and 33 (44.6%) of 74 GBM patients. It was significantly associated with both longer overall and progression-free survival time in AA but not GBM patients. CONCLUSIONOur results demonstrate that MGMT promoter hypermethylation is associated with longer survival time in patients with AA who were treated with surgery, radiotherapy, and ACNU-based chemotherapy but not in patients with GBM.


Japanese Journal of Cancer Research | 2002

Expression of Hqk Encoding a KH RNA Binding Protein Is Altered in Human Glioma

Zheng Zhe Li; Tatsuya Kondo; Tomoaki Murata; Thomas A. Ebersole; Toru Nishi; Kenji Tada; Yukitaka Ushio; Ken Ichi Yamamura; Kuniya Abe

The quaking gene family encodes single KH domain RNA‐binding proteins that play vital roles in cell differentiation, proliferation, and apoptotic processes. The human quaking gene, Hqk, maps to 6q25–q26, where cytogenetic alterations associated with a variety of human malignancies, including gliomas have been reported. To assess possible relationships of Hqk with human diseases such as glial tumors, we first isolated the Hqk gene, characterized its structure and expression pattern, and carried out mutational analysis of Hqk in primary tumor samples. The Hqk gene contains 8 exons spanning a ∼200 kb genomic region, and generating at least four alternatively spliced transcripts, Hqk–5, Hqk–6, Hqk–7 and Hqk–7B, of which Hqk–7 is abundantly expressed in brain. Analysis of primary tumors demonstrated a high incidence of expression alterations of Hqk in gliomas (30%; 6/20), but not in other tumors such as schwannomas (0/3), or meningiomas (0/8). Among the tumor samples showing expression alterations, two were devoid of all three major transcripts, one was missing only the Hqk–5 message, and only the Hqk–7 message was absent in two cases. Our results thus imply the involvement of Hqk in human glial tumor progression.


Frontiers in Bioscience | 2003

Correlation of molecular genetic analysis of p53, MDM2, p16, PTEN, and EGFR and survival of patients with anaplastic astrocytoma and glioblastoma.

Yukitaka Ushio; Kenji Tada; Shoji Shiraishi; Takanori Kamiryo; Naoki Shinojima; Masato Kochi; Hideyuki Saya

This article reviews studies on the correlation between genetic abnormalities in malignant astrocytic tumors and patient survival. It is almost certain that alterations of PTEN on chromosome 10 represent a significant unfavorable prognostic factor in glioblastoma patients. The association of alterations in p53, MDM2, p16 or EGFR with the survival of patients with anaplastic astrocytoma or glioblastoma remains controversial. It is possible that the p16 alteration and EGFR amplification are associated with poor survival in certain groups of patients and that there might be a relationship with age. Malignant transformation of astrocytic cells are driven by the sequential acquisition of genetic alteration. Therefore, it is reasonable to subgroup gliomas by their patterns of genetic alterations. However the studies that correlated the multiple genetic alterations with survival are still limited. Further studies on large cohorts are necessary to elucidate the genetic factors that affect the prognosis and response to therapy of patients with malignant gliomas and to develop effective management strategies.


Neuro-oncology | 2003

Preliminary observations on genetic alterations in pilocytic astrocytomas associated with neurofibromatosis 1

Kenji Tada; Masato Kochi; Hideyuki Saya; Jun Ichi Kuratsu; Shoji Shiraishi; Takanori Kamiryo; Naoki Shinojima; Yukitaka Ushio

Neurofibromatosis 1 (NF1) is an autosomal dominant disorder that predisposes sufferers to various forms of neoplasia. Among affected individuals, 15%-20% develop astrocytomas, especially pilocytic astrocytomas (PA), which are benign and classified as grade I by the World Health Organization. They are generally well circumscribed, and their progression is slow. NF1-associated PAs (NF1-PAs) occasionally behave as aggressive tumors. To elucidate underlying genetic events in clinically progressive NF1-PAs, we performed molecular genetic analysis on 12 PAs, including 3 NF1-PAs, for pS3, p16, and epidermal growth factor receptor genes, as well as loss of heterozygosity (LOH) on chromosome 1p, 10, 17, and 19q. None of the obvious genetic alterations typically seen in higher grade astrocytomas were found in 9 sporadic PAs. However, in 2 of 3 NF1-PAs, microsatellite analysis showed LOH10, including the PTEN (phosphatase and tensin homolog deleted on chromosome 10) gene locus, despite the diagnosis of pilocytic astrocytoma;one of these also manifested homozygous deletion of the p16 gene. The other NF1-PA harbored only LOH of the NF1 gene locus (17q). Our preliminary results support the hypothesis that some NF1-PAs differ genetically from sporadic PAs.


Journal of Neuro-oncology | 2000

Randomized comparison of intra-arterial versus intravenous infusion of ACNU for newly diagnosed patients with glioblastoma

Masato Kochi; Isao Kitamura; Tomoaki Goto; Toru Nishi; Hideo Takeshima; Yoshiki Saito; Keizo Yamamoto; Takahiro Kimura; Takeshi Kino; Kenji Tada; Shoji Shiraishi; Shozaburo Uemura; Tazuko Iwasaki; Jun Ichi Kuratsu; Yukitaka Ushio

This prospective randomized trial was performed to compare the effectiveness of intra-arterial ACNU with intravenous ACNU in newly diagnosed patients with supratentorial glioblastoma. The primary end points were overall survival and progression-free survival. Within 3 weeks after surgery, patients were randomly assigned to receive either intravenous or intra-arterial ACNU (80 mg/m2) once every 6 weeks concomitant with radiotherapy. Intra-arterial ACNU was administered for the first 3 courses followed by intravenous administration. Eighty-four patients were enrolled onto this study and among them 82 patients who passed eligibility criteria were analyzed. Patients characteristics were not different significantly between 2 treatment arms. Median survival and progression-free survival time was 59 and 24 weeks, respectively for intra-arterial arm and 56 and 45 weeks, respectively for intravenous arm. There was no significant difference respectively between two treatment arms. Among the prognostic variables including age, Karnofsky performance status, extent of surgery and treatment arm, Coxs proportional hazards model showed that age was the only significant factor for both survival and progression-free survival (P=0.003 and 0.016, respectively). With regard to toxicity, there was no significant difference between two treatment arms. Leukoencephalopathy was not observed in intra-arterial arm. In conclusion, intra-arterial ACNU when administered by the method in this study does not increase the survival and progression-free survival of newly diagnosed patients with glioblastoma over that afforded by intravenous ACNU.


Cancer Research | 2003

Prognostic Value of Epidermal Growth Factor Receptor in Patients with Glioblastoma Multiforme

Naoki Shinojima; Kenji Tada; Shoji Shiraishi; Takanori Kamiryo; Masato Kochi; Hideo Nakamura; Keishi Makino; Hideyuki Saya; Hirofumi Hirano; Jun Ichi Kuratsu; Koji Oka; Yasuji Ishimaru; Yukitaka Ushio


Journal of Cell Biology | 2000

Zyxin, a Regulator of Actin Filament Assembly, Targets the Mitotic Apparatus by Interacting with H-Warts/Lats1 Tumor Suppressor

Toru Hirota; Tetsuro Morisaki; Yasuyuki Nishiyama; Tomotoshi Marumoto; Kenji Tada; Toshihiro Hara; Norio Masuko; Masaki Inagaki; Katsuyoshi Hatakeyama; Hideyuki Saya


Journal of Neurosurgery | 1991

Increased MR signal intensity due to cervical myelopathy : analysis of 29 surgical cases

Yasutaka Matsuda; Kazumi Miyazaki; Kenji Tada; Atsushi Yasuda; Tomitaka Nakayama; Hitoshi Murakami; Michimasa Matsuo


Journal of Neurosurgery | 2004

The influence of sex and the presence of giant cells on postoperative long-term survival in adult patients with supratentorial glioblastoma multiforme

Naoki Shinojima; Masato Kochi; Jun-ichiro Hamada; Hideo Nakamura; Shigetoshi Yano; Keishi Makino; Hiromasa Tsuiki; Kenji Tada; Jun Ichi Kuratsu; Yasuji Ishimaru; Yukitaka Ushio


Journal of Neurosurgery | 2001

Analysis of loss of heterozygosity on chromosome 10 in patients with malignant astrocytic tumors: Correlation with patient age and survival

Kenji Tada; Shoji Shiraishi; Takanori Kamiryo; Hideo Nakamura; Hirofumi Hirano; Jun Ichi Kuratsu; Masato Kochi; Hideyuki Saya; Yukitaka Ushio

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