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Dive into the research topics where Yoko Nakasu is active.

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Featured researches published by Yoko Nakasu.


Acta Neuropathologica | 1994

bcl-2 Protein expression in tumors of the central nervous system

Satoshi Nakasu; Yoko Nakasu; Hirofumi Nioka; Masayuki Nakajima; Jyoji Handa

Abstractbcl-2 protein (BCL-2) expression was immunohistochemically studied in 140 varied central nervous system tumors. The protein was most frequently expressed in neuronomas and ependymomas, and in normal ependymal cells and Schwann cells. Most pituitary adenomas could be classified into one of two subgroups, diffusely positive or diffusely negative tumors, while BCL-2 localized heterogeneously in normal pituitary glands. Although the protein was not detected in normal astrocytes, it was positive in reactive hypertrophic astrocytes observed in various pathological conditions. Similarly, astrocytic tumor cells often expressed BCL-2. Since lowgrade astrocytomas more often exhibited the protein than malignant gliomas, the degree of BCL-2 expression appeared to be related to the degree of malignancy of the gliomas. On the other hand, 7 out of 17 recurrent gliomas and medulloblastomas showed an increase in the frequency of protein expression compared with specimens from initial treatments. One recurrent astrocytic tumor which demonstrated anaplastic change showed a decrease in the frequency of BCL-2-positive cells. It is concluded that the frequency of BCL-2 expression in CNS tumors is increased when the non-neoplastic counterparts of the tumors exhibit the protein. Although it has been reported that overexpression of BCL-2 protects cells from damage by radiation and/or chemotherapy, we could not find any significant relationship between the degree of BCL-2 expression and the length of survival of patients with glioblastomas or medulloblastomas.


Cancer | 2011

Benefits of interferon-β and temozolomide combination therapy for newly diagnosed primary glioblastoma with the unmethylated MGMT promoter: A multicenter study.

Kazuya Motomura; Atsushi Natsume; Yugo Kishida; Hiroyuki Higashi; Yutaka Kondo; Yoko Nakasu; Tatsuya Abe; Hiroki Namba; Kenji Wakai; Toshihiko Wakabayashi

The aim of the current study was to catalog genomic and epigenomic abnormalities in newly diagnosed glioblastoma patients and determine the correlation among clinical, genetic, and epigenetic profiles and clinical outcome.


Neurosurgery | 1995

Meningioma: proliferating potential and clinicoradiological features.

Satoshi Nakasu; Masayuki Nakajima; Ken-ichi Matsumura; Yoko Nakasu; Jyoji Handa

We examined the proliferative potentials of meningiomas in 120 patients using the MIB-1 antibody against the Ki-67 antigen and compared them with the clinicoradiological features. The Ki-67 staining index (SI) did not relate to the age and sex of the patients or the location of the tumors. Asymptomatic meningiomas showed significantly lower SIs (mean +/- standard deviation [SD], 0.87 +/- 0.56%) than symptomatic meningiomas (mean +/- SD, 1.63 +/- 2.17%). We found no relation between SIs and clinical symptoms and signs in the symptomatic meningiomas. A weak correlation was found between the size of tumors and Ki-67 SIs (r = 0.21; P = 0.024). There were significant differences in SIs between calcified (mean +/- SD, 0.77 +/- 0.41%) and noncalcified tumor (mean +/- SD, 1.75 +/- 2.25%). Diffusely calcified tumors (mean +/- SD, 0.57 +/- 0.34%) showed lower SIs than focally calcified tumors (mean +/- SD, 0.92 +/- 0.41%). Lobulated tumors showed higher SIs (mean +/- SD, 2.85 +/- 3.68%) than round tumors (mean +/- SD, 1.06 +/- 0.67%). Tumors with perifocal edema or unclear borders had higher SIs than did those without such features. Signal intensities on T1-weighted magnetic resonance images had no relation to SIs, whereas low-intensity tumors on T2-weighted images, most of which presented diffuse calcification on computed tomographic scans, showed lower SIs. This study indicates that several clinicoradiological features relate to the proliferative potential of meningiomas and that they may contribute to the management of patients.


PLOS ONE | 2011

The global DNA methylation surrogate LINE-1 methylation is correlated with MGMT promoter methylation and is a better prognostic factor for glioma.

Fumiharu Ohka; Atsushi Natsume; Kazuya Motomura; Yugo Kishida; Yutaka Kondo; Tatsuya Abe; Yoko Nakasu; Hiroki Namba; Kenji Wakai; Takashi Fukui; Hiroyuki Momota; Kenichiro Iwami; Sayano Kinjo; Maki Ito; Masazumi Fujii; Toshihiko Wakabayashi

Gliomas are the most frequently occurring primary brain tumor in the central nervous system of adults. Glioblastoma multiformes (GBMs, WHO grade 4) have a dismal prognosis despite the use of the alkylating agent, temozolomide (TMZ), and even low grade gliomas (LGGs, WHO grade 2) eventually transform to malignant secondary GBMs. Although GBM patients benefit from promoter hypermethylation of the O 6-methylguanine-DNA methyltransferase (MGMT) that is the main determinant of resistance to TMZ, recent studies suggested that MGMT promoter methylation is of prognostic as well as predictive significance for the efficacy of TMZ. Glioma-CpG island methylator phenotype (G-CIMP) in the global genome was shown to be a significant predictor of improved survival in patients with GBM. Collectively, we hypothesized that MGMT promoter methylation might reflect global DNA methylation. Additionally in LGGs, the significance of MGMT promoter methylation is still undetermined. In the current study, we aimed to determine the correlation between clinical, genetic, and epigenetic profiles including LINE-1 and different cancer-related genes and the clinical outcome in newly diagnosed 57 LGG and 54 GBM patients. Here, we demonstrated that (1) IDH1/2 mutation is closely correlated with MGMT promoter methylation and 1p/19q codeletion in LGGs, (2) LINE-1 methylation levels in primary and secondary GBMs are lower than those in LGGs and normal brain tissues, (3) LINE-1 methylation is proportional to MGMT promoter methylation in gliomas, and (4) higher LINE-1 methylation is a favorable prognostic factor in primary GBMs, even compared to MGMT promoter methylation. As a global DNA methylation marker, LINE-1 may be a promising marker in gliomas.


Lung Cancer | 2011

Continuous EGFR-TKI administration following radiotherapy for non-small cell lung cancer patients with isolated CNS failure.

Takehito Shukuya; Toshiaki Takahashi; Tateaki Naito; Rieko Kaira; Akira Ono; Yukiko Nakamura; Asuka Tsuya; Hirotsugu Kenmotsu; Haruyasu Murakami; Hideyuki Harada; Koichi Mitsuya; Masahiro Endo; Yoko Nakasu; Kazuhisa Takahashi; Nobuyuki Yamamoto

INTRODUCTION Based on previous reports, patients who experience isolated central nervous system (CNS) failure may not have systemic acquired resistance to EGFR-TKI therapy. However, because there are few articles that have reported on the clinical efficacy of continuous EGFR-TKI administration following progressive disease (PD) in isolated CNS metastasis, we retrospectively investigated the possibility of using the treatment. PATIENTS AND METHODS From July 2002 to December 2009, 17 non-small cell lung cancer patients showed isolated CNS failure after clinical benefit (partial response or stable disease longer than 6 months) from EGFR-TKIs and continuously received EGFR-TKIs following radiotherapy (whole brain radiotherapy or stereotactic radiotherapy) to the CNS metastases. RESULTS The response rate and the disease control rate of CNS lesions were 41% and 76%, respectively. The median progression free survival, extracranial progression free survival and the median overall survival time were 80 days, 171 days and 403 days, respectively. The toxicities which were observed during the first EGFR-TKI treatments were sustained, but did not worsen during this study period. The acute toxicities caused by radiotherapy to the CNS were controllable. There were no remarkable late toxicities related to the treatment. CONCLUSIONS Continuous administration of EGFR-TKI following radiotherapy after PD in isolated CNS metastasis appears to be a valid treatment option.


BMC Cancer | 2012

α-type-1 polarized dendritic cell-based vaccination in recurrent high-grade glioma: a phase I clinical trial.

Yasuto Akiyama; Chie Oshita; Akiko Kume; Akira Iizuka; Haruo Miyata; Masaru Komiyama; Tadashi Ashizawa; Mika Yagoto; Yoshiaki Abe; Koichi Mitsuya; Reiko Watanabe; Takashi Sugino; Ken Yamaguchi; Yoko Nakasu

BackgroundHigh-grade gliomas including glioblastoma multiforme (GBM) are among the most malignant and aggressive of tumors, and have a very poor prognosis despite a temozolomide-based intensive treatment. Therefore, a novel therapeutic approach to controlling recurrence is needed. In the present study, we investigated the effect of activated dendritic cell (DC) (α-type-1 polarized DC)-based immunotherapy on high-grade glioma patients with the HLA-A2 or A24 genotype.MethodsNine patients with recurrent high-grade gliomas including 7 with GBMs who fulfilled eligibility criteria were enrolled into a phase I study of monocyte-derived DC-based immunotherapy. HLA-genotyping revealed 1 case of HLA-A*0201 and 8 cases of A*2402. Enriched monocytes obtained using OptiPrepTM from leukapheresis products on day1, were incubated with GM-CSF and IL-4 in a closed serum-free system, and activated on day6 with TNF-α, IL-1β, IFN-α, IFN-γ, and poly I/C. After pulsing with a cocktail of 5 synthetic peptides (WT-1, HER2, MAGE-A3, and MAGE-A1 or gp100) restricted to HLA-A2 or A24 and KLH, cells were cryopreserved until used. Thawed DCs were injected intradermally in the posterior neck at a dose per cohort of 1.0, 2.0 and 5.0× 107/body.ResultsThe frequency of CD14+ monocytes increased to 44.6% from 11.9% after gradient centrifugation. After a 7-day-incubation with cytokines, the mean percentage of DCs rated as lin-HLA-DR+ in patients was 56.2 ± 19.1%. Most DCs expressed high levels of maturation markers, co-stimulatory molecules and type-1 phenotype (CD11c+HLA-DR+) with a DC1/2 ratio of 35.6. The amount of IL-12 produced from activated DCs was 1025 ± 443 pg/ml per 105 cells. All 76 DC injections were well tolerated except for transient liver dysfunction with grade II. Six patients showed positive immunological responses to peptides in an ELISPOT assay, and positive skin tests to peptide-pulsed DC and KLH were recognized in 4 cases. The clinical response to DC injections was as follows :1 SD and 8 PD. Interestingly, the SD patient, given 24 DC injections, showed a long-term recurrence-free and immunological positive response period.ConclusionsThese results indicate peptide cocktail-treated activated α-type-1 DC-based immunotherapy to be a potential therapeutic tool against recurrent high-grade glioma with mainly HLA-A*2402.Trial registrationCurrent non-randomized investigational trial UMIN-CTR UMIN ID: 000000914.


Surgical Neurology | 1984

Aneurysms of the proximal anterior cerebral artery

Jyoji Handa; Yoko Nakasu; Masayuki Matsuda; Kazumitsu Kyoshima

The authors report eight cases of aneurysm of the anterior cerebral artery proximal to the anterior communicating artery (A1 segment). In six of these cases, the aneurysms arose from the proximal anterior cerebral artery at the origin of either a cortical branch (on case), the accessory middle cerebral artery (one case), or a perforating branch (four cases). In another case the aneurysm arose at the proximal end of the fenestration, whereas in the one remaining case no branch was present at the site of the aneurysmal neck.


International Journal of Oncology | 2013

Effect of the STAT3 inhibitor STX-0119 on the proliferation of cancer stem-like cells derived from recurrent glioblastoma.

Tadashi Ashizawa; Haruo Miyata; Akira Iizuka; Masaru Komiyama; Chie Oshita; Akiko Kume; Masahiro Nogami; Mika Yagoto; Ichiro Ito; Takuma Oishi; Reiko Watanabe; Koichi Mitsuya; Kenji Matsuno; Toshio Furuya; Tadashi Okawara; Masami Otsuka; Naohisa Ogo; Akira Asai; Yoko Nakasu; Ken Yamaguchi; Yasuto Akiyama

Signal transducer and activator of transcription (STAT) 3, a member of a family of DNA-binding molecules, is a potential target in the treatment of cancer. The highly phosphorylated STAT3 in cancer cells contributes to numerous physiological and oncogenic signaling pathways. Furthermore, a significant association between STAT3 signaling and glioblastoma multiforme stem-like cell (GBM-SC) development and maintenance has been demonstrated in recent studies. Previously, we reported a novel small molecule inhibitor of STAT3 dimerization, STX-0119, as a cancer therapeutic. In the present study, we focused on cancer stem-like cells derived from recurrent GBM patients and investigated the efficacy of STX-0119. Three GBM stem cell lines showed many stem cell markers such as CD133, EGFR, Nanog, Olig2, nestin and Yamanaka factors (c-myc, KLF4, Oct3/4 and SOX2) compared with parental cell lines. These cell lines also formed tumors in vivo and had similar histological to surgically resected tumors. STAT3 phosphorylation was activated more in the GBM-SC lines than serum-derived GB cell lines. The growth inhibitory effect of STX-0119 on GBM-SCs was moderate (IC50 15-44 µM) and stronger compared to that of WP1066 in two cell lines. On the other hand, the effect of temozolomide was weak in all the cell lines (IC50 53-226 µM). Notably, STX-0119 demonstrated strong inhibition of the expression of STAT3 target genes (c-myc, survivin, cyclin D1, HIF-1α and VEGF) and stem cell-associated genes (CD44, Nanog, nestin and CD133) as well as the induction of apoptosis in one stem-like cell line. Interestingly, VEGFR2 mRNA was also remarkably inhibited by STX-0119. In a model using transplantable stem-like cell lines in vivo GB-SCC010 and 026, STX-0119 inhibited the growth of GBM-SCs at 80 mg/kg. STX-0119, an inhibitor of STAT3, may serve as a novel therapeutic compound against GBM-SCs even in temozolomide-resistant GBM patients and has the potential for GBM-SC-specific therapeutics in combination with temozolomide plus radiation therapy.


Acta Neurochirurgica | 1991

Mechanism of mutism following the transcallosal approach to the ventricles

Yoko Nakasu; Takahiro Isozumi; Hirofumi Nioka; Jyoji Handa

SummaryTransient mutism has been known as a common manifestation following callosotomy for medically intractable epilepsy, but its cause has not been clearly elucidated. In this paper, we report three cases of mutism following a transcallosal approach to tumours in the lateral and third ventricles and retrospectively analyze the surgical, neurological and radiological features which may suggest the cause of this type of mutism.Mutism may be a result of division of the corpus callosum. Suppression of the limbic system caused by lesions in the anterior cingulate gyrus, septum pellucidum, and fornix may have been of importance in at least two of these three cases. Impairments of the supplementary motor cortex, thalamus and basal ganglia may also be factors reducing speech production. The mechanism of such transient mutism seems to be a complex of two or more of these factors, and their combinations may be different from one case to the other.


Surgical Neurology | 1987

Monitoring of somatosensory-evoked potentials during aneurysm surgery

Minoru Kidooka; Yoko Nakasu; Kazuyoshi Watanabe; Masayuki Matsuda; Jyoji Handa

Somatosensory-evoked potentials were recorded during and after 31 operations for intracranial aneurysms, and the changes in the central conduction times, namely, the interpeak latencies between the N14 and N20 peaks in response to bipolar stimulation of the median nerve, were studied. Neuroleptanalgesia and routine intracranial operative procedures such as opening the dura mater, drainage of the cerebrospinal fluid, gentle retraction of the brain, and microsurgical dissection of the circle of Willis, were found to have no significant adverse effect on the evoked responses, whereas the temporary clipping of the major cerebral artery or premature rupture of the aneurysm associated with hypotension or both, often caused significant prolongation of the central conduction time. Prolongation of the central conduction time exceeding 1.2 ms or disappearance of the N20 peak adversely affected the postoperative conditions in 8 of 13 patients (62%).

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Jyoji Handa

Shiga University of Medical Science

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Satoshi Nakasu

Shiga University of Medical Science

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Masayuki Matsuda

Shiga University of Medical Science

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Ken Yamaguchi

Mitsubishi Chemical Corporation

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Tadashi Ashizawa

Kumamoto Health Science University

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Yasuto Akiyama

Kumamoto Health Science University

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Akira Iizuka

Tokyo Medical and Dental University

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Reiko Watanabe

Saitama Medical University

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