Kyushu University Academic Staff Educational and Research Activities Database
List of Papers
Nobuhiro Hata Last modified date:2019.06.07

Lecturer / Department of Neurosurgery, Graduate School of Medical Sciences, Kyushu University / Neurosurgery / Kyushu University Hospital


Papers
1. Kikuchi K, Hiwatashi A, Togao O, Yamashita K, Kamei R, Momosaka D, Hata N, Iihara K, Suzuki SO, Iwaki T, Honda H., Intravoxel Incoherent Motion MR Imaging of Pediatric Intracranial Tumors: Correlation with Histology and Diagnostic Utility., AJNR Am J Neuroradiol. 40(5):878-884, 2019. , 10.3174/ajnr.A6052., 40, 5, 878-884, 2019.05.
2. Togao O, Hiwatashi A, Yamashita K, Momosaka D, Obara M, Nishimura A, Arimura K, Hata N, Iihara K, Van Cauteren M, Honda H, Acceleration-selective arterial spin labeling MR angiography for visualization of brain arteriovenous malformations., Neuroradiology. 2019 (in press), 10.1007/s00234-019-02217-w., 2019.06.
3. Yamashita K, Hatae R, Hiwatashi A, Togao O, Kikuchi K, Momosaka D, Yamashita Y, Kuga D, Hata N, Yoshimoto K, Suzuki SO, Iwaki T, Iihara K, Honda H., Predicting TERT promoter mutation using MR images in patients with wild-type IDH1 glioblastoma., Diagn Interv Imaging. S2211-5684(19)30067-1, 2019 , 10.1016/j.diii.2019.02.010., 2019.04.
4. Michiwaki Y, Hata N, Amano T, Suzuki SO, Akagi Y, Kuga D, Onozuka D, Momosaki S, Nakamizo A, Yoshimoto K, Yoshimoto K, Iwaki T, Iihara K, Predictors of recurrence and postoperative outcomes in patients with non-skull base meningiomas based on modern neurosurgical standards, Interdisciplinary Neurosurgery 15:30-37. 2019, 15, 30-37, 2019.03.
5. Togao O, Hiwatashi A, Obara M, Yamashita K, Momosaka D, Nishimura A, Arimura K, Hata N, Yoshimoto K, Iihara K, Van Cauteren M, Honda H., 4D ASL-based MR angiography for visualization of distal arteries and leptomeningeal collateral vessels in moyamoya disease: a comparison of techniques., Eur Radiol. , 10.1007/s00330-018-5462-7., 28, 11, 4871-4881, 2018.11.
6. Akagi Y, Yoshimoto K, Hata N, Kuga D, Hatae R, Amemiya T, Sangatsuda Y, Suzuki SO, Iwaki T, Mizoguchi M, Iihara K., Reclassification of 400 consecutive glioma cases based on the revised 2016WHO classification, Brain Tumor Pathology. 2018, 10.1007/s10014-018-0313-4, 2018.04.
7. Kuga D, Hata N, Akagi Y, Amemiya T, Sangatsuda Y, Hatae R, Yoshimoto K, Mizoguchi M, Iihara K., The Effectiveness of Salvage Treatments for Recurrent Lesions of Oligodendrogliomas Previously Treated with Upfront Chemotherapy., World Neurosurg. S1878-8750(18)30547-3, 10.1016/j.wneu.2018.03.069., 2018.06.
8. Yoshimoto K, Hatae R, Suzuki SO, Hata N, Kuga D, Akagi Y, Amemiya T, Sangatsuda Y, Mukae N, Mizoguchi M, Iwaki T, Iihara K, High-resolution melting and immunohistochemical analysis efficiently detects mutually exclusive genetic alterations of adamantinomatous and papillary craniopharyngiomas., Neuropathoogy 38: 3-10, 2018, 10.1111/neup.12408, 38, 3-10, 2018.02.
9. Yoshimoto K, Hatae R, Sangatsuda Y, Suzuki SO, Hata N, Akagi Y, Kuga D, Hideki M, Yamashita K, Togao O, Hiwatashi A, Iwaki T, Mizoguchi M, Iihara K, Prevalence and clinicopathological features of H3.3 G34-mutant high-grade gliomas: a retrospective study of 411 consecutive glioma cases in a single institution., Brain Tumor Pathol. 34: 103-112, 2017, 10.1007/s10014-017-0287-7, 34, 103-112, 2017.07.
10. Mukae N, Mizoguchi M, Mori M, Hashiguchi K, Kawaguchi M, Hata N, Amano T, Nakamizo A, Yoshimoto K, Sayama T, Iihara K, Hashizume M. , The usefulness of arcuate fasciculus tractography integrated navigation for glioma surgery near the language area; Clinical Investigation, Interdisciplinary Neurosurgery 7:22-28. 2017, 2017.07.
11. Nobuhiro Hata, Koji Yoshimoto, Ryusuke Hatae, DAISUKE KUGA, Yojiro Akagi, Yuhei Sangatsuda, Satoshi O Suzuki, Tadahisa Shono, Masahiro Mizoguchi, Koji Iihara, Add-on bevacizumab can prevent early clinical deterioration and prolong survival in newly diagnosed partially resected glioblastoma patients with a poor performance status., Oncotargets and Therapy, 10.2147/OTT.S125587, 10, 429-437, 2017.01, Purpose: The AVAglio trial established the beneficial effect of add-on bevacizumab (BEV) for the treatment of newly diagnosed glioblastomas (nd-GBMs) that led to the approval of BEV for the treatment of these patients in Japan. However, the rationality of using BEV as a first-line treatment for nd-GBMs remains controversial. The purpose of this study was to analyze the outcomes of a case series of nd-GBM patients.
Patients and methods: The outcomes of 69 nd-GBM patients treated after 2006 were retrospectively analyzed. Clinical and genetic analyses were performed, and estimates of progression-free survival (PFS) and overall survival (OS) were calculated using the Kaplan–Meier method. Since add-on BEV therapy was only used for partially resected GBMs (pr-GBMs) after its approval in 2013, the patients were subdivided into 3 treatment groups: Type I, partial removal with temozolomide (TMZ)/BEV and concurrent radiotherapy (CCRT); Type II, partial removal with TMZ and CCRT; and Type III, gross total removal with TMZ and CCRT.
Results: The PFS rate of Type I patients was significantly higher than that of Type II patients (P=0.014), but comparable to that of Type III patients. Differences in OS rates between Type I and Type II patients were less apparent (P=0.075), although the median OS of Type I patients was ∼8 months higher than that of Type II patients (17.4 vs 9.8 months, respectively). The clinical deterioration rate during initial treatment was significantly (P=0.024) lower in Type I than in Type II patients (7.7% vs 47.4%, respectively). Differences in OS rates between Type I and Type II patients with a poor performance status (PS) were significant (P=0.017).
Conclusion: Our findings suggest that add-on BEV can prevent early clinical deterioration of pr-GBM patients and contribute to a prolonged survival, especially for those with a poor PS..
12. Nobuhiro Hata, Ryusuke Hatae, Koji Yoshimoto, Hideki Murata, DAISUKE KUGA, Yojiro Akagi, Yuhei Sangatsuda, Satoshi O Suzuki, Toru Iwaki, Masahiro Mizoguchi, Koji Iihara, Insular primary glioblastomas with IDH mutations: Clinical and biological specificities., Neuropathology, 10.1111/neup.12362., in press, 2017.01, Isocitrate dehydrogenase (IDH) mutation is a good prognostic marker for glioblastoma (GBM). Although it is infrequent in primary tumors, it is found in most lower grade gliomas. Thus, it is unclear whether IDH mutation is
a marker for a specific phenotype of apparently primary de novo GBMs (pGBMs), or a marker for secondary tumors
(sGBMs). We addressed this issue by analyzing clinical, radiographic and molecular findings in our institutional case
series. Our cases included 92 pGBMs, with five cases of IDH1 mutations at R132 and no IDH2 mutations. The
median overall survival of these five patients was 29 months (range: 4 to >40 months), which is considered good prognoses. Clinical and radiographic characteristics were distinct from IDH-wildtype (IDH-wt) pGBMs. IDH-mutant
(IDH-mut) tumors consistently involved insular lesions and were subdivided into: (i) the two cases of elderly patients with long clinical histories and features implying multistep tumor development; and (ii) the three cases of younger patients with diffusely swelling insular tumors, slight contrast enhancement and no necrosis. Genetic and expression analyses of IDH-mut pGBMs were similar to those of sGBMs, suggesting that they are indeed distinct from their IDH-wt counterparts. TERT promoter mutation, a genetic marker of oligodendroglial derivation, was detected in one long-surviving case, but genetic alterations in the astrocyte sGBM pathway were generally prevalent in IDH-mut pGBMs. Our results present a unique phenotype of IDH-mutpGBMs arising frominsular cortex region, the molecular backgrounds of which are similar to sGBMs..
13. Nobuhiro Hata, Koji Yoshimoto, Ryusuke Hatae, DAISUKE KUGA, Yojiro Akagi, Satoshi O Suzuki, Toru Iwaki, Tadahisa Shono, Masahiro Mizoguchi, Koji Iihara, Deferred radiotherapy and upfront procarbazine-ACNU-vincristine administration for 1p19q codeleted oligodendroglial tumors are associated with favorable outcome without compromising patient performance, regardless of WHO grade., OncoTargets and Therapy, 10.2147/OTT.S115911, 9, 7123-7131, 2016.12, [URL].
14. Ryusuke Hatae, Nobuhiro Hata, Satoshi O Suzuki, Koji Yoshimoto, DAISUKE KUGA, Hideki Murata, Yojiro Akagi, Yuhei Sangatsuda, Toru Iwaki, Masahiro Mizoguchi, Koji Iihara, A comprehensive analysis identifies BRAF hotspot mutations associated with gliomas with peculiar epithelial morphology., Neuropathology, 10.1111/neup.12347., in press, 2016.08.
15. Ryusyke Hatae, Nobuhiro Hata, Koji Yoshimoto, DAISUKE KUGA, Yojiro Akagi, Hideki Murata, Satoshi O Suzuki, Masahiro Mizoguchi, Koji Iihara, Precise Detection of IDH1/2 and BRAF Hotspot Mutations in Clinical Glioma Tissues by a Differential Calculus Analysis of High-Resolution Melting Data., PLOS ONE, 11, 8, e0160489, 2016.08.
16. Hideki Murata, Koji Yoshimoto, Ryusuke Hatae, Yojiro Akagi, Masahiro Mizoguchi, Nobuhiro Hata, DAISUKE KUGA, Akira Nakamizo, TOSHIYUKI AMANO, Sayama Tetsuro, Koji Iihara, Detection of proneural/mesenchymal marker expression in glioblastoma: temporospatial dynamics and association with chromatin-modifying gene expression., Journal of Neurooncology, 125, 1, 33-41, 2015.01.
17. Ma X, Yoshimoto K, Guan Y, Hata N, Mizoguchi M, Sagata N, Murata H, Kuga D, Amano T, Nakamizo A, Sasaki T., Associations between microRNA expression and mesenchymal marker gene expression in glioblastoma., Neuro Oncol. , 14, 9, 1153-1162, 2012.09, [URL], The subclassification of glioblastoma (GBM) into clinically relevant subtypes using microRNA (miRNA)- and messenger RNA (mRNA)-based integrated analysis has been attempted. Because miRNAs regulate multiple gene-signaling pathways, understanding miRNA-mRNA interactions is a prerequisite for understanding glioma biology. However, such associations have not been thoroughly examined using high-throughput integrated analysis. To identify significant miRNA-mRNA correlations, we selected and quantified signature miRNAs and mRNAs in 82 gliomas (grade II: 14, III: 16, IV: 52) using real-time reverse-transcriptase polymerase chain reaction. Quantitative expression data were integrated into a single analysis platform that evaluated the expression relationship between miRNAs and mRNAs. The 21 miRNAs include miR-15b, -21, -34a, -105, -124a, -128a, -135b, -184, -196a-b, -200a-c, -203, -302a-d, -363, -367, and -504. In addition, we examined 23 genes, including proneural markers (DLL3, BCAN, and OLIG2), mesenchymal markers (YKL-40, CD44, and Vimentin), cancer stem cell-related markers, and receptor tyrosine kinase genes. Primary GBM was characterized exclusively by upregulation of mesenchymal markers, whereas secondary GBM was characterized by significant downregulation of mesenchymal markers, miR-21, and -34a, and by upregulation of proneural markers and miR-504. Statistical analysis showed that expression of miR-128a, -504, -124a, and -184 each negatively correlated with the expression of mesenchymal markers in GBM. Our functional analysis of miR-128a and -504 as inhibitors demonstrated that suppression of miR-128a and -504 increased the expression of mesenchymal markers in glioblastoma cell lines. Mesenchymal signaling in GBM may be negatively regulated by miR-128a and -504..
18. Mizoguchi M, Yoshimoto K, Ma X, Guan Y, Hata N, Amano T, Nakamizo A, Suzuki SO, Iwaki T, Sasaki T., Molecular characteristics of glioblastoma with 1p/19q co-deletion., Brain Tumor Pathol. , 29, 3, 148-153, 2012.03, Recent developments in molecular analysis have revealed genetic alterations in human gliomas. Loss of heterozygosity (LOH) is a critical molecular marker for classification of human glioma, and is useful for predicting outcome. Our previous LOH study identified a small subgroup of glioblastoma (GBM), with 1p/19q co-deletion, with a favorable clinical outcome. In this study, we investigated molecular pathological features of eight GBM with 1p/19q co-deletion compared with "classic" GBM and anaplastic oligodendroglioma (AO). We estimated EGFR gene amplification, EGFRvIII expression, CDKN2A (p16) homozygous deletion, and isocitrate dehydrogenase 1/2 (IDH1/2) gene mutations. We also conducted an analysis of the expression of proneural genes (DLL3, OLIG2, SOX2). On histopathological review, only one GBM was diagnosed as glioblastoma with oligodendroglioma component (GBMO). Loss of chromosomes 10 and 17p is common, and neither IDH1/2 mutations nor EGFRvIII expression were detected in GBM with 1p/19q co-deletion. The expression profile revealed high expression of the OLIG2 gene in this subgroup. High expression of proneural gene OLIG2 without EGFRvIII expression may be associated with a favorable clinical outcome; however, IDH1/2 gene status and the extent of LOH regions may indicate that this small subgroup of GBM is a distinct genetic subgroup from oligodendroglial tumors..
19. Yoshimoto K, Ma X, Guan Y, Mizoguchi M, Nakamizo A, Amano T, Hata N, Kuga D, Sasaki T., Expression of stem cell marker and receptor kinase genes in glioblastoma tissue quantified by real-time RT-PCR., Brain Tumor Pathol. , 28, 4, 291-296, 2011.10, Glioblastoma is dependent on a specific signaling pathway to maintain its tumor phenotype. The receptor tyrosine kinase (RTK) family mediates the multiple oncogenic growth factor receptor signaling and contributes to the pathogenesis of glioblastoma. Recently, many studies have shown that the expression of stem cell marker in glioblastoma tissue has prognostic significance, which indicates that the quantification of stem cell markers and RTK genes yields biological information about glioblastoma. In this study, we quantified RNA expression levels of stem cell markers [CD133, Nestin, BMI-1, maternal embryonic leucine zipper kinase (MELK), and Notch1-4] as well as RTKs (EGFR, ErbB4, VEGFR1-3, FGFR1, -2, PDGFRΑ, and PDGFRΒ) in 42 clinical samples of glioblastoma by the real-time RT-PCR method. We demonstrated that the expression of MELK is exclusively upregulated in glioblastoma tissue. Notch receptor expression is moderately upregulated and is correlated with that of VEGFR2, VEGFR3, and PDGFRβ. Unsupervised clustering identified one unique sample group that showed high expression of most of the genes analyzed. Our results suggest that quantification of these stem cell markers and RTK genes can stratify patients based on the expression profile, which might provide insight into the glioma biology in each cluster..
20. Hata N, Hisada K, Torisu R, Suzuki SO, Kameda K, Sasaki T., Foreign body granuloma associated with dura-cranioplasty after resection of convexity meningioma with extracranial extension: case report., Neurol Med Chir (Tokyo), 51, 3, 236-238, 2011.03.
21. Guan Y, Mizoguchi M, Yoshimoto K, Hata N, Shono T, Suzuki SO, Araki Y, Kuga D, Nakamizo A, Amano T, Ma X, Hayashi K, Sasaki T , MiRNA-196 is upregulated in glioblastoma but not in anaplastic astrocytoma and has prognostic significance.
, Clin Cancer Res. 16: 4289-4297. 2010, 16, 16, 4289-4297, 2010.08.
22. Hata N, Shinojima N, Gumin J, Yong R, Marini F, Andreeff M, Lang FF., Platelet-derived growth factor BB mediates the tropism of human mesenchymal stem cells for malignant gliomas., Neurosurgery. 66: 144-156. 2010, 66, 1, 144-156, 2010.01.
23. Kuga D, Mizoguchi M, Guan Y, Hata N, Yoshimoto K, Shono T, Suzuki SO, Kukita Y, Tahira T, Nagata S, Sasaki T, Hayashi K., Prevalence of copy-number neutral LOH in glioblastomas revealed by genomewide analysis of laser-microdissected tissues., Neuro Oncol 10: 995-1003. 2008, 10, 6, 995-1003, 2008.12.
24. Hata N, Yoshimoto K, Yokoyama N, Mizoguchi M, Shono T, Guan Y, Tahira T, Kukita Y, Higasa K, Nagata S, Iwaki T, Sasaki T, Hayashi K, Allelic losses of chromosome 10 in glioma tissues detected by quantitative single-strand conformation polymorphism analysis. , Clin Chem. 52: 370-378. 2006, 52, 3, 370-378, 2006.03.
25. Guan Y, Hata N, Kuga D, Yoshimoto K, Mizoguchi M, Shono T, Suzuki SO, Tahira T, Kukita Y, Higasa K, Yokoyama N, Nagata S, Iwaki T, Sasaki T, Hayashi K, Narrowing of the regions of allelic losses of chromosome 1p36 in meningioma tissues by an improved SSCP analysis., Int J Cancer 122: 1820-1826. 2008, 122, 8, 1820-1826, 2008.04.