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Nobuhiro Hata Last modified date:2018.08.08

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


Graduate School


E-Mail
Homepage
http://www.ns.med.kyushu-u.ac.jp//
Phone
092-642-5524
Fax
092-642-5526
Academic Degree
Ph.D.
Field of Specialization
Neurosurgery, genomics
Outline Activities
Clinical Neurosurgery,
Genetic analysis of malignant brain tumor,
Chemotherapy of malignant brain tumor,
Clinical oncology of malignant brain tumor
Research
Research Interests
  • Clinical efficacy of Anti-VEGF therapy for glioma
    keyword : glioma, clinical oncology, bevacizumab, VEGF
    2017.04~2019.04.
  • Development of the novel genetic analysis method, which can lead widespread utilization of taylor-made medicine for gliomas
    keyword : glioma, genetic analysis, taylor-made medicine
    2010.09~2019.03.
Academic Activities
Papers
1. 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.
2. 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.
3. Nobuhiro Hata, Koji Yoshimoto, Ryusuke Hatae, DAISUKE KUGA, 赤木 洋二郎, 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., 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..
4. Nobuhiro Hata, Ryusuke Hatae, Koji Yoshimoto, Hideki Murata, DAISUKE KUGA, 赤木 洋二郎, 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..
5. Nobuhiro Hata, Koji Yoshimoto, Ryusuke Hatae, DAISUKE KUGA, 赤木 洋二郎, 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].
6. Ryusuke Hatae, Nobuhiro Hata, Satoshi O Suzuki, Koji Yoshimoto, DAISUKE KUGA, Hideki Murata, 赤木 洋二郎, 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.
7. Ryusyke Hatae, Nobuhiro Hata, Koji Yoshimoto, DAISUKE KUGA, 赤木 洋二郎, 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.
8. 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.
9. 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.
10. 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.
11. 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.
Presentations
1. Nobuhiro Hata, Koji Yoshimoto, Ryusuke Hatae, Daisuke Kuga, Yojiro Akagi, Yuhei Sangatsuda, Takeo Amemiya, 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 , ASNO, 2017.10, Purpose: The rationality of using Bevacizumab (BEV) for newly-diagnosed glioblastomas (nd-GBMs) remains controversial. The purpose of this study was to analyze the outcomes of this treatment.
Methods: The outcomes of 69 nd-GBM patients treated after 2006 were retrospectively analyzed. 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 three treatment groups: Type I, partial removal with 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 approximately 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).
Conclusions: 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.
.
2. Usefulness of FISH and bioluminescent imaging for evaluation the fate of
human mesenchymal stem cell of gliomas.