Mitsuhiro Hara

Osaka City University, Ōsaka, Ōsaka, Japan

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Publications (3)9.49 Total impact

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    ABSTRACT: RCAS1, one of the tumor cell surface antigens, is strongly expressed in aggressive tumors. RCAS1 suppresses the in vitro growth of immune effector cells. We investigated the expression of RCAS1 in 57 gliomas using immunohistochemistry. Furthermore, we examined the association of the RCAS1 expression with the infiltration of tumor infiltrating lymphocyte (TIL). RCAS1 overexpression was significantly correlated with high histological grade and poor prognosis. Reduced infiltration and increased apoptosis of TILs was observed in RCAS1-positive regions. Apoptotsis of TILs appeared to be induced by RCAS1. RCAS1 expression in gliomas may play roles in tumor progression and tumor immune escape.
    Cancer Letters 03/2007; 246(1-2):182-9. · 5.02 Impact Factor
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    ABSTRACT: Cathepsin B, one of the lysosomal cysteine proteases, has been related to tumor invasiveness. Cystatin C is the strongest inhibitor of cathepsin B. Knowledge of its participation in the progression of gliomas is limited. We investigated the expression of cystatin C and its association with the clinicopathologic features of 57 gliomas. Cystatin C and cathepsin B expressions were evaluated by immunohistochemical methods and by semiquantitative real-time polymerase chain reaction analysis for the corresponding messenger RNA. Disease-free survival was analyzed by the Kaplan-Meier method. Tumors with low cystatin C protein expression and high cathepsin B protein expression were significantly more likely to be of high grade, and this pattern was significantly correlated with high Ki-67 LI and tumor recurrence. Depressed expression of cystatin C messenger RNA in glioblastomas compared with low-grade astrocytomas was demonstrated. Multivariate analysis demonstrated high tumor grade, high Ki-67 labeling index, high cathepsin B expression, and low cystatin C expression correlated significantly with shorter disease-free survival. These results suggest that gliomas in patients with an unfavorable clinical outcome are characterized by depressed expression of cystatin C. Evaluation of cystatin C expression in gliomas provides useful clinical information, especially as a prognostic indicator.
    Human Pathlogy 10/2005; 36(9):1008-15. · 2.84 Impact Factor
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    ABSTRACT: Unconstrained cell proliferation is characteristic of tumors. It is caused by the functional disorders of proteins that constitute the cell cycle mechanism. The cell cycle is controlled by cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors. Many reports have proved, in cancers, that cyclins, cyclin-dependent kinases, and cyclin-dependent kinase inhibitors are out of control. Cyclin A is a protein that regulates critical transition of the cell cycle. The expression of cyclin A in meningiomas by immunohistochemical method was investigated. Furthermore, the correlation among cyclin A expression, clinical course, and proliferative potential were also evaluated. Seventy-seven meningiomas were studied. The mean cyclin A labeling indices were as follows: benign meningiomas, 1.01% +/- 0.62%; atypical meningiomas, 4.23% +/- 1.82%; and anaplastic meningiomas, 7.72% +/- 0.88%. Analyses of variance showed that significant differences existed between tumor grades for cyclin A labeling indices. A linear positive correlation between the cyclin A labeling index and bromodeoxyuridine labeling index was observed. The multivariate analysis using Cox's hazards model showed a high cyclin A labeling index (>3%) was a significant risk factor for recurrence. A high Ki-67 labeling index (>5%) and high tumor grade (World Health Organization grade II, III) were also significant risk factors for recurrence. These results suggested that the evaluation of cyclin A expression in meningiomas provides significant clinical information, especially as an independent prognostic indicator.
    Applied immunohistochemistry & molecular morphology: AIMM / official publication of the Society for Applied Immunohistochemistry 03/2003; 11(1):9-14. · 1.63 Impact Factor

Publication Stats

27 Citations
9.49 Total Impact Points


  • 2005
    • Osaka City University
      • Department of Neurosurgery
      Ōsaka, Ōsaka, Japan
  • 2003
    • Kochi Medical School
      Kôti, Kōchi, Japan