Publications by authors named "Arun H Shastry"

Introduction: Chordoid meningiomas (CMs) are a rare subgroup of tumors, accounting for approximately 0.5% of all meningiomas. These tumors correspond to World Health Organization (WHO) Grade II lesions and behave aggressively, with an increased likelihood of recurrence.

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Background: Hospital-based cancer registries (HBCRs) provide information on the magnitude and distribution of cancers in a given hospital. Hospital-based brain tumor registry (HBBTR) data on primary intracranial tumors from a tertiary care neurological center is presented. This is compared with related national and international data.

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Background: Upregulation of insulin-like growth factor binding protein 2 (IGFBP-2) is often associated with aggressiveness of glioblastoma (GBM) and contributes to poor prognosis for GBM patients. In view of the regulation of β-catenin by IGFBP-2 in breast cancer and the crucial role of β-catenin pathway in glioma invasion, proliferation and maintenance of glioma stem cells, the mechanism of regulation of β-catenin by IGFBP-2, and its role in GBM prognosis was studied.

Methods: Regulation of the β-catenin pathway was studied by immunocytochemistry, Western blot analysis, luciferase assays, and real-time RT-PCR.

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Background: Manganese super oxide dismutase (MnSOD) has been previously identified as one of the top regulated genes associated with poor survival in glioblastoma (GBM) patients. In the current study we have evaluated the protein expression of MnSOD across various grades of astrocytoma, studied its influence on survival of GBM patients and following recurrence.

Methods: The protein expression of MnSOD was analyzed on tumor tissue sections by immunohistochemistry on 30 diffuse astrocytomas (DA), 50 anaplastic astrocytomas (AA), 30 paired (primary and recurrent) GBM samples and 30 non-tumor brain tissues.

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Background: Protein phosphatase 1 α (PP1A) is an enzyme intimately associated with cell cycle, the over expression of which has been demonstrated in glioblastoma (GBM). Further, the nuclear expression of PP1A has been shown to be highly specific to GBM. In addition, PP1A has been shown to be a connecting molecule in the p53 containing GBM sub network.

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Background: Despite the conventional acceptance of the matrix metalloproteinases (MMP)-2 and MMP-9, as markers of invasion in glioblastoma (GBM), there is no large body of evidence supporting their role as prognostic markers. Since the co-expression of MMPs with p53 was noted to be prognostic in other cancers, we evaluated the protein expression of MMP-2 and MMP-9 in GBM and explored their prognostic relevance with respect to p53 expression.

Materials And Methods: Tumor tissues from a uniformly treated cohort of 132 GBM patients were examined for MMP-2, MMP-9, and p53 protein expression by immunohistochemistry (IHC).

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Background: Insulin-like growth factor binding proteins (IGFBPs) are known to be differentially expressed in brain tumours. The role of some IGFBPs in malignant CNS tumours, except glioblastoma, is unknown. We evaluated the protein expression of 3 IGFBP isoforms (IGFBP-2, -3, -5) in medulloblastoma and correlated them with histological subtypes and clinical parameters.

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Object: Insulin-like growth factor binding proteins (IGFBPs) have been implicated in the pathogenesis of glioma. In a previous study the authors demonstrated that IGFBP-3 is a novel glioblastoma biomarker associated with poor survival. Since signal transducer and activator of transcription 1 (STAT-1) has been shown to be regulated by IGFBP-3 during chondrogenesis and is a prosurvival and radioresistant molecule in different tumors, the aim in the present study was to explore the functional significance of IGFBP-3 in malignant glioma cells, to determine if STAT-1 is indeed regulated by IGFBP-3, and to study the potential of STAT-1 as a biomarker in glioblastoma.

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S100A2, an EF hand calcium-binding protein, is a potential biomarker in several cancers and is also a TGF-β (transforming growth factor-β)-regulated gene in melanoma and lung cancer cells. However, the mechanism of S100A2 regulation by TGF-β and its significance in cancer progression remains largely unknown. In the present study we report the mechanism of S100A2 regulation by TGF-β and its possible role in TGF-β-mediated tumour promotion.

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