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Fengming Lan, Qing Qin, Huiming Yu and Xiao Yue

G lioma is reported to be the most common primary intracranial tumor of adults, and glioblastoma (GBM) is the most frequently occurring and most malignant form of glioma. Even with combination treatment with surgery and chemoradiotherapy, the prognosis of GBM patients remains poor, with a 5-year survival rate lower than 5%. 1 Radiotherapy is an important and irreplaceable treatment modality for GBM patients; therefore, methods for enhancing the radiosensitivity of GBM are urgently needed. To date, various researchers have shown that the presence of GBM is

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Qiang Jia, Yanhe Li, Desheng Xu, Zhenjiang Li, Zhiyuan Zhang, Yipei Zhang, Dong Liu, Xiaomin Liu, Peiyu Pu and Chunsheng Kang

from activation of protooncogenes and inactivation of tumor suppressor genes. 2 One promising strategy involving the enhancement of antitumor effects by combining radiation therapy with gene therapy has been reported: due to the increased radiosensitivity achieved with gene therapy, lower doses of radiation can often be used. In a previous study in tumor-bearing rats, in which we used EGFR antisense RNA combined with GKT, we demonstrated that it was possible to effectively inhibit glioma cell proliferation and significantly increase apoptosis as well as prolong

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Manabu Takase and Osamu Watanabe

I ntracranial hemangiopericytomas are neoplasms which are thought to arise from blood vessels because their biological behavior is distinctly different from benign meningiomas. This report describes a case of a radiosensitive hemangiopericytoma located on the falx cerebri. Case Report This 58-year-old woman experienced the sudden onset of transient expressive aphasia 1 month prior to her first admission. Her general physical and neurological examination on admission were within normal limits. Computerized tomography (CT) of the head and carotid

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William C. Broaddus, Yue Liu, Laura L. Steele, George T. Gillies, Peck-Sun Lin, William G. Loudon, Kristoffer Valerie, Rupert K. Schmidt-Ullrich and Helen L. Fillmore

supporting this hypothesis in 9L rat gliosarcoma cells, which express mutant rat p53 . Whether such an approach would be effective in glioma cells already expressing wild-type p53 or whether it might only be applicable to the subset of tumors expressing mutant p53 is not yet clear. We report here results of similar studies in which RT2 rat glioblastoma cells were used; these cells express wild-type rat p53 as a baseline, which suggests the ability of transduction with wild-type p53 to enhance the radiosensitivity of these cells markedly. Western blot studies

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Christina Stache, Christiane Bils, Rudolf Fahlbusch, Jörg Flitsch, Michael Buchfelder, Harald Stefanits, Thomas Czech, Udo Gaipl, Benjamin Frey, Rolf Buslei and Annett Hölsken

restored radiosensitivity after combined treatment with radiotherapy and TKI. 52 A clinical phase II study revealed promising results of a combined gefitinib treatment strategy in childhood brainstem glioma. 55 Another promising group of agents are histone deacetylase (HDAC) inhibitors, described as radiosensitizers in esophageal cancer and prostate carcinoma, potentially acting via intrinsic apoptosis. 13 , 71 CUDC-101 is a combined inhibitor, blocking HDACs, human epidermal growth factor receptor 2 ( HER2), and EGFR signaling simultaneously. In vitro assays

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Frederick F. Lang, W. K. Alfred Yung, Uma Raju, Floralyn Libunao, Nicholas H. A. Terry and Philip J. Tofilon

to ionizing radiation. We found that transfection of Ad5CMV-p53 enhanced the radiosensitivity of p53 wild-type U87MG cells and that the mechanism of this p53 radiosensitization is associated with an increased frequency of radiation-induced apoptosis. Materials and Methods Human Glioma Cell Cultures The human glioma cell lines U87MG and U251MG were maintained in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10% fetal bovine serum and incubated at 37°C in a humidified atmosphere containing 5% CO 2 /95% air. The U87MG cells have homozygous wild

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Carl D. Lordo, Eric C. Stroude and Rolando F. Del Maestro

Res (Tokyo) 25: 215–224, 1984 21. Lordo CD , Stroude EC , Del Maestro RF : The effects of diphenylhydantoin on murine astrocytoma radiosensitivity. J Neurooncol 5 : 339 – 350 , 1987 Lordo CD, Stroude EC, Del Maestro RF: The effects of diphenylhydantoin on murine astrocytoma radiosensitivity. J Neurooncol 5: 339–350, 1987 22. Megyesi JF , Del Maestro RF : Nuclear magnetic resonance in the investigation of cerebral tumors and cerebral edema: a clue to the cellular alterations that may affect

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Desheng Xu, Qiang Jia, Yanhe Li, Chunsheng Kang and Peiyu Pu

radiosensitivity of these tumors is the hot spot in the radiotherapy research. It has been reported that enhancing the antitumor effects by combining radiation with other agents often allows lower doses to be used, thereby minimizing radiation side effects. Gene therapy in combination with radiation is one such promising strategy. Evidence indicates that p53 gene may play a role in improving the radiosensitivity of tumors by inducing cell cycle arrest and apoptosis. 5–7 Meanwhile, many authors have reported that fractionated radiotherapy in combination with adenoviral p53 can

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Leopoldo Casentini, Umberto Fornezza, Zeno Perini, Egle Perissinotto and Federico Colombo

multisession SRS schedules depending on different hypothetical α/β ratios No. of Fractions α/β = 2 α/β = 5 α/β = 10 3 19.8 Gy 18.3 Gy 16.8 Gy 4 22.4 Gy 20.4 Gy 18 Gy 5 24.5 Gy 22 Gy 19 Gy Our data suggest that the radiobiology of VSs is still unclear; genetic markers determining radiosensitivity need further investigation. 46 In any case, various reports demonstrate that SRS or fractionated stereotactic radiotherapy can achieve a tumor control rate of about 90%–96% treating VS, 7 , 9 , 14 , 16 , 18 , 23 , 28 , 29

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Eric K. Oermann, Marie-Adele S. Kress, Jonathan V. Todd, Brian T. Collins, Riane Hoffman, Huma Chaudhry, Sean P. Collins, David Morris and Matthew G. Ewend

the treatment of intracranial metastatic disease. Classic radioresistance (to fractionated therapy) is not a known predictor of response to radiosurgery. 1 , 12 For the treatment of larger metastatic lesions, it is increasingly common to fractionate the radiosurgical dose to minimize toxicity. It is unknown whether this fractionated radiosurgery would be equally effective in both classically radiosensitive and radioresistant tumors (analogous to single-fraction radiosurgery) or display less efficacy in radioresistant tumors (analogous to fractionated radiotherapy