Molecular Advances of Brain Tumors in Radiation Oncology

Noda, Shin‐ei; El‐Jawahri, Areej; Patel, Disha; Lautenschlaeger, Tim; Siedow, Michael; Chakravarti, Arnab

doi:10.1016/j.semradonc.2009.02.005

Cited by 57 publications

(50 citation statements)

References 75 publications

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“…2 Radiation therapy provides a survival benefit, but resistance of glioma cells to radiation limits the therapeutic efficacy of this standard adjuvant treatment. 3 Therefore, innovative approaches are urgently needed to overcome such resistance and thereby enhance the treatment outcome.…”

Section: Introductionmentioning

confidence: 99%

Silver nanoparticles outperform gold nanoparticles in radiosensitizing U251 cells in vitro and in an intracranial mouse model of glioma

Liu¹,

Jin²,

Guo³

et al. 2016

IJN

113

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Radiotherapy performs an important function in the treatment of cancer, but resistance of tumor cells to radiation still remains a serious concern. More research on more effective radiosensitizers is urgently needed to overcome such resistance and thereby improve the treatment outcome. The goal of this study was to evaluate and compare the radiosensitizing efficacies of gold nanoparticles (AuNPs) and silver nanoparticles (AgNPs) on glioma at clinically relevant megavoltage energies. Both AuNPs and AgNPs potentiated the in vitro and in vivo antiglioma effects of radiation. AgNPs showed more powerful radiosensitizing ability than AuNPs at the same mass and molar concentrations, leading to a higher rate of apoptotic cell death. Furthermore, the combination of AgNPs with radiation significantly increased the levels of autophagy as compared with AuNPs plus radiation. These findings suggest the potential application of AgNPs as a highly effective nano-radiosensitizer for the treatment of glioma.

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Section: Introductionmentioning

confidence: 99%

Silver nanoparticles outperform gold nanoparticles in radiosensitizing U251 cells in vitro and in an intracranial mouse model of glioma

Liu¹,

Jin²,

Guo³

et al. 2016

IJN

113

View full text Add to dashboard Cite

show abstract

“…However, this treatment remains a challenge for radiation oncologists because of tumor radioresistance. The intrinsic radiosensitivity of gliomas is a pivotal factor that determines the effectiveness of radiotherapy (3). Many factors, including genetic alterations and microenvironments, affect tumor response to ionizing radiation (4).…”

Section: Introductionmentioning

confidence: 99%

Cycling hypoxia increases U87 glioma cell radioresistance via ROS induced higher and long-term HIF-1 signal transduction activity

Hsieh¹,

Lee

Liang³

et al. 2010

Oncol Rep

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Abstract. Glioblastoma multiforme (GBM) tumors are the most common type of brain tumors and resistance to radiotherapy. This study aimed to investigate the differential effect and mechanism of tumor microenvironments, cycling hypoxia and non-interrupted hypoxia, on tumor cell radiosensitivity in the human U87 glioblastoma tumor model. We exposed U87 cells and mice bearing U87 glioma to experimentally imposed cycling or non-interrupted hypoxic stress in vitro and in vivo prior to treatment with ionizing irradiation. Clonogenic survival assay and tumor growth measurements were performed to determine tumor radiosensitivity. The differential regulation of non-interrupted vs. cycling hypoxia by hypoxia-inducible factor-1 (HIF-1) and the impact of HIF-1· on hypoxia-induced radioresistance were assessed by molecular assay and RNAiknockdown technology. Our results demonstrated that cycling hypoxia induced higher and longer term HIF-1 signal transduction activity via reactive oxygen species (ROS) in U87 cells compared with non-interrupted hypoxia. Cycling hypoxiainduced HIF-1· activation reflected ROS mediated HIF-1· synthesis and stabilization, whereas non-interrupted hypoxiainduced HIF-1· activation was due to decreased HIF-1· degradation resulting from decreased prolyl hydroxylation. With regard to tumor radiosensitivity, cycling hypoxia induced more tumor cell radioresistance and a decreased response to radiotherapy in U87 cells compared with non-interrupted hypoxia. HIF-1 knockdown during in vitro and in vivo hypoxic stresses combined with radiotherapy suppressed cycling and non-interrupted hypoxia-induced radioresistance while increasing overall tumor radiosensitivity. Our results suggest that cycling hypoxia induces more radioresistance than non-interrupted hypoxia in U87 gliomas, and ROS mediated HIF-1· activation is a crucial mechanism involved in hypoxia-induced differential radioresistant in U87 gliomas.

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“…Therefore it is thought that p53 mutations are a hallmark of low-grade gliomas and consequently also occur in secondary GBM that arise from lower grade gliomas (Noda et al, 2009). Loss of p53 is observed in grade II astrocytomas (35-60%), grade III astrocytomas (~50%), primary GBM (~30%), and secondary GBM (~60-65%) (Sulman et al, 2009;Bourne & Schiff, 2010;Gladson et al, 2010).…”

Section: Cell Cycle Regulation 221 P53mentioning

confidence: 99%

“…Overexpression of p53 has also been observed in ~50% of GBM cases (Kim et al, 2010). Interestingly, tumors that harbor 1p/19q co-deletions do not contain p53 mutations (Noda et al, 2009;Fischer & Aldape, 2010). MDM2, a negative regulator of p53, has also been reported to be amplified or mutated in anaplastic astrocytoma (AA) (13-43%) and in glioblastoma (~10-27%) (Gladson et al, 2010;Kim et al, 2010).…”

Section: Cell Cycle Regulation 221 P53mentioning

confidence: 99%