Radiosensitivity and Capacity to Recover from Radiation-Induced Damage in Pimonidazole-Unlabeled Oxygenated Intratumor Quiescent Cells Depend on p53 Status of Tumor Cells

2016 ◽  
Vol 96 (2) ◽  
pp. E557-E558
Author(s):  
S.I. Masunaga ◽  
K. Tano ◽  
Y. Sanada ◽  
Y. Sakurai ◽  
H. Tanaka ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Quiescent Cells ◽  
Radiation Induced ◽  
P53 Status

scholarly journals Impact of the p53 Status of the Tumor Cells on the Effect of Reactor Neutron Beam Irradiation, with Emphasis on the Response of Intratumor Quiescent Cells

2002 ◽  
Vol 93 (12) ◽  
pp. 1366-1377 ◽  
Author(s):  
Shin-ichiro Masunaga ◽  
Koji Ono ◽  
Akihisa Takahashi ◽  
Yoshinori Sakurai ◽  
Ken Ohnishi ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Neutron Beam ◽  
Reactor Neutron ◽  
Beam Irradiation ◽  
Quiescent Cells ◽  
P53 Status

scholarly journals Effects of p53 Status of Tumor Cells and Combined Treatment With Mild Hyperthermia, Wortmannin or Caffeine on Recovery From Radiation-Induced Damage

2019 ◽  
Vol 10 (3) ◽  
pp. 132-141 ◽  
Author(s):  
Shin-ichiro Masunaga ◽  
Keizo Tano ◽  
Yu Sanada ◽  
Minoru Suzuki ◽  
Akihisa Takahashi ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Combined Treatment ◽  
Mild Hyperthermia ◽  
Radiation Induced ◽  
P53 Status

Tumor cells suppress radiation-induced immunity by hijacking caspase 9 signaling

2020 ◽  
Vol 21 (5) ◽  
pp. 546-554 ◽  
Author(s):  
Chuanhui Han ◽  
Zhida Liu ◽  
Yunjia Zhang ◽  
Aijun Shen ◽  
Chunbo Dong ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Caspase 9 ◽  
Radiation Induced ◽  
Induced Immunity

scholarly journals CBIO-11. NOVEL THERAPY TO TARGET PR-RECURRENT GLIOMA

2020 ◽  
Vol 22 (Supplement_2) ◽  
pp. ii17-ii18
Author(s):  
Masum Rahman ◽  
Ian E Olson ◽  
Rehan Saber ◽  
Jibo Zhang ◽  
Lucas P Carlstrom ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Tumor Recurrence ◽  
Primary Brain Tumor ◽  
Differential Sensitivity ◽  
Proliferating Cells ◽  
Novel Therapy ◽  
Conventional Radiation ◽  
Long Time ◽  
Radiation Induced

Abstract BACKGROUND Glioblastoma is a fatal infiltrative primary brain tumor, and standard care includes maximal safe surgical resection followed by radiation and Temozolomide (TMZ). Therapy-resistant residual cells persist in a latent state a long time before inevitable recurrence. Conventional radiation and Temozolomide (TMZ) treatment cause oxidative stress and DNA damage resulting senescent-like state of cell-cycle arrest. However, increasing evidence demonstrates escaping senescence leads to tumor recurrence. Thus, the ablation of senescent tumor cells after chemoradiation may be an avenue to limit tumor recurrence. METHODS 100uM TMZ for 7days or 10-20Gy radiation (cesium gamma radiator) was used for senescence induction in human glioblastoma in vitro and confirmed by SA-Beta gal staining and PCR. Replication arrest assessed by automated quantification of cellular confluence (Thermo Scientific Series 8000 WJ Incubator). We evaluated the IC50 for several senolytics targeting multiple SCAPs, including Dasatinib, Quercetin, AMG-232, Fisetin, Onalespib, Navitoclax, and A1331852, and in senescent vs. proliferating cells. RESULTS Among the senolytic tested, the Bcl-XL inhibitors A1331852 and Navitoclax both shown senolytic effect by selectively killing radiated, senescent tumor cells at lower concentrations as compared to 0Gy treated non-senescent cells. Across 12 GBM cell lines, IC50 for senescent cells was 6–500 times lower than non-senescent GBM(p< 0.005). Such differential sensitivity to Bcl-XL inhibition after radiation has also observed by BCL-XL knockdown in radiated glioma. CONCLUSION These findings suggest the potential to harness radiation-induced biology to ablate surviving quiescent cells and demonstrate Bcl-XL dependency as a potential vulnerability of surviving tumor cells after exposure to chemoradiation.

scholarly journals Inhibition of Rac1 attenuates radiation-induced lung injury while suppresses lung tumor in mice

2022 ◽  
Vol 8 (1) ◽  
Author(s):  
Ni An ◽  
Zhenjie Li ◽  
Xiaodi Yan ◽  
Hainan Zhao ◽  
Yajie Yang ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Lung Injury ◽  
Mouse Model ◽  
Tumor Cells ◽  
Nuclear Translocation ◽  
Lung Tumor ◽  
Lung Epithelial Cells ◽  
Normal Lung ◽  
Limiting Factor ◽  
Radiation Induced

AbstractThe lung is one of the most sensitive tissues to ionizing radiation, thus, radiation-induced lung injury (RILI) stays a key dose-limiting factor of thoracic radiotherapy. However, there is still little progress in the effective treatment of RILI. Ras-related C3 botulinum toxin substrate1, Rac1, is a small guanosine triphosphatases involved in oxidative stress and apoptosis. Thus, Rac1 may be an important molecule that mediates radiation damage, inhibition of which may produce a protective effect on RILI. By establishing a mouse model of radiation-induced lung injury and orthotopic lung tumor-bearing mouse model, we detected the role of Rac1 inhibition in the protection of RILI and suppression of lung tumor. The results showed that ionizing radiation induces the nuclear translocation of Rac1, the latter then promotes nuclear translocation of P53 and prolongs the residence time of p53 in the nucleus, thereby promoting the transcription of Trp53inp1 which mediates p53-dependent apoptosis. Inhibition of Rac1 significantly reduce the apoptosis of normal lung epithelial cells, thereby effectively alleviating RILI. On the other hand, inhibition of Rac1 could also significantly inhibit the growth of lung tumor, increase the radiation sensitivity of tumor cells. These differential effects of Rac1 inhibition were related to the mutation and overexpression of Rac1 in tumor cells.

scholarly journals Radiation Induced Upregulation of DNA Sensing Pathways is Cell-Type Dependent and Can Mediate the Off-Target Effects

Cancers ◽  
2020 ◽  
Vol 12 (11) ◽  
pp. 3365
Author(s):  
Tanja Jesenko ◽  
Masa Bosnjak ◽  
Bostjan Markelc ◽  
Gregor Sersa ◽  
Katarina Znidar ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Checkpoint Inhibitors ◽  
Cell Types ◽  
Immunofluorescent Staining ◽  
Dna Sensing ◽  
Radiation Induced ◽  
Underlying Mechanisms ◽  
Sting Pathway ◽  
Abscopal Effects ◽  
Target Effects

Irradiation of tumors generates danger signals and inflammatory cytokines that promote the off-target bystander and abscopal effects, evident especially when radiotherapy is administered in combination with the immune checkpoint inhibitors (ICI). The underlying mechanisms are not fully understood; however, cGAS-STING pathway was recognized as the main mediator. In our study, we demonstrate by immunofluorescent staining that tumor cells as well as macrophages, cell types abundant in the tumor microenvironmeent (TME) accumulate DNA in their cytosol soon after irradiation. This accumulation activated several distinct DNA sensing pathways, most prominently activated DNA sensors being DDX60, DAI, and p204 in tumor cells and DDX60, DAI, p204, and RIG-I in macrophages as determined by PCR and immunofluorescence imaging studies. This was accompanied by increased expression of cytokines evaluated by flow cytometry, TNFα, and IFNβ in tumor cells and IL1β and IFNβ in macrophages, which can alter the TME and mediate off-target effects (bystander or abscopal effects). These results give insight into the mechanisms involved in the stimulation of antitumor immunity by radiation.

Abstract C218: Relevance of p53 status for the response of tumor cells to MET inhibitors combined with irradiation.

2013 ◽  
Author(s):  
Kei Mikami ◽  
Michaela Medová ◽  
Bruno Streit ◽  
Mario P. Tschan ◽  
Andree Blaukat ◽  
...  
Keyword(s):  
Tumor Cells ◽  
P53 Status

Abstract 2066: Albumin-binding doxorubicin prodrug selectively activated by radiation-induced apoptotic tumor cells

2016 ◽  
Author(s):  
Seung Woo Chung ◽  
Kwangmeyung Kim ◽  
Seong Who Kim ◽  
In-San Kim ◽  
Sang Yoon Kim ◽  
...  
Keyword(s):  
Tumor Cells ◽  
Albumin Binding ◽  
Radiation Induced
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