TH-A-BRB-04: Vascular Response to Microbeam Radiation Therapy in Vivo Using a Murine Window Chamber Tumor Model

2012 ◽  
Vol 39 (6Part29) ◽  
pp. 3983-3983 ◽  
Author(s):  
M Dewhirst ◽  
A Fontanella ◽  
G Palmer ◽  
M Boss ◽  
J Zhang ◽  
...  
Keyword(s):  
Radiation Therapy ◽  
Tumor Model ◽  
Vascular Response ◽  
Microbeam Radiation Therapy ◽  
Window Chamber

scholarly journals Current Topics in Esophageal Squamous Cell Carcinoma

Cancers ◽  
2020 ◽  
Vol 12 (10) ◽  
pp. 2898
Author(s):  
Hiroki Kurumi ◽  
Hajime Isomoto
Keyword(s):  
Squamous Cell Carcinoma ◽  
Radiation Therapy ◽  
Esophageal Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Three Dimensional ◽  
Intensity Modulated Radiation Therapy ◽  
Tumor Model ◽  
Stromal Cell Derived Factor

Esophageal squamous cell carcinoma (ESCC) is one of the most deadly cancers due to its extremely aggressive nature and poor survival rate. Central to East Asia is one of regions with the highest incidence of ESCC. In these five papers, the international leaders of ESCC in Asia have taken various approaches to ESCC. Lin et al. compared intensity-modulated radiation therapy with three-dimensional stereoscopic radiation therapy with respect to treatment of ESCC. Song et al. demonstrated that (S)-10-Hydroxycamptothecin is useful in the ESCC cell lines as well as in vivo using a patients-derived xenograft tumor model in mice. Chen et al. showed Stromal cell-derived factor-1α expression is an independent prognostic predictor of ESCC. Lin et al. showed that the SUVLN/SUVTumor ratio of PET-CT was associated with ESCC prognosis. Yoon et al. investigated the association between sarcopenia and prognosis in the ESCC patients. All reports are an essential approach to overcoming ESCC.

Diode in Vivo Dosimetry for Patients Receiving External Beam Radiation Therapy

10.37206/88 ◽  
2005 ◽  
Author(s):  
Ellen Yorke ◽  
Rodica Alecu ◽  
Li Ding ◽  
Doracy Fontenla ◽  
Andre Kalend ◽  
...  
Keyword(s):  
Radiation Therapy ◽  
External Beam Radiation Therapy ◽  
External Beam Radiation ◽  
In Vivo Dosimetry ◽  
External Beam ◽  
Beam Radiation

Long Non-Coding RNA ARAP1-AS1 Facilitates the Progression of Cervical Cancer by Regulating miR-149-3p and POU2F2

Pathobiology ◽  
2021 ◽  
pp. 1-12
Author(s):  
Ling Zhou ◽  
Xiao-li Xu
Keyword(s):  
Cervical Cancer ◽  
Tumor Model ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Non Coding Rna ◽  
Injection Model ◽  
Rna Immunoprecipitation ◽  
Long Non Coding Rna

<b><i>Background:</i></b> Emerging research has demonstrated that long non-coding RNAs (lncRNAs) attach great importance to the progression of cervical cancer (CC). LncRNA ARAP1-AS1 was involved in the development of several cancers; however, its role in CC is far from being elucidated. <b><i>Methods:</i></b> Real-time PCR (RT-PCR) was employed to detect ARAP1-AS1 and miR-149-3p expression in CC samples. CC cell lines (HeLa and C33A cells) were regarded as the cell models. The biological effect of ARAP1-AS1 on cancer cells was measured using CCK-8 assay, colony formation assay, flow cytometry, Transwell assay and wound healing assay in vitro, and subcutaneous xenotransplanted tumor model and tail vein injection model in vivo. Furthermore, interactions between ARAP1-AS1 and miR-149-3p, miR-149-3p and POU class 2 homeobox 2 (POU2F2) were determined by bioinformatics analysis, qRT-PCR, Western blot, luciferase reporter and RNA immunoprecipitation assay, respectively. <b><i>Results:</i></b> The expression of ARAP1-AS1 was enhanced in CC samples, while miR-149-3p was markedly suppressed. Additionally, ARAP1-AS1 overexpression enhanced the viability, migration, and invasion of CC cells. ARAP1-AS1 downregulated miR-149-3p via sponging it. ARAP1-AS1 and miR-149-3p exhibited a negative correlation in CC samples. On the other hand, ARAP1-AS1 enhanced the expression of POU2F2, which was validated as a target gene of miR-149-3p. <b><i>Conclusion:</i></b> ARAP1-AS1 was abnormally upregulated in CC tissues and indirectly modulated the POU2F2 expression via reducing miR-149-3p expression. Our study identified a novel axis, ARAP1-AS1/miR-149-3p/POU2F2, in CC tumorigenesis.

PO-1606: Measurement of dose distribution of cardiosynchronous brain motion in microbeam radiation therapy

2020 ◽  
Vol 152 ◽  
pp. S874
Author(s):  
M. Petasecca ◽  
M. Duncan ◽  
M. Donzelli ◽  
P. Pellicioli ◽  
E. Brauer-Krisch ◽  
...  
Keyword(s):  
Radiation Therapy ◽  
Dose Distribution ◽  
Microbeam Radiation Therapy ◽  
Brain Motion

scholarly journals Multi-Modal Multi-Spectral Intravital Microscopic Imaging of Signaling Dynamics in Real-Time during Tumor–Immune Interactions

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 499
Author(s):  
Tracy W. Liu ◽  
Seth T. Gammon ◽  
David Piwnica-Worms
Keyword(s):  
Molecular Imaging ◽  
Single Cell ◽  
Real Time ◽  
Bioluminescence Imaging ◽  
Emission Spectra ◽  
Ccd Camera ◽  
Microscopic Imaging ◽  
Signaling Dynamics ◽  
Window Chamber

Intravital microscopic imaging (IVM) allows for the study of interactions between immune cells and tumor cells in a dynamic, physiologically relevant system in vivo. Current IVM strategies primarily use fluorescence imaging; however, with the advances in bioluminescence imaging and the development of new bioluminescent reporters with expanded emission spectra, the applications for bioluminescence are extending to single cell imaging. Herein, we describe a molecular imaging window chamber platform that uniquely combines both bioluminescent and fluorescent genetically encoded reporters, as well as exogenous reporters, providing a powerful multi-plex strategy to study molecular and cellular processes in real-time in intact living systems at single cell resolution all in one system. We demonstrate that our molecular imaging window chamber platform is capable of imaging signaling dynamics in real-time at cellular resolution during tumor progression. Importantly, we expand the utility of IVM by modifying an off-the-shelf commercial system with the addition of bioluminescence imaging achieved by the addition of a CCD camera and demonstrate high quality imaging within the reaches of any biology laboratory.

scholarly journals Metformin induces Ferroptosis by inhibiting UFMylation of SLC7A11 in breast cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Jingjing Yang ◽  
Yulu Zhou ◽  
Shuduo Xie ◽  
Ji Wang ◽  
Zhaoqing Li ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Treatment ◽  
Morphological Changes ◽  
Tumor Model ◽  
Independent Manner ◽  
Regulated Cell Death ◽  
Anti Cancer ◽  
Cancer Agent ◽  
Approved Drugs

Abstract Background Ferroptosis is a newly defined form of regulated cell death characterized by the iron-dependent accumulation of lipid peroxidation and is involved in various pathophysiological conditions, including cancer. Targeting ferroptosis is considered to be a novel anti-cancer strategy. The identification of FDA-approved drugs as ferroptosis inducers is proposed to be a new promising approach for cancer treatment. Despite a growing body of evidence indicating the potential efficacy of the anti-diabetic metformin as an anti-cancer agent, the exact mechanism underlying this efficacy has not yet been fully elucidated. Methods The UFMylation of SLC7A11 is detected by immunoprecipitation and the expression of UFM1 and SLC7A11 in tumor tissues was detected by immunohistochemical staining. The level of ferroptosis is determined by the level of free iron, total/lipid Ros and GSH in the cells and the morphological changes of mitochondria are observed by transmission electron microscope. The mechanism in vivo was verified by in situ implantation tumor model in nude mice. Results Metformin induces ferroptosis in an AMPK-independent manner to suppress tumor growth. Mechanistically, we demonstrate that metformin increases the intracellular Fe2+ and lipid ROS levels. Specifically, metformin reduces the protein stability of SLC7A11, which is a critical ferroptosis regulator, by inhibiting its UFMylation process. Furthermore, metformin combined with sulfasalazine, the system xc− inhibitor, can work in a synergistic manner to induce ferroptosis and inhibit the proliferation of breast cancer cells. Conclusions This study is the first to demonstrate that the ability of metformin to induce ferroptosis may be a novel mechanism underlying its anti-cancer effect. In addition, we identified SLC7A11 as a new UFMylation substrate and found that targeting the UFM1/SLC7A11 pathway could be a promising cancer treatment strategy.

scholarly journals Offset of apparent hyperpolarized 13 C lactate flux by the use of adjuvant metformin in ionizing radiation therapy in vivo

2021 ◽  
Author(s):  
Young‐Suk Choi ◽  
Joonsung Lee ◽  
Han‐Sol Lee ◽  
Jae Eun Song ◽  
Dong‐Hyun Kim ◽  
...  
Keyword(s):  
Radiation Therapy ◽  
Ionizing Radiation
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