scholarly journals Early detection of antiangiogenic treatment responses in a mouse xenograft tumor model using quantitative perfusion MRI

2014 ◽  
Vol 3 (1) ◽  
pp. 47-60 ◽  
Author(s):  
Reshmi Rajendran ◽  
Wei Huang ◽  
Annie Mei Yee Tang ◽  
Jie Ming Liang ◽  
Stephanie Choo ◽  
...  
Keyword(s):  
Early Detection ◽  
Tumor Model ◽  
Perfusion Mri ◽  
Xenograft Tumor ◽  
Antiangiogenic Treatment ◽  
Mouse Xenograft ◽  
Quantitative Perfusion ◽  
Xenograft Tumor Model ◽  
Treatment Responses

Abstract 2605: Mithramycin enhances the efficacy of etoposide in Ewing sarcoma cells and a mouse xenograft tumor model

2019 ◽  
Author(s):  
Anish Ray ◽  
Umesh T. Sankpal ◽  
Lina Albeer ◽  
Abigail Hunter ◽  
Holly Lout ◽  
...  
Keyword(s):  
Ewing Sarcoma ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Mouse Xenograft ◽  
Xenograft Tumor Model ◽  
Sarcoma Cells

Dynamic Contrast-Enhanced Folate-Receptor-Targeted MR Imaging Using a Gd-loaded PEG-Dendrimer–Folate Conjugate in a Mouse Xenograft Tumor Model

2009 ◽  
Vol 12 (2) ◽  
pp. 145-154 ◽  
Author(s):  
Wei-Tsung Chen ◽  
Dhakshanamurthy Thirumalai ◽  
Tiffany Ting-Fang Shih ◽  
Ran-Chou Chen ◽  
Shin-Yang Tu ◽  
...  
Keyword(s):  
Mr Imaging ◽  
Folate Receptor ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Mouse Xenograft ◽  
Dynamic Contrast Enhanced ◽  
Contrast Enhanced ◽  
Xenograft Tumor Model ◽  
Folate Conjugate

Abstract 2605: Mithramycin enhances the efficacy of etoposide in Ewing sarcoma cells and a mouse xenograft tumor model

2019 ◽  
Author(s):  
Anish Ray ◽  
Umesh T. Sankpal ◽  
Lina Albeer ◽  
Abigail Hunter ◽  
Holly Lout ◽  
...  
Keyword(s):  
Ewing Sarcoma ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Mouse Xenograft ◽  
Xenograft Tumor Model ◽  
Sarcoma Cells

scholarly journals Combining Sodium Butyrate With Cisplatin Increases the Apoptosis of Gastric Cancer In Vivo and In Vitro via the Mitochondrial Apoptosis Pathway

2021 ◽  
Vol 12 ◽  
Author(s):  
Yangbo Li ◽  
Pengzhan He ◽  
Yinghui Liu ◽  
Mingming Qi ◽  
Weiguo Dong
Keyword(s):  
Sodium Butyrate ◽  
Intestinal Flora ◽  
Tumor Model ◽  
Mitochondrial Apoptosis ◽  
Xenograft Tumor ◽  
Mouse Xenograft ◽  
Xenograft Tumor Model ◽  
Related Pathway

Introduction: The gastrointestinal malignancy, gastric cancer (GC), has a high incidence worldwide. Cisplatin is a traditional chemotherapeutic drug that is generally applied to treat cancer; however, drug tolerance affects its efficacy. Sodium butyrate is an intestinal flora derivative that has general anti-cancer effects in vitro and in vivo via pro-apoptosis effects and can improve prognosis in combination with traditional chemotherapy drugs. The present study aimed to assess the effect of sodium butyrate combined with cisplatin on GC.Methods: A Cell Counting Kit-8 assay was used to assess the viability of GC cells in vitro. Hoechst 33,258 staining and Annexin V-Phycoerythrin/7-Aminoactinomycin D were used to qualitatively and quantitatively detect apoptosis in GC cells. Intracellular reactive oxygen species (ROS) measurement and a mitochondrial membrane potential (MMP) assay kit were used to qualitatively and quantitatively reflect the function of mitochondria in GC cells. Western blotting was used to verify the above experimental results. A nude mouse xenograft tumor model was used to evaluate the anti-tumor efficacity of sodium and cisplatin butyrate in vivo.Results: Cisplatin combined with sodium butyrate increased the apoptosis of GC cells. In the nude mouse xenograft tumor model, sodium butyrate in combination with cisplatin markedly inhibited the growth of the tumor more effectively than either single agent. The combination of sodium butyrate and cisplatin increased the intracellular ROS, decreased the MMP, and suppressed the invasion and migration abilities of GC cells. Western blotting verified that the combination of sodium butyrate and cisplatin remarkably enhanced the levels of mitochondrial apoptosis-related pathway proteins.Conclusion: Sodium butyrate, a histone acetylation inhibitor produced by intestinal flora fermentation, combined with cisplatin enhanced the apoptosis of GC cells through the mitochondrial apoptosis-related pathway, which might be considered as a therapeutic option for GC.

Responsiveness of Human Prostate Carcinoma Bone Tumors to Interleukin-2 Therapy in a Mouse Xenograft Tumor Model

1999 ◽  
Vol 23 (5) ◽  
pp. 408-416 ◽  
Author(s):  
Sosa V. Kocheril ◽  
David J. Grignon ◽  
Ching Y. Wang ◽  
Richard L. Maughan ◽  
Emily J. Montecillo ◽  
...  
Keyword(s):  
Prostate Carcinoma ◽  
Bone Tumors ◽  
Interleukin 2 ◽  
Tumor Model ◽  
Human Prostate ◽  
Xenograft Tumor ◽  
Mouse Xenograft ◽  
Human Prostate Carcinoma ◽  
Xenograft Tumor Model

Antitumor Activity of γδ T Cells Reactive against Cytomegalovirus-Infected Cells in a Mouse Xenograft Tumor Model

2009 ◽  
Vol 69 (9) ◽  
pp. 3971-3978 ◽  
Author(s):  
Christel Devaud ◽  
Eric Bilhere ◽  
Séverine Loizon ◽  
Vincent Pitard ◽  
Charlotte Behr ◽  
...  
Keyword(s):  
T Cells ◽  
Antitumor Activity ◽  
Γδ T Cells ◽  
Tumor Model ◽  
Xenograft Tumor ◽  
Mouse Xenograft ◽  
Xenograft Tumor Model ◽  
Infected Cells

scholarly journals Wnt5b-induced PCP/JNK Activation Promotes PD-L1 Expression and the Malignant Phenotype of Non-small Cell Lung Cancer 

2020 ◽  
Author(s):  
Guangping Wu ◽  
Yuan Luo ◽  
Yusai Xie ◽  
Yang Han ◽  
Di Zhang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Tumor Model ◽  
Small Cell ◽  
Xenograft Tumor ◽  
Small Cell Lung ◽  
Malignant Phenotype ◽  
Membrane Recruitment ◽  
Xenograft Tumor Model

Abstract Background: Wnt5b is noncanonical Wnt ligand, and programmed-death ligand 1 (PD-L1) is a targeted agent for immunotherapy, but the mechanism by which Wnt5b regulates PD-L1 expression in non-small cell lung cancer (NSCLC) is unclear. Methods: Wnt5b and PD-L1 expressions were detected in NSCLC specimens by immunohistochemistry. The interrelationship connecting Wnt5b with PD-L1 was verified using dual-luciferase assay, immunofluorescence, coimmunoprecipitation, western blot，real-time PCR and xenograft tumor model. Results: Wnt5b and PD-L1 expressions were positively correlated in NSCLC specimens. Five-year survival time in the group with their coexpression was significantly lower than that without coexpression. Under the effect of Wnt5b, Frizzled-3 (Fzd3) initiated Dishevellde-3 (Dvl-3) membrane recruitment via DEP domain by Dvl-3 phosphorylation, contributing to activate PCP/JNK signaling through the small GTPase Rac1, and then upregulate PD-L1 expression and promote the malignant phenotype of NSCLC in vivo and in vitro. After PD-L1 antibody treatment, Wnt5b induced tumor growth was inhibited significantly in xenograft tumor model. Conclusion: We demonstrate a new signal transduction pathway: Wnt5b initiates Dvl-3 membrane recruitment via DEP domain by Fzd3 so as to promote Rac1–PCP/JNK–PD-L1 pathway, which provides a potential target for clinical intervention and immunotherapy in lung cancer.

Sign in / Sign up

Export Citation Format

Share Document