scholarly journals Tet2 ‐deficency in immune cells exacerbates tumor progression by increasing angiogenesis in a lung cancer model

2021 ◽  
Author(s):  
Yen T.M. Nguyen ◽  
Manabu Fujisawa ◽  
Tran B. Nguyen ◽  
Yasuhito Suehara ◽  
Sakamoto Tatsuhiro ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tumor Progression ◽  
Immune Cells ◽  
Cancer Model ◽  
Lung Cancer Model

scholarly journals Knockout of c-mos gene does not affect tumor progression in murine models of lung and colorectal cancer

2017 ◽  
Author(s):  
Zhengxi Chen ◽  
Ju Qiao ◽  
Zhenqi Chen ◽  
Qian Xiao
Keyword(s):  
Colorectal Cancer ◽  
Lung Cancer ◽  
Tumor Progression ◽  
Cancer Patients ◽  
Survival Rates ◽  
Intestinal Cancer ◽  
Murine Models ◽  
Cancer Model ◽  
Poor Survival ◽  
Lung Cancer Model

Background. The c-mos proto-oncogene was one of the first proto-oncogenes to be cloned. Apart from its role in meiosis, many efforts have been made to illuminate the mechanisms by which c-mos acts as an oncogene. c-mos or its coding messenger RNA have been confirmed in most somatic tissues at low levels. However, a detailed role of c-mos as an oncogene in somatic cells remains unknown. Methods. In this study, we analyzed online databases to find out the correlation between Mos expression and poor survival rates in human cancer patients. Then, we investigated whether the involvement of c-mos in tumor progression via applying Apcmin intestinal cancer model and KrasG12D lung cancer model. Results. First, we found the expression of Mos differed between human and mice, and a significant correlation between high Mos expression and poor survival rates in lung cancer patients. Interestingly, we tested that the effects of deficient c-mos in both Apcmin intestinal cancer model and KrasG12D lung cancer model. Despite the abovementioned significant correlation, the results did not show a strong inhibitory effect on murine models of lung and intestine tumors. We find no evidence of a direct role for c-mos in tumor progression in abovementioned mice models. Discussion. It indicated that functions of c-mos gene might be species-specific and that c-mos involvement in tumor progression was circumstantial and it probably depended on other oncogene activation. Keywords: c-mos, Kras, Apc, survival rate, murine model, lung cancer, colorectal cancer

scholarly journals Knockout of c-mos gene does not affect tumor progression in murine models of lung and colorectal cancer

2017 ◽  
Author(s):  
Zhengxi Chen ◽  
Ju Qiao ◽  
Zhenqi Chen ◽  
Qian Xiao
Keyword(s):  
Colorectal Cancer ◽  
Lung Cancer ◽  
Tumor Progression ◽  
Cancer Patients ◽  
Survival Rates ◽  
Intestinal Cancer ◽  
Murine Models ◽  
Cancer Model ◽  
Poor Survival ◽  
Lung Cancer Model

Background. The c-mos proto-oncogene was one of the first proto-oncogenes to be cloned. Apart from its role in meiosis, many efforts have been made to illuminate the mechanisms by which c-mos acts as an oncogene. c-mos or its coding messenger RNA have been confirmed in most somatic tissues at low levels. However, a detailed role of c-mos as an oncogene in somatic cells remains unknown. Methods. In this study, we analyzed online databases to find out the correlation between Mos expression and poor survival rates in human cancer patients. Then, we investigated whether the involvement of c-mos in tumor progression via applying Apcmin intestinal cancer model and KrasG12D lung cancer model. Results. First, we found the expression of Mos differed between human and mice, and a significant correlation between high Mos expression and poor survival rates in lung cancer patients. Interestingly, we tested that the effects of deficient c-mos in both Apcmin intestinal cancer model and KrasG12D lung cancer model. Despite the abovementioned significant correlation, the results did not show a strong inhibitory effect on murine models of lung and intestine tumors. We find no evidence of a direct role for c-mos in tumor progression in abovementioned mice models. Discussion. It indicated that functions of c-mos gene might be species-specific and that c-mos involvement in tumor progression was circumstantial and it probably depended on other oncogene activation. Keywords: c-mos, Kras, Apc, survival rate, murine model, lung cancer, colorectal cancer

scholarly journals DNA vaccine elicits an efficient antitumor response by targeting the mutant Kras in a transgenic mouse lung cancer model

Gene Therapy ◽  
2014 ◽  
Vol 21 (10) ◽  
pp. 888-896 ◽  
Author(s):  
T-Y Weng ◽  
M-C Yen ◽  
C-T Huang ◽  
J-J Hung ◽  
Y-L Chen ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Transgenic Mouse ◽  
Dna Vaccine ◽  
Mouse Lung ◽  
Cancer Model ◽  
Antitumor Response ◽  
Lung Cancer Model

Refinement of an Orthotopic Lung Cancer Model in the Nude Rat

2001 ◽  
Vol 38 (5) ◽  
pp. 483-490 ◽  
Author(s):  
T. H. March ◽  
P. G. Marron-Terada ◽  
S. A. Belinsky
Keyword(s):  
Lung Cancer ◽  
Cancer Model ◽  
Nude Rat ◽  
Lung Cancer Model

scholarly journals Combination Therapy of VEGF-Trap and Gemcitabine Results in Improved Anti-Tumor Efficacy in a Mouse Lung Cancer Model

PLoS ONE ◽  
2013 ◽  
Vol 8 (7) ◽  
pp. e68589 ◽  
Author(s):  
Shuang Zhou ◽  
Yang Yang ◽  
Yaoqin Yang ◽  
Huihong Tao ◽  
Dong Li ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Combination Therapy ◽  
Mouse Lung ◽  
Cancer Model ◽  
Lung Cancer Model ◽  
Vegf Trap

scholarly journals Ex Vivo Four-Dimensional Lung Cancer Model Mimics Metastasis

2015 ◽  
Vol 99 (4) ◽  
pp. 1149-1156 ◽  
Author(s):  
Dhruva K. Mishra ◽  
Chad J. Creighton ◽  
Yiqun Zhang ◽  
Fengju Chen ◽  
Michael J. Thrall ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Ex Vivo ◽  
Cancer Model ◽  
Lung Cancer Model

scholarly journals Combination Therapy with Vidaza and Entinostat Suppresses Tumor Growth and Reprograms the Epigenome in an Orthotopic Lung Cancer Model

2011 ◽  
Vol 71 (2) ◽  
pp. 454-462 ◽  
Author(s):  
Steven A. Belinsky ◽  
Marcie J. Grimes ◽  
Maria A. Picchi ◽  
Hugh D. Mitchell ◽  
Chris A. Stidley ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Combination Therapy ◽  
Tumor Growth ◽  
Cancer Model ◽  
Lung Cancer Model
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