scholarly journals new bIologIcal model of moderate InhIbItIon of tumor and metastases growth wIth prolonged leukopenIa In mIce

2016 ◽  
Vol 1 (5) ◽  
pp. 121-125
Author(s):  
Зуева ◽  
Elena Zueva ◽  
Разина ◽  
Tatyana Razina ◽  
Ермакова ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Tumor Therapy ◽  
Biological Model ◽  
Tumor Growth Inhibition ◽  
Lewis Lung ◽  
Inhibition Of Tumor Growth ◽  
Toxic Manifestation ◽  
Cyclophosphamide Dose

A new biological model of moderate inhibition of tumor growth and metastases with prolonged leukopenia on C57Bl/6 mice with the Lewis Lung Carcinoma was designed. The model was created by the injection of cyclophosphamide (dose 83.3mg/kg) on 6th, 12th, 18th days after tumor cells transplantation on animals. Experiment showed that 3-fold cyclo-phosphamide use leads to growth of primary tumor and metastases inhibition. Tumor growth inhibition was 34% on 21st day after cyclophosphamide inject. The number of metastases decreased by 4.7times (p<0,01). Metastatic area reduced. Metastasis frequency made 100%. In addition, the course of cyclophosphamide application caused inhibition of granulocytic and lymphoid hematopoiesis. The reducing the number of segmented neutrophils and lymphocytes was showed on the 3rd day after 1, 2 and 3 injections of cyclophosphamide. The model can be used to study the efficacy of drugs in tumor therapy and in correction of such toxic manifestation of chemotherapy as leukopenia.

Effect of Navelbine on Inhibition of Tumor Growth, Cellular Differentiation and Estrogen Receptor Status on Lewis Lung Carcinoma

Chemotherapy ◽  
2000 ◽  
Vol 46 (3) ◽  
pp. 188-194 ◽  
Author(s):  
A. Papageorgiou ◽  
P. Stravoravdi ◽  
D. Sahpazidou ◽  
K. Natsis ◽  
E. Chrysogelou ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Tumor Growth ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Cellular Differentiation ◽  
Estrogen Receptor Status ◽  
Lewis Lung ◽  
Receptor Status ◽  
Inhibition Of Tumor Growth

scholarly journals Paclitaxel Combined with Ticagrelor Inhibits B16F10 and Lewis Lung Carcinoma Cell Metastasis

2021 ◽  
Author(s):  
Xingjun Meng ◽  
Zhihui Cao ◽  
Renfeng Liu ◽  
Kai Zheng ◽  
Shuai Ding ◽  
...  
Keyword(s):  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Tumor Metastasis ◽  
Tumor Therapy ◽  
Microtubule Assembly ◽  
Dominant Factor ◽  
Migration And Invasion ◽  
Lewis Lung ◽  
Coronary Syndrome ◽  
Lymphatic Circulation

Abstract It is widely accepted that tumor metastasis is the dominant factor leading to cancer-related death. Tumor metastasis is mediated by cell invasion, blood circulation and lymphatic circulation. Paclitaxel, as a common anti-tumor drug and a mitotic inhibitor, promotes microtubule assembly and inhibits microtubule depolymerization. In addition, ticagrelor, an anti-platelet drug, is used to treat acute coronary syndrome. An increasing numbers of studies have reported that platelets can facilitate tumor metastasis. Therefore, inhibiting the effects of platelets can serve as a novel therapeutic strategy for cancer. To explore the effect of anti-tumor and anti-platelet drugs on tumor progression, the murine melanoma cell line, B16F10, and Lewis Lung carcinoma (LLC) cells were treated with paclitaxel and/or ticagrelor. Interestingly, the results demonstrated that paclitaxel and ticagrelor could not only suppress the proliferation, migration and invasion of B16F10 and LLC cells, but they could also prevent tumor metastasis to the lungs. Furthermore, the inhibitory effect of paclitaxel and ticagrelor was more apparent when both drugs were used in combination. Collectively, the current study demonstrated that the combination of paclitaxel and ticagrelor could be considered as a potential anti-tumor therapy approach.

scholarly journals ATIQCTPC targeting MMP-9: a key step to slowing primary tumor growth and inhibiting metastasis of lewis lung carcinoma in vivo

Oncotarget ◽  
2017 ◽  
Vol 8 (38) ◽  
pp. 63881-63889 ◽  
Author(s):  
Yuji Wang ◽  
Xinyi Xu ◽  
Ce Song ◽  
Jianhui Wu ◽  
Xi Hu ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Lung Carcinoma ◽  
Primary Tumor ◽  
Lewis Lung Carcinoma ◽  
Lewis Lung ◽  
Primary Tumor Growth

scholarly journals Superoxide- and no-dependent mechaniSmS of antitumor and antimetaStatic effect of L-arginine hydrochLoride and coenzyme Q10

2016 ◽  
Vol 38 (1) ◽  
pp. 31-35 ◽  
Author(s):  
A P Burlaka ◽  
I I Ganusevich ◽  
V V Golotiuk ◽  
A V Vovk ◽  
S M Lukin
Keyword(s):  
Tumor Growth ◽  
Lewis Lung Carcinoma ◽  
Superoxide Radical ◽  
Tumor Growth Inhibition ◽  
Low Doses ◽  
Lewis Lung ◽  
Combined Use ◽  
Arginine Hydrochloride ◽  
Radical Generation ◽  
High Doses

Aim: To study the redox-dependent mechanism of antiradical, antitumor and antimetastatic action of L-arginine hydrochloride (L-Arg) and coenzyme Q10 (CoQ10) in vivo. Materials and Methods: The study was performed on С57Вl mice with transplanted Lewis lung carcinoma treated by intraperitoneal injections of L-Arg at low or high doses (60 and 360 mg/kg body weight), CoQ10 (0.2 and 1.2 mg/kg body weight) or their combinations. Electron paramagnetic resonance was applied for analysis of mitochondrial electron transport chain, СoQ10 levels, free iron (FI), the level of NO, and the rate of superoxide radical generation. The activity of matrix metalloproteinase (MMP)-2 and -9 in tumor tissue was determined by zymography method in polyacrylamide gel. Results: Administration of L-Arg at high doses caused an inhibition of tumor growth by 48 ± 8.0%, increase of superoxide radical generation rate and NO levels to a value of 1.23 ± 0.14 аnd 2.26 ± 0.31 nm/g tissue · min, and decreased activity of MMP-2 and -9 (3.55 ± 0.8 and 4.8 ± 1.0 r.u., respectively). Treatment with L-Arg at low doses stimulated tumor growth and increased the levels of MMP-2 and -9 activities (8.44 ± 2.7 and 9.8 ± 3.1 r.u., respectively). Administration of СoQ10 at high doses significantly decreased superoxide radical generation rate to the values of 0.44 ± 0.09 nm/g tissue · min, levels of free iron and NO, and caused tumor growth inhibition by 54 ± 11.3%. The combined use of L-Arg and СoQ10 at high doses caused tumor growth inhibition by 51 ± 7.4% compared to Lewis lung carcinoma-bearing untreated animals (р < 0.05). Conclusions: Administration of L-Arg and СoQ10 caused the dose-dependent effect on the rate of generation of superoxide radicals, level of ubisemyquinone, complexes NOFeS-proteins, levels of FI and NO. L-Arg at low doses positively modulated MMP-9 activity that promoted tumor progression. Upon combined use of L-Arg and СoQ10, superoxide radicals and NO form the redox state that causes decrease of MMP-2, -9 activities with consequent inhibition of tumor invasion and metastasis.

Hybrid-primed lymphocytes and hybrid vaccination prevent tumor growth of lewis lung carcinoma in mice

Pneumologie ◽  
2006 ◽  
Vol 60 (S 1) ◽  
Author(s):  
S Rajkumar ◽  
R Schermuly ◽  
M Schneider ◽  
S Pullamsetti ◽  
F Grimminger ◽  
...  
Keyword(s):  
Tumor Growth ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Lewis Lung ◽  
Prevent Tumor Growth
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