scholarly journals Effect of Warfarin, Warfarin Enantiomers and Defibrase on Lewis Lung Carcinoma Metastasis Growth in Mice

1977 ◽  
Author(s):  
M.B. Donati ◽  
A. Poggi ◽  
L. Mussoni ◽  
L. Kornblihtt ◽  
G.de Gaetano ◽  
...  
Keyword(s):  
Lung Carcinoma ◽  
Primary Tumor ◽  
Lewis Lung Carcinoma ◽  
Lung Metastases ◽  
Tumor Development ◽  
Surgical Removal ◽  
Lewis Lung ◽  
Complex Activity ◽  
Metastasis Growth ◽  
Warfarin Enantiomers

The Lewis Lung Carcinoma (3LL) is a spontaneously metastasizing tumor, the development of which is eccompanied by marked hemostatic changes. Acceleration of labelled fibrinogen turnover and fibrin accumulation at the tumor and metastasis sites have been observed in 3LL bearing mice. Both the number and the weight of lung metastases were significantly lower in mice anti-coagulated with racemic sodium warfarin during the whole tumor development period (prothrombin complex activity around 20%). This treatment had less effect on the primary tumor. The anti-metastatic effect was slightly greater with larger doses of warfarin, which lowered the prothrombin complex activity to less than 5%. Continuous anticoagulation also protected the animals from pulmonary growth of blood-borne tumor emboli following intravenous injection of 3LL cells. This effect appeared to be closely associated with the anticoagulant activity of warfarin; indeed experiments performed with the resolved warfarin enantiomers showed that R-warfarin had virtually no anticlotting activity in mice and did not modify the metastatic growth of 3LL cells; the opposite was true for S-warfarin.Lung metastasis growth was increased in mice kept defibrinogenated during the whole period of tumor development by treatment with batrcxobin; in contrast, in mice kept defibrinated only during the period of metastasis growth, with or without surgical removal of the primary tumor, metastasis formation was slightly decreased. This suggests that fibrin may play different roles in various phases of metastaticspreading of the same tumor.

Can irradiation of lewis lung carcinoma primary tumor cause the growth of lung metastases?

1998 ◽  
Vol 42 (1) ◽  
pp. 169
Author(s):  
Mohamed K. Khan ◽  
Michael S. O'Reilly ◽  
Goulshan Ara ◽  
C. Norman Coleman ◽  
Judah Folkman
Keyword(s):  
Lung Carcinoma ◽  
Primary Tumor ◽  
Lewis Lung Carcinoma ◽  
Lung Metastases ◽  
Lewis Lung

scholarly journals Production of cytokines by cell-effectors of natural cytotoxicity system in mice under development of Lewis lung carcinoma

2004 ◽  
Vol 3 (2) ◽  
pp. 24-29
Author(s):  
Ye. Yu. Sherstoboyev ◽  
O. A. Kaplya ◽  
Ye. P. Zuyeva ◽  
T. G. Razina ◽  
O. I. Epstein
Keyword(s):  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Tumor Development ◽  
Peritoneal Macrophages ◽  
Interferon Γ ◽  
Lewis Lung ◽  
Natural Cytotoxicity ◽  
Tnf Α ◽  
Factor Α ◽  
T Helpers

Cytokine production by cell-effectors of natural cytotoxicity system under Lewis lung carcinoma development in F1(CBAxC57B1/6) line mice has been studied. It has been revealed the increase of interleukin-1β (IL-1β) production and tumor necrosis factor-α (TNF-α) by peritoneal macrophages. At this the balance of cytokines produced by T-helpers (Th)  has  been displaced to Th2 side, IL-4 production has increased and interferon-γ (IFN-γ) and IL-2 production has decreased. The rise of IL-10 production by lymphocytes has been observed in the later terms of tumor development.

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

In Vitro and in Vivo Selection of two Lewis Lung Carcinoma Cell Lines

1979 ◽  
Vol 65 (6) ◽  
pp. 657-664 ◽  
Author(s):  
Ada Sacchi ◽  
Anna Corsi ◽  
Marco Caputo ◽  
Gabriella Zupi
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Lung Metastases ◽  
Tumor Cell Lines ◽  
Lewis Lung ◽  
Selection Of

Two tumor cell lines adapted to grow in vitro were originated from an explant of lung metastases of Lewis lung carcinoma. These lines differ in their malignancy when reinoculated into syngeneic animals; nevertheless, they do not show any difference for their in vitro clonogenic ability. From these lines 2 in vivo sublines of 3LL carcinoma were developed. The TD 50 of the 2 in vivo sublines are different, and both the values obtained are lower than that of the original line. These results are interpreted as a selection of more malignant tumor cell lines.

Paracrine Suppression of VEGF Secretion by Erythropoietin Inhibits Tumor Growth.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 3909-3909
Author(s):  
Carroll R. Smith ◽  
Kenneth J. Salleng ◽  
Vaia Y. Sigounas ◽  
Adam Asch ◽  
George Sigounas
Keyword(s):  
Tumor Growth ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Lung Metastases ◽  
Control Group ◽  
Lewis Lung ◽  
Average Volume ◽  
Primary Tumors ◽  
Significant Difference

Abstract Several studies have reported that erythropoietin (Epo) is a pleiotropic cytokine with biological properties in addition to its primary function in regulating maturation, growth and survival along the erythroid lineage. Recently, a number of investigators have reported that various neoplastic tissues and human cancer cell lines express Epo and the Epo receptor (EpoR), raising suspicion for the presence of an autocrine-paracrine Epo-EpoR system. It has been shown that inhibition of vascular endothelial growth factor (VEGF) results in an increase of Epo secretion and increased hematocrit in vivo. In this study, we used an in vivo Lewis lung carcinoma model to examine a converse Epo effect on VEGF production and metastasis. Lewis lung carcinoma (LLC) cells were injected subcutaneously into C57BL mice. The plasma levels of VEGF, the tumor vessel formation, the size of the primary tumors and the extent of lung metastatic disease were determined. In addition, intravenously injected LLC cells seeded in the lungs were assessed. Tumor-bearing animals treated with Epo had 23.6% less VEGF in the plasma compared to saline treated mice (p<0.04). There was no correlation between VEGF concentration and hemoglobin levels in either group of animals. Tumor sections indicated that the number of blood vessels was higher (10.7% for inner and 23.8% for outer, respectively) in tumors obtained from animals treated with saline compared to Epo-treated mice (p>0.05). Using non-parametric analysis, we found that there was a statistically significant difference in tumor growth between saline-treated and Epo-treated animals (p<0.05). However, the number of lung metastases derived from primary tumors was similar in both groups. In assessing size of the metastatic tumors, we found that the average volume of lung nodules was 24.2% higher in saline-injected animals compared to Epo-treated mice. The number of tumors seeded in the lungs following intravenous injection of LLC cells was similar in animals treated with a high dosage of Epo, low dosage of Epo or saline. In addition, the average volume of the nodules was reduced by 42% in animals treated with high and low concentrations of Epo compared to the control group (p = 0.03). In conclusion, Epo exerts a paracrine suppressive effect on VEGF secretion resulting in slower tumor growth in this model.

EFFECT OF ENTEROSORPTION ON PARANEOPLASTIC SYNDROME MANIFESTATIONS IN MICE WITH HIGHLY ANGIOGENIC VARIANT OF LEWIS LUNG CARCINOMA

2015 ◽  
Vol 37 (4) ◽  
pp. 255-261 ◽  
Author(s):  
V V Sarnatskaya ◽  
V G Nikolaev ◽  
L A Yushko ◽  
L M Paziuk ◽  
O M Karaman ◽  
...  
Keyword(s):  
Lung Carcinoma ◽  
Paraneoplastic Syndrome ◽  
Peripheral Blood ◽  
Lewis Lung Carcinoma ◽  
Lung Metastases ◽  
Morphological Structure ◽  
Histological Structure ◽  
Lewis Lung ◽  
Morphological Examination ◽  
Biochemical Indices

Aim: To study the correcting effects of microgranulated HSGD enterosorbent on hematological, morphological and biochemical indices of paraneoplastic syndrome in mice with highly angiogenic variant of Lewis lung carcinoma LLC/R9. Methods: The study was performed on male С57/ВL6 mice with transplanted LLC/R9. Enterosorbent HSGD was administered daily at a dose of 0.625 g/kg for 2 weeks starting from 7th day after tumor cell transplantation. When enterosorption was completed, an analysis of peripheral blood, biochemical indices and morphological structure of tumor, lung, liver, spleen and thymus was carried out by standard methods. Results: It has been shown that administration of enterosorbent did not affect LLC/R9 growth but resulted in nearly two fold decrease of the volume of lung metastases (p < 0.05). Erythrocyte number and hemoglobin level were higher by 30.0% (p < 0.05) and 23.3% (p < 0.05), respectively, in mice treated with enterosorbents as compared to untreated animals. In addition sorbent treatment completely normalized the thrombocyte index resulting in elevation of platelet number by 54.5% (p < 0.01) up to their level in intact mice. The morphological examination of liver and biochemical analysis of peripheral blood evidenced on significant positive correcting effect of enterosorption on histological structure of this organ and its functional activ ity. Normalization of total proteins and serum albumin level as well as significant decrease of total lipid concentration by 29% (p < 0.01) in blood of treated mice were observed. Conclusion: Positive influence of microgranulated carbon sorbent on some hematological, morphological and biochemical indices of tumor associated symptoms in LLC/R9-bearing mice denotes that enterosorption-based therapy can be considered as a prospective treatment for correction of some paraneoplastic syndrome signs in cancer patients.

THE EFFECTS OF EARLY POSTOPERATIVE IMMUNIZATION WITH XENOGENEIC EMBRYO PROTEINS ON LEWIS LUNG CARCINOMA MODEL

2018 ◽  
Vol 40 (4) ◽  
pp. 275-281 ◽  
Author(s):  
T V Symchych ◽  
N I Fedosova ◽  
O M Karaman ◽  
I M Voeykova ◽  
G V Didenko
Keyword(s):  
Cytotoxic Activity ◽  
Lung Carcinoma ◽  
Lewis Lung Carcinoma ◽  
Nk Cell ◽  
Tumor Resection ◽  
Surgical Removal ◽  
Blast Transformation ◽  
Lewis Lung ◽  
Transformation Activity

Aim: To investigate the effect of chicken embryo proteins (CEP) as a prototype of xenogeneic vaccine on immune reactions in mice immunized after Lewis lung carcinoma (LLC) surgical removal. Materials and Methods: C57Bl male mice were immunized on days 1, 8, and 15 after surgical removal of LLC. The immune response was assessed on days 7, 14, 21 and 28 after tumor resection. Cytotoxic activity of natural killer cells (NK) and cytotoxic T-lymphocytes as well as antibody dependent cellular cytotoxicity was estimated in MTT-assay; specific antibodies were detected in ELISA; lymphocyte proliferation was tested in reaction of in vitro blast transformation. Results: None of the immunized mice developed LLC metastases. Immunization with CEP seems to prevent the potential decrease in NK cell cytotoxic activity and spontaneous blast transformation activity of lymphocytes following the surgically induced stress. Further research on improving immunization schedule and elucidating the mechanisms of NK modulation with CEP is needed.

Influence of Adriamycin on Growth Kinetics of Lewis Lung Carcinoma and Its Lung Metastases

Oncology ◽  
1983 ◽  
Vol 40 (2) ◽  
pp. 124-131 ◽  
Author(s):  
M. Madonna ◽  
T. Colombo ◽  
M.G. Donelli ◽  
G. Dagnino
Keyword(s):  
Lung Carcinoma ◽  
Growth Kinetics ◽  
Lewis Lung Carcinoma ◽  
Lung Metastases ◽  
Lewis Lung ◽  
Kinetics Of

scholarly journals Lipidomic Composition of Lewis Lung Carcinoma Metastases from Mice Fed an Obesogenic, High-fat Diet (P08-126-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Lin Yan ◽  
Sneha Sundaram ◽  
Michael Bukowski ◽  
Aaron Mehus ◽  
Matthew Picklo
Keyword(s):  
Fatty Acids ◽  
Fatty Acid Composition ◽  
Fatty Acid ◽  
Acid Composition ◽  
Lung Carcinoma ◽  
Primary Tumor ◽  
High Fat Diet ◽  
Lewis Lung Carcinoma ◽  
Lewis Lung ◽  
High Fat

Abstract Objectives Metastasis is a hallmark of cancer. Diet-induced obesity enhances lung metastasis from the primary tumor of Lewis lung carcinoma (LLC) in mice and the lipidomic profile of LLC primary tumor reflects the fatty acid composition of the diet. The objective of this study was to evaluate the impact of feeding an obesogenic, high-fat diet (HFD) on the lipidomic composition of resulting LLC metastases in mice. Methods Lung metastases were obtained from LLC primary tumor-bearing mice fed the AIN93G diet or a HFD providing 16% or 45% of energy from soybean oil. Triacylglycerols (TAG) in the metastases were analyzed by using a mass spectrometry method wherein the ion source was calibrated with an equimolar TAG standard. Neutral mass losses were used to determine the relative content of selected fatty acids across Brutto structures. Lipidomic data were analyzed by using MetaboAnalyst software (Version 4.0) with a false discovery rate of 0.05. Results Analysis of TAG composition in metastases identified 51 separate TAGs by Brutto structure. Six TAGs were significantly different between the two diet groups. Concentrations of TAGs containing 48 and 50 acyl carbons were lower and those containing 54 acyl carbons were higher in the HFD-fed mice. In mice fed the HFD, TAG 54:6 was higher whereas TAGs 48:1 and 50:1 were lower in the metastases than in mice-fed the AIN93G diet. The volcano plot analysis of TAGs showed that differences in 3 TAGs between the two groups were at least two-fold. In neutral loss analysis, the acyl chain C and saturation values of 36:4 and 36:5 corresponding to 18:2_18:2 and 18:2_18:3, respectively, were significantly higher in the HFD group than in the AIN93G group. Increases in these linoleic and linolenic acid-containing species reflected the higher concentrations of these fatty acids in the HFD. Conclusions The lipidomic profile of LLC metastases reflects the fatty acid composition of the diet. It suggests that lipidomic alteration of the metastases by an obesogenic diet may contribute to the aggressiveness of metastatic growth in the lungs. Funding Sources USDA ARS 3062-51000-050-00D.

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