Morphologic Changes in the Tumor and Liver in Mice with Transplanted RLS40 Lymphosarcoma during Increase of Its Drug Resistance

Sen’kova, Aleksandra V.; Агеева, Т. А.; Zenkova, Marina A.

doi:10.1007/s10517-010-0921-4

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“…Tumor model. The cyclophosphamide resistant murine lymphosarcoma RLS (38,39) obtained from the repository of Institute of Cytology and Genetics SBRAS was used as a model. For grafting, cells were sampled from mice with 10-day ascites, diluted with physiological saline solution and inoculated into animals at the amount of 10 6 per mouse to produce the ascitic form of the tumor.…”

Section: Methodsmentioning

confidence: 99%

Approbation of the Cancer Treatment Approach Based on the Eradication of TAMRA+ Cancer Stem Cells in a Model of Murine Cyclophosphamide Resistant Lymphosarcoma

et al. 2020

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Background/Aim: We previously have described the "3+1" tumors cure approach consisting of individual time schedule of cyclophosphamide and dsDNA preparation administrations. The aim of the study was to adapt the "3+1" approach based on eradication of cancer stem cells to the model of murine ascitic cyclophosphamide-resistant lymphosarcoma (RLS). Materials and Methods: Adaptation of the "3+1" approach includes the identification of the timing to disrupt the tumorigenic potential of a certain tumor. Results: The proposed therapeutic scheme allowed complete reduction of primary RLS ascites in experimental animals. However, reduction of primary ascites due to the complementary action of cyclophosphamide and dsDNA was inevitably followed by the development of a secondary one, most likely arising from a solid carcinomatous formation in the peritoneal wall. Conclusion: The "3+1" approach resulted in the elimination of cancer stem cells, and, as a consequence, in the complete reduction of RLS ascites.Malignant neoplasms rank second in the world after cardiovascular disorders in overall mortality rates. Recent studies indicate a much higher complexity of the disease than previously thought. The main characteristic of this complexity determining the unpredictable response of neoplasms to a variety of therapeutic procedures and the difficulties in their cure is the heterogeneity of malignant cells that include a subpopulation of almost "indestructible" cells, which possess an incredible survival and proliferative potency, and is designated as tumor-initiating stem cells or cancer stem cells (CSCs) (1, 2).The main hallmarks of cancer stem cells are their capabilities of (1) self-renewal in through unlimited replicative cycles, (2) producing a progeny of committed cells with high proliferative activity, but incapable of inducing a new tumor, and (3) retaining a potency to induce new tumors with similar histological properties in a series of transplantations (3). CSCs possess a number of features allowing their dominance in co-existence with organism: self-sufficiency in proliferative stimuli (4), reduced sensitivity to anti-proliferative ones (5), immortalization (6, 7), dedifferentiation (8), genomic instability (9), increased efflux and metabolism of xenobiotics (10, 11), reversed "Warburg effect" (12, 13), suppression of pro-apoptotic signals ( 14), as well as stimulation of pathways causing apoptosis evasion (15). Another essential for disease development property of CSCs is their migratory capacity, allowing exit into the bloodstream, and formation of new growth foci in distant organs (16)(17)(18)(19)(20). Thus, the aforementioned properties of CSCs are such that they create 795

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Section: Methodsmentioning

confidence: 99%