Neural Progenitor and Hemopoietic Stem Cells Inhibit the Growth of Low-Differentiated Glioma

Baklaushev, V. P.; Grinenko, N. F.; Savchenko, Ekaterina; Bykovskaya, S. N.; Yusubalieva, Gaukhar M.; Viktorov, I. V.; Bryukhovetskii, A. S.; Bryukhovetskii, I. S.; Chekhonin, V. P.

doi:10.1007/s10517-012-1562-6

Cited by 4 publications

(2 citation statements)

References 12 publications

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“…After conventional treatments, every cancer patient should receive an obligatory course of immune therapy with well-known anti-cancer vaccines [41] and the preparations of CTLs; 5. The intrathecal transfusion of haploidentical HSCs of close relatives [58]. In the case of relapse, the consequent stages of the treatment should include all cytoreductive, cytostatic and cytotoxic approaches and end in the cytoregulatory personalized preparation with remodeled proteome [50].…”

Section: The Reasons For the Failures In The Mbt Therapy And Possiblementioning

confidence: 99%

Malignant Brain Tumors: Death Sentence, No Mercy

Bryukhovetskiy¹

2016

World. J. Oncol. Res.

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The article presents critical analysis of current methodological approaches, the standard and the options of complex therapy of malignant brain tumors (MBT). Author defines the main reasons for low effectiveness of MBT therapy. Relying on post-genome innovations (mass-spectrometry proteome mapping and whole transcriptome profiling of gene expression of cancer cells (CCs), cancer stem cells (CSCs) and tissue-specific stem cells (TSSCs) of the cancer patient, and their comparative analysis) the author proposes systemic solution for the MBT complex therapy that consists in a new alternative paradigm of cytoregulatory anti-cancer treatment of the MBT that is aimed at rigid control, management and regulation of the number of CCs and CSCs in the body. The goal of a new treatment paradigm is to transfer acute, uncontrollable and mortal process into chronic and non-lethal disease, and, thus, to improve survival rates and life quality of the patients. The instrument to implement the new paradigm is a sparing algorithm of conventional therapeutic methods and immune therapy, supplemented with personalized anti-tumor proteome-based cell therapy. The therapy implies transfusions of transcriptome-modified autologous TSSCs with specified properties to regulate the reproductive functions of the CSCs. The author proposes the complex therapy of the MBT and shows its social and economic significance for the society and neuroscience.

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Section: The Reasons For the Failures In The Mbt Therapy And Possiblementioning

confidence: 99%

Malignant Brain Tumors: Death Sentence, No Mercy

Bryukhovetskiy¹

2016

World. J. Oncol. Res.

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“…On the other hand, normal stem and progenitor cells can migrate to the pathological focus characterized by overexpression CXC-and CC-chemokines and their receptors (CXCR, CCR, CX3C -CX3CR) [34]. Stem cells introduced into tumor focus interact with glioma cells [25] and migrate into the peritumoral area of glioma invasion [3]. The tropism of these cells to the tumor focus allows considering stem cells as a potential vector for targeted therapy of gliomas [5,15,27,29].…”

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confidence: 99%

Functionally Active Gap Junctions between Connexin 43-Positive Mesenchymal Stem Cells and Glioma Cells

Габашвили

Baklaushev

Grinenko³

et al. 2015

Bull Exp Biol Med

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The formation of functional gap junctions between mesenchymal stem cells and cells of low-grade rat glioma C6 cells was studied in in vitro experiments. Immunocytochemical analysis with antibodies to connexin 43 extracellular loop 2 showed that mesenchymal stem cells as well as C6 glioma cells express the main astroglial gap junction protein connexin 43. Analysis of migration activity showed that mesenchymal stem cells actively migrate towards C6 glioma cells. During co-culturing, mesenchymal stem cells and glioma C6 form functionally active gap junctions mediating the transport of cytoplasmic dye from glioma cells to mesenchymal stem cells in the opposite direction. Fluorometry showed that the intensity of transport of low-molecular substances through heterologous gap junctions between mesenchymal stem cells and glioma cells is similar to that through homologous gap junctions between glioma cells. This phenomenon can be used for the development of new methods of cell therapy of high-grade gliomas.

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Antitumor Activity of Rat Mesenchymal Stem Cells during Direct or Indirect Co-Culturing with C6 Glioma Cells

et al. 2016

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The tumor-suppressive effect of rat mesenchymal stem cells against low-differentiated rat C6 glioma cells during their direct and indirect co-culturing and during culturing of C6 glioma cells in the medium conditioned by mesenchymal stem cells was studied in an in vitro experiment. The most pronounced antitumor activity of mesenchymal stem cells was observed during direct co-culturing with C6 glioma cells. The number of live C6 glioma cells during indirect co-culturing and during culturing in conditioned medium was slightly higher than during direct co-culturing, but significantly differed from the control (C6 glioma cells cultured in medium conditioned by C6 glioma cells). The cytotoxic effect of medium conditioned by mesenchymal stem cells was not related to medium depletion by glioma cells during their growth. The medium conditioned by other "non-stem" cells (rat astrocytes and fibroblasts) produced no tumor-suppressive effect. Rat mesenchymal stem cells, similar to rat C6 glioma cells express connexin 43, the main astroglial gap junction protein. During co-culturing, mesenchymal stem cells and glioma C6 cells formed functionally active gap junctions. Gap junction blockade with connexon inhibitor carbenoxolone attenuated the antitumor effect observed during direct co-culturing of C6 glioma cells and mesenchymal stem cells to the level produced by conditioned medium. Cell-cell signaling mediated by gap junctions can be a mechanism of the tumor-suppressive effect of mesenchymal stem cells against C6 glioma cells. This phenomenon can be used for the development of new methods of cell therapy for high-grade malignant gliomas.

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Neural Progenitor and Hemopoietic Stem Cells Inhibit the Growth of Low-Differentiated Glioma

Cited by 4 publications

References 12 publications

Malignant Brain Tumors: Death Sentence, No Mercy

Malignant Brain Tumors: Death Sentence, No Mercy

Functionally Active Gap Junctions between Connexin 43-Positive Mesenchymal Stem Cells and Glioma Cells

Antitumor Activity of Rat Mesenchymal Stem Cells during Direct or Indirect Co-Culturing with C6 Glioma Cells

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