Horizontal gene transfers and cell fusions in microbiology, immunology and oncology (Review)

Sinkovics, Joseph G.

doi:10.3892/ijo_00000357

Cited by 6 publications

(8 citation statements)

References 275 publications

(392 reference statements)

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“…It is naturally essential to clarify the promoter factor inducing the malignant transformation of stromal cells in tumors. Several factors have been considered in previous studies, including horizontal transmission of malignancy by cell fusion ( 38 – 42 ), exosomes (or microvesicles) ( 43 , 44 ) or even sera ( 45 , 46 ). However, more significant is the fact that, if the change in stromal cells in the development of tumors in patients is consistent with the transplanted tumor model, the results of this study have added a new basis to the theory that malignant tumors have heterogeneity ( 47 ), with practical value in research on resistance to radiation and chemotherapy of heterogeneous tumors ( 48 ).…”

Section: Discussionmentioning

confidence: 99%

Experimental research of host macrophage canceration induced by glioma stem progenitor cells

Wang

Cui

Fei

et al. 2014

Molecular Medicine Reports

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The involvement of tumor-associated macrophages in tumor progression is an indisputable fact. However, whether the growth-promotion effects of macrophages towards tumors in the aggressive stage affect their own canceration remains unknown. In the present study, human glioma stem/progenitor cells transfected with red fluorescent protein gene (SU3-RFP) were seeded inside the abdominal cavity of transgenic nude mice, of which all nucleated cells could express green fluorescent protein (GFP), forming a tumor model with a double-color RFP/GFP fluorescent tracer. Ascites and tumor nodules from tumor-bearing mice were cultured, then the GFP+ cells were separated for clonal culture and further related phenotypic characterization and tumorigenicity tests. It was observed that the GFP+ cells isolated from ascites and solid tumors exhibited unlimited proliferative potential; the monoclonal cells were mouse-original, had a cancer cell phenotype and expressed the macrophage marker protein CD68. Thus, in the abdominal tumor model with double-color fluorescent tracer, macrophages recruited by tumor cells not only promoted tumor cell growth, but also exhibited their own canceration. This discovery is significant for the further study of tumor tissue remodeling and the tumor microenvironment.

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Section: Discussionmentioning

confidence: 99%

Experimental research of host macrophage canceration induced by glioma stem progenitor cells

Wang

Cui

Fei

et al. 2014

Molecular Medicine Reports

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“…This notion is in line with the observation that local ECs and stromal fibroblasts in cancers are also capable of acquiring genetic changes of neighbor tumor cells (Hida et al, 2004; Streubel et al, 2004). Various mechanisms could account for acquiring these genotypical changes, like cell fusion (Sinkovics, 2009), entosis (Janssen and Medema, 2011), horizontal (lateral) gene transfers (Sinkovics, 2009), and transdifferentiation (French et al, 2002). The finding that none of the glioma genetic aberrations were present in the circulating EPCs in the blood samples of the same patients would suggest that the genetic alterations are not acquired prior to the time these cells enter the tumors.…”

Section: Discussionmentioning

confidence: 99%

Intratumoral, not circulating, endothelial progenitor cells share genetic aberrations with glial tumor cells

Zheng

Weiden

Spek

et al. 2013

Journal Cellular Physiology

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Literature data indicate that glioma stem cells may give rise to both tumor cells and endothelial progenitor cells (EPCs). Malignant glioma patients usually have increased levels of circulating (EPCs) and these cells are known to contribute to the glioma neovasculature. In this study we compared the intratumoral and circulating EPCs of glioma patients for a set of common glioma genotypical aberrations (amplification of EGFR; deletion of PTEN and aneusomy of chromosomes 7 and 10). We found that the EPCs present in the tumor tissues, not the circulating EPCs, share genetic aberrations with the tumor cells. EPCs with EGFR amplification were found in 46% and with PTEN deletion in 36% of the cases. EPCs with polysomy 7 and monosomy 10 were detected in 56% and 38% of the cases while centrosomal abnormalities in EPCs were found in 68% of the cases. The presence of genetic aberrations of glioma cells in intratumoral EPCs may point to transdifferentiation of glioma stem cells into EPCs. However, the tissue specific CD133 splice variant of blood EPCs was detected in the glioma tissues but not in control brains, suggestive of a blood origin of at least part of the intratumoral EPCs. The findings highlight the complexity of the cellular constituents of glioma neovascularization which should be taken into account when developing anti-angiogenic strategies for gliomas.

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“…These breast cancer cells metastasize to the regional (axillary) lymph nodes [755]. Sinkovics proposed the term of traitor/transforming T cells (T/T T cells) for this class of host T lymphocytes [756]. The generation of T/T T lymphoid cell clones have nor as yet shown in B. fragilis enterotoxin-exposed colon cells, but it is documented in the microenvironment of human breast cancer that a subpopulation of reactive T lymphocytes (T/T T cells) with upregulated ILEI genes (interleukin-like epidermal-to-mesenchymal transition inducer) produce TGF-β [755].…”

Section: The Epithelial-to-mesenchymal Transformationmentioning

confidence: 99%

Horizontal Gene Transfers with or without Cell Fusions in All Categories of the Living Matter

Sinkovics

2011

Advances in Experimental Medicine and Biology

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This article reviews the history of widespread exchanges of genetic segments initiated over 3 billion years ago, to be part of their life style, by sphero-protoplastic cells, the ancestors of archaea, prokaryota, and eukaryota. These primordial cells shared a hostile anaerobic and overheated environment and competed for survival. "Coexist with, or subdue and conquer, expropriate its most useful possessions, or symbiose with it, your competitor" remain cellular life's basic rules. This author emphasizes the role of viruses, both in mediating cell fusions, such as the formation of the first eukaryotic cell(s) from a united crenarchaeon and prokaryota, and the transfer of host cell genes integrated into viral (phages) genomes. After rising above the Darwinian threshold, rigid rules of speciation and vertical inheritance in the three domains of life were established, but horizontal gene transfers with or without cell fusions were never abolished. The author proves with extensive, yet highly selective documentation, that not only unicellular microorganisms, but the most complex multicellular entities of the highest ranks resort to, and practice, cell fusions, and donate and accept horizontally (laterally) transferred genes. Cell fusions and horizontally exchanged genetic materials remain the fundamental attributes and inherent characteristics of the living matter, whether occurring accidentally or sought after intentionally. These events occur to cells stagnating for some 3 milliard years at a lower yet amazingly sophisticated level of evolution, and to cells achieving the highest degree of differentiation, and thus functioning in dependence on the support of a most advanced multicellular host, like those of the human brain. No living cell is completely exempt from gene drains or gene insertions.

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Horizontal gene transfers and cell fusions in microbiology, immunology and oncology (Review)

Cited by 6 publications

References 275 publications

Experimental research of host macrophage canceration induced by glioma stem progenitor cells

Experimental research of host macrophage canceration induced by glioma stem progenitor cells

Intratumoral, not circulating, endothelial progenitor cells share genetic aberrations with glial tumor cells

Horizontal Gene Transfers with or without Cell Fusions in All Categories of the Living Matter

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