Literature DB >> 26898918

Radiation-resistant B-1 cells: A possible initiating cells of neoplastic transformation.

Caroline Ferreira Guimarães-Cunha1, Anuska Marcelino Alvares-Saraiva2, Juliana de Souza Apostolico1, Ana Flavia Popi3.   

Abstract

The role of B-1 cells in the hyperproliferative hematologic disease has been described. Several reports bring evidences that B-1 cells are the main cell population in the chronic lymphatic leukemia. It is also described that these cells have an important involvement in the lupus erythematous systemic. The murine model used to investigate both disease models is NZB/NZW. Data from literature point that mutation in micro-RNA 15a and 16 are the responsible for the B-1 hyperplasia in these mice. Interestingly, it was demonstrated that NZB/NZW B-1 cells are radioresistant, contrariwise to observe in other mouse lineage derived B-1 cells and B-2 cells. However, some reports bring evidences that a small percentage of B-1 cells in healthy mice are also able to survive to irradiation. Herein, we aim to investigate the malignant potential of ionizing-radiation resistant B-1 cells in vitro. Our main goal is to establish a model that mimics the neoplastic transformation originate to a damage exposure of DNA, and not only related to intrinsic mutations. Data shown here demonstrated that radiation-resistant B-1 cells were able to survive long periods in culture. Further, these cells show proliferation index increase in relation to non-irradiated B-1 cells. In addition, radiation resistant B-1 cells showed hyperploid, morphologic alterations, increased induction of apoptosis after anti-IgM stimulation. Based on these results, we could suggest that radiation resistant B-1 cells showed some modifications in that could be related to induction of malignant potential.
Copyright © 2016. Published by Elsevier GmbH.

Entities:  

Keywords:  B-1 Cells; Bcl-2; Irradiation; Leukemia; Malignant cells

Mesh:

Substances:

Year:  2016        PMID: 26898918     DOI: 10.1016/j.imbio.2016.01.010

Source DB:  PubMed          Journal:  Immunobiology        ISSN: 0171-2985            Impact factor:   3.144


  4 in total

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  4 in total

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