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The Influence of Erythropoietin (EPO) on Cancer Cells and its Role in the Cancer Treatment


The Influence of Erythropoietin (EPO) on Cancer Cells and its Role in the Cancer Treatment
Authors : Almedina Kozić, Lejla Gurbeta, Enisa Omanović-mikličanin
Publication Date: 03-07-2017

Authors

Author(s):  Almedina Kozić, Lejla Gurbeta, Enisa Omanović-mikličanin

Published in:   International Journal of Engineering Research & Technology

License:  This work is licensed under a Creative Commons Attribution 4.0 International License.

Website: www.ijert.org

Volume/Issue:   Volume. 6 - Issue. 07 , July - 2017

e-ISSN:   2278-0181

Abstract

The hormone erythropoietin (EPO) is essential for the survival, proliferation and differentiation of the erythrocytic progenitors. The EPO receptor (EPO-R) of erythrocytic cells belongs to the cytokine class I receptor family and signals through various protein kinases and STAT transcription factors. The EPO-R is also expressed in many organs outside the bone marrow, suggesting that EPO is a pleiotropic anti-apoptotic factor. The controversial issue as to whether the EPO-R is functional in tumor tissue is critically reviewed. Importantly, most studies of EPO-R detection in tumor tissue have provided falsely positive results because of the lack of EPO-R specific antibodies. However, endogenous EPO appears to be necessary to maintain the viability of endothelial cells and to promote tumor angiogenesis. This review paper reviews EPO use in cancer patients and its management of anemia. While the findings promise beneficial effects of endogenous EPO and its therapeutic analogues as tissue-protective factors, for example in ischemic and degenerative heart and brain diseases, fear has also arisen that EPO may promote tumor cell survival and stimulate tumor growth. If the cancer patient is being treated with curative intent, the use of ESAs should be avoided. If the treatment plan is more conservative or palliative, ESA should be considered for anemia treatment, but the treatment should be controlled.

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