Derkaoui Kheira Dalia
Oran University, Algeria
Samia Mourah
Oran University, Algeria
Marie Pierre Podgorniak
Oran University, Algeria
Irene Joab
Oran University, Algeria
Camelia Radulescy
Oran University, Algeria
Boucherit Elhassen
Oran University, Algeria
Elkebir Fatima Zohra
Oran University, Algeria
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How to cite this article
Derkaoui Kheira Dalia, Samia Mourah, Marie Pierre Podgorniak, Irene Joab, Camelia Radulescy, Boucherit Elhassen and Elkebir Fatima Zohra, 2015. Research of Epstein-Barr Virus Genome and Quantification of Viral Load in Algerian
Frozen Tissue of Breast Cancer. International Journal of Cancer Research, 11: 32-40.
DOI: 10.3923/ijcr.2015.32.40
URL: https://scialert.net/abstract/?doi=ijcr.2015.32.40
DOI: 10.3923/ijcr.2015.32.40
URL: https://scialert.net/abstract/?doi=ijcr.2015.32.40
Richard E. Kast, MD Reply
Nice work. Profound differences of markers and, as you demonstrate, viral infection of cells, is underappreciated. Tumors are heterogeneous within themselves even when H&E homogeneous, we agree. We make similar point in our glioblastoma treatment regimen,Oncotarget. 2014;5(18):8052-82.
Also consider breast H.pylori infection, as in Med Hypotheses. 2007;68(5):1041-6.
DERKAOUI-GRIBI DALIA
dear colleague, I'm flattered that you positively commented on my work.
Here is a short explanation:
Breast cancer etiology is multifactorial, it is a heterogeneous tumor with different histological types,
Data on the EBV virus as breast cancer cofactors, provide an essential but not conclusive part, despite numerous studies that highlight the presence of EBV in tumor progression of breast cancer. However, the heterogenicity of the viral load may be itself a proof of non-association of the EBV breast cancer. Indeed, although few cells are infected with EBV in breast cancer, it remains to know the role of these cells in carcinogenesis and tumor progression.
Two hypotheses have been advanced to explain the heterogenicity viral load in breast cancer:
Either that EBV infects early mammary epithelial cells before the formation of the tumor followed by a phenomenon of "Hit and Run" this phenomenon is described as a mechanism for the cell transformation by human DNA virus, when the viral genetic information can not be detected in long term cultures of transformed host cells in vitro or after in vivo passage. In fact, this mechanism consists of the cell modified by a virus which is then lost "
The second hypothesis is that EBV infects cells at a late stage of tumor development that could lead to phenomena such as angiogenesis or metastasis.