Special Issue "DNA Viruses in Human Cancer"
A special issue of Cancers (ISSN 2072-6694).
Deadline for manuscript submissions: closed (31 May 2014)
Dr. Elena Kashuba
Department of Microbiology, Tumor and Cell Biology (MTC), Karolinska Institutet, Box 280, S-171 77, Stockholm, Sweden
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Fax: +46 8 33 04 98
Interests: cell transformation; virus-induced cell transformation; Epstein-Barr virus; protein–protein interaction; cell cycle regulation; tumor cell metabolism; nuclear receptors; mitochondrial ribosomal protein S18-2; cell differentiation, cancerogenesis
As you are well aware, DNA tumor viruses normally induce an S-phase in the natural host cell which is linked with cell transformation. In the case of small and medium sized DNA tumor viruses (Simian virus 40 (SV40), polyoma, and transforming adenoviruses) the induction of the S-phase is associated with the inactivation of the RB and the p53 pathways. Human papillomavirus, for example, encodes the E6 antigen that binds to p53 and to the cellular ubiquitin-protein ligase, E3A (UBE3A), also known as E6-associated protein. This binding leads to polyubiquitination of p53 and its proteasomal degradation. Large T encoded by SV40 binds to the DNA-binding domain of p53, and also to RB, and inhibits their functional activity.
In the much larger and more complex herpesviruses, this is not so straightforward. For example, ORF72 of human herpesvirus 8 (Kaposi’s sarcoma herpesvirus, KSHV) encodes a cyclin, homologous to cyclin D2, that binds to cdk6. This leads to the phosphorylation of RB and release of E2F1. The transactivating activity of p53 is blocked by KSHV-encoded LANA protein and the functionally corresponding ORF73 of Herpesvirus saimiri.
Epstein-Barr virus (EBV) is a human gamma herpesvirus that immortalizes B-cells. Six EBV-encoded nuclear antigens (EBNAs) and three latent membrane proteins (LMPs) constitute the growth transformation program III (also called latency III), that is not used in non-B-cells. Although the mechanism of EBV-induced B-cell transformation is not fully understood, it is already apparent that the virus exploits the normal signaling pathways of the B-lymphocyte. The growth transformation-associated viral proteins promote cell proliferation and protect the cells from apoptosis.
In this Special Issue of Cancers, “DNA viruses in human cancer”, experts are invited to contribute original research papers or review articles that will provide further insights on the role of DNA tumor viruses in cancerogenesis.
Dr. Elena Kashuba
Manuscript Submission Information
Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.
Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cancers is an international peer-reviewed open access monthly journal published by MDPI.
Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.
- DNA tumor virus
- Epstein-Barr virus
- cell transformation
- tumor suppressor gene
- cell proliferation
- cell metabolism
- cell signaling
- protein–protein interaction