About this Research Topic
In this special issue of Frontiers in Oncology, the Guest Editor Prof. Mauro Tognon and the Co-Guest Editor Prof. Axel zur Hausen, propose a collection of 10 reviews on the association between small DNA tumor viruses and human cancers. The goal of these reviews is to summarize the present knowledge in the field of human tumors associated with small DNA tumor viruses, such as polyoma- and papilloma-viruses. Attention will be given to the mechanism of transformation of these oncogenic viruses in human cells and the oncogenic activities responsible of the tumor onset. In different reviews, authors will deal, together with the tumor biology, with the molecular mechanism operated by the viral oncogenic proteins during the oncogenesis steps. The immunology of small DNA tumor viruses will be considered too. The aim of this special issue is to address an overview of different study models in the viral oncogenesis. Some examples are reported below.
In recent years, many investigations were published on the human polyomaviruses (HPyV), such as BK (BKPyV), JC (JCPyV) and their involvement in distinct human pathologies, including tumors of different histotypes. Moreover, since 2007 a new wave of investigation allowed to identify new human polyomaviruses, such as KI and WU, and then in 2008 the oncogenic Merkel cell polyomavirus (MCPyV) found to be the etiological agent of the Merkel cell carcinoma, a rare but very aggressive tumor of the skin of neuroendocrine origin. At present, the number of HPyV account for 13 different viruses and many subtypes. The study of the association between these HPyV and human pathologies/tumors is a very active topic in the scientific research worldwide.
The human papillomaviruses (HPV) account for more than 200 types. Some HPV types are more oncogenic, such as HPV-16 and HPV-18, than other types (HPV-31; 33 etc), while the great majority of HPV types are not oncogenic. It is of interest to understand why some HPV are of high risk for the tumor onset, whereas other types are considered at low risk for their oncogenic potential. In recent years different HPV vaccines were introduced in the market with results that are during these days analyzed for their impact in the young females vaccinated more than 10 years ago.
It is of interest to note that from the biology point of view the tumorigenic potential of both HPyV and HPV is due to their viral oncoproteins, the large T antigen and small t antigen for HPyVs, E6 and E7 gene products for HPVs. The biological features of these viral oncoproteins are similar and act as activated oncogenes. However, biological differences in their oncogenic activities are responsible for the high or low risk in the oncogenesis/tumor onset.
Our special issue will deal with these interesting topics, which are very innovative and timely.
In recent years, many investigations were published on the human polyomaviruses (HPyV), such as BK (BKPyV), JC (JCPyV) and their involvement in distinct human pathologies, including tumors of different histotypes. Moreover, since 2007 a new wave of investigation allowed to identify new human polyomaviruses, such as KI and WU, and then in 2008 the oncogenic Merkel cell polyomavirus (MCPyV) found to be the etiological agent of the Merkel cell carcinoma, a rare but very aggressive tumor of the skin of neuroendocrine origin. At present, the number of HPyV account for 13 different viruses and many subtypes. The study of the association between these HPyV and human pathologies/tumors is a very active topic in the scientific research worldwide.
The human papillomaviruses (HPV) account for more than 200 types. Some HPV types are more oncogenic, such as HPV-16 and HPV-18, than other types (HPV-31; 33 etc), while the great majority of HPV types are not oncogenic. It is of interest to understand why some HPV are of high risk for the tumor onset, whereas other types are considered at low risk for their oncogenic potential. In recent years different HPV vaccines were introduced in the market with results that are during these days analyzed for their impact in the young females vaccinated more than 10 years ago.
It is of interest to note that from the biology point of view the tumorigenic potential of both HPyV and HPV is due to their viral oncoproteins, the large T antigen and small t antigen for HPyVs, E6 and E7 gene products for HPVs. The biological features of these viral oncoproteins are similar and act as activated oncogenes. However, biological differences in their oncogenic activities are responsible for the high or low risk in the oncogenesis/tumor onset.
Our special issue will deal with these interesting topics, which are very innovative and timely.
Keywords: Polyomavirus, Papillomavirus, tumor, oncogenesis, transformation
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