Editorial Recent Patents on Biomarkers 2014, Vol. 4, No. 2 65 Editorial Oncoviruses and Head and Neck Cancer: An Impending Facts Oncoviruses are the viruses which cause cancer and exploration of these viruses is of importance to understand the biology of these cancers [1]. The fact of viruses being a causative factor for cancer has always created deception among researchers. Since viruses are infectious and transmissible, initially it was difficult to accept the fact, oncoviruses. The International Agency for Research in Cancer (IARC) has termed many viruses as group I carcinogens [2], including DNA viruses like human papil- loma viruses (HPVs), Epstein-Barr virus (EBV), Kaposi’s Sarcoma-Associated Herpesviruses (KSHV), Hepatitis B Virus (HBV) and the Merkel Cell Polyomavirus (MCV). Among the RNA viruses, hepatitis C virus (HCV) and the Human T-cell Leukemia Virus Type 1 (HTLV- 1)-retrovirus are associated with human malignancies [3]. According to Rossini et al. Head and neck squamous cell carcinomas (HNSCC) are the sixth most common cancers world- wide, accounting for 633000 new cases annually. Oropharyngeal squamous cell carcinoma (OPSCC) is one component of HNSCC. The etiology of HNSCC is considered to be multifactorial. Smoking and excessive alcohol consumption are well es- tablished risk factors for HNSCCs [4]. HPV, particularly subtype 16, is one of the important etiological risk factors in Oral Squamous Cell Carcinoma (OSCC) development. Other oncogenic virus species i.e. Epstein Barr Virus and Herpes Simplex Virus Type 1 are also been implicated in oral carcinogenesis. Recent trends show that there is a decrease in the incidence of oropharyngeal squamous cell carcinoma associated with tobacco use and increase in the human papilloma virus associated with OPSCC. OSCC affects approximately 650,000 patients worldwide and 350,000 die of this disease every year. This disease is increasing and is appearing every day more in younger people. The risk factors most studied for OPSCC are tobacco and alco- hol but several studies indicate that HPV is a risk factor for OPSCC [5]. In the last two years, there has been an acceleration of activities in research focusing on identification of HPV in oral cancer and treatment modalities. Nearly about six patents have been published on this aspect in the year 2013 and 2014. Two patents published describe about how HPV DNA can be identi- fied and also how differentiation of high risk and low risk type can be done [6, 7]. Remaining four patents mainly deal with the therapeutic aspect of HPV and oral cancer [8-11]. EBV as an etiological factor is linked with four types of cancers: Burkitt’s lymphoma (one of the most dreaded diseases in sub-Saharan Africa), Hodgkin’s lymphoma, nasopharyngeal carcinoma (the most common tumor of males in southern China), and non-Hodgkin lymphoma associated with post-transplant or HIV Immunosuppression [12-14]. EBV is of two types Type A and Type B. Type A is most commonly associated with lymphoma and its role has been very well established in the past. Very recently the role of Type B virus has been explored [15]. Rickinson et al. showed that the immortalization capacity of type B virus is much lesser than the type A virus. Like Type A virus, Type B virus has no geographical restriction and can be seen in areas other than Africa [16]. Tushako K proved the role of EBV in OSCC through polymerase chain reaction (PCR). According to his finding, 46 of 60 cases were positive for EBV [17]. Higa et al. reported that incidence of OSCC in Okinawa is influenced by EBV type B infection and the slight differences in the EBNA2 gene [15]. The role of type B virus in OSCC is still to be es- tablished in other parts of world where it is multifaceted. Recently, in year 2013, very interesting therapeutic modality has been patented. This patent is about how EBV infected cytotoxic T cells can be used to treat nasopharyngeal carcinoma [18]. The role of Cytomegalovirus (CMV) in salivary gland malignancy has been clearly depicted by a new study from the Labo- ratory for Developmental Genetics at the Herman Ostrow School of Dentistry of USC. Professor and lead author Michael Mel- nick have also shown the role of CMV in an oncovirus in human salivary gland tumors and salivary glands of postnatal mice [19]. Even though many researchers are working hard to prove the role of CMV in salivary gland oncology, the other side of the coin has shown its face where many scholars like Karja et al. and Lanne et al. have already disproved the association of CMV with salivary gland pathology [20, 21]. In the last two years, three patented research are published which mainly focus on CMV and its relation with cancer and its oncovirus nature [22-24]. This special issue is the result of growing interest of many researchers in the field of oncoviruses and head and neck cancer. The association of oncoviruses with cancer of other body parts has already been well established and evolved but association of oncoviruses with head and neck cancer is a new domain and has attracted many researchers to conduct extensive research. In the first topic of this minithematic issue, the author have focused on how the world of oncoviruses was explored and how these viruses causing transformation of normal tissue to neoplastic tissue with discussion on current concepts and current pat- ents. Also the pathogenesis of HPV, EBV and CMV has been discussed. The topic ends with recent patents of the last two years for HPV, EBV and CMV and their association with oropharyngeal carcinoma. The second topic is contributed by Gerardo Meza-Garcia and coworkers mainly designed to reveal the role of p16INK4 as a Biomarker in OPSCC. The potential of single protein p16 to cause OPSCC will be discussed. In this paper, authors have re- viewed p16INK4 and its pathogenesis with OPSCC, as well as its relation to HPV and its possible role as a biomarker of the dis- ease and current brand patent literature. In the third topic, Arora from Malaysia deals with diagnostic approach towards oncoviruses especially HPV in OPSCC. It also encompass advanced techniques for diagnosis. In this topic, different techniques like PCR, in situ hybridization, immu- nostaining etc. are well discussed in relation to techniques, applications, and shortcoming. She has also included the patented publications of last three years specifically about advanced detection methods of HPV. 66 Recent Patents on Biomarkers 2014, Vol. 4, No. 2 Editorial The fourth topic is a totally new topic elaboaratively discussed by Dr. Nidhi and coworkers, trying to build relation between CMV and salivary gland tumors. This review is an attempt to gather correlations between cytomegalovirus and salivary gland pathology. It brings the various discovered patents of CMV and its association with salivary gland pathology under the same roof. An inclusive understanding of biomarker related to CMV would help diagnose disease reliably, and also open new vistas of multiple therapeutic alternatives to benefit the patients. Keywords: Biomarkers, human papilloma virus, oncoviruses, oral cancer, patents. CONFLICT OF INTEREST The authors confirm that this article content has no conflict of interest. ACKNOWLEDGEMENTS Declared none. REFERENCES [1] Linda Z, Kuan-Teh J. Human cancer viruses: Past, present and future. National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892. P 30-34. [2] Boccardo E, Villa LL.Viral origins of human cancer. Curr Med Chem 2007; 14(24): 2526-39. [3] Phelan JA.Viruses and neoplastic growth. Dent Clin North Am 2003; 47(3): 533-43. [4] Rossini ARAL, Hashimoto CL, Iriya K, Zerbini C, Baba ER, Moraes-Filho JPP. Dietary habits, ethanol and tobacco consumption as predictive factors in the development of esophageal carcinoma in patients with head and neck neoplasms. Dis Esophagus 2008; 21(4): 316-21. [5] Syrjänen S. The role of human papillomavirus infection in head and neck cancers. Ann Oncol 2010; 5(Supplement 7): 243-5. [6] Elizabeth, F., Lutecia, P., Isildinha, M., Reis, R.C. Duncan methods for detecting human papilloma virus and providing prognosis for head and neck squamous cell carcinoma. WO2013074793 (2013). [7] Karl, P., Tobey, G. Prognosis papilloma virus (HPV) detection using nucleic acid probes, microbeads and Fluorescent-Activated Cell Sorter (FACS). US8389217 (2013). [8] Kai, K., Ayumi T. Mucosal immunity-stimulating agent and oral pharmaceutical composition for treating HPV infection. WO2013191225 (2013). [9] Richard, S. Use of artemisinin for treating tumors induced by oncogenic viruses and for treating viral infections. US8394849 (2013). [10] Chackerian, B., Peabody, D.S., Tumban, E. Immunogenic HPV L2-containing vlps and related compositions, constructs, and therapeutic methods. US20140105924 (2014). [11] Parimal, S.A., Padigaru, M., Agarwal, V.R., Deshpande, G.A. Compounds for the treatment of cancers associated with human papillomavirus. US20140142159 (2014). [12] de Martel C, Franceschi S. Infections and cancer: Established associations and new hypotheses. Crit Rev Oncol Hematol 2009; 70(3): 183-94. [13] Persing DH, Prendergast F.G. Infection, immunity, and cancer. Arch Pathol Lab Med 1999; 123(11): 1015-22. [14] Taylor, GS, Blackbourn DJ. Infectious agents in human cancers: lessons in immunity and immunomodulation from gamma herpesviruses EBV and KSHV. Cancer Lett 2011; 305(2): 263-78. [15] Higa M, Kinjo T, Kamiyama K, Iwamasa T, Hamada T, Iyama K. Epstein-Barr virus (EBV) subtype in EBV related oral squamous cell carcinoma in Okinawa, a subtropical island in southern Japan, compared with Kitakyushu and Kumamoto in mainland Japan. J Clin Pathol 2002; 55: 414-23. [16] Rickinson AB, Young LS, Rowe M. Influence of the Epstein-Barr virus nuclear antigen EBNA 2 on the growth phenotype of virus-transformed B cells. J Virol 1987; 61: 1310-17.
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