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Colorectal cancer (CRC) is the third most common malignancy in both men and women worldwide. Colorectal carcinogenesis is a complex, multistep process involving environmental and lifestyle features as well as sequential genetic changes in addition to bacterial and viral infections. Viral infection has a proven role in the incidence of approximately 20% of human cancers including gastric malignancies. Accordingly, Epstein-Barr virus (EBV) has been recently shown to be present in human gastric cancers, which could play an important role in the initiation and progression of these cancers. Therefore, this work explores the prevalence of EBV in 102 CRC tissues from the Syrian population using polymerase chain reaction (PCR) and tissue microarray (TMA) analysis. We found that EBV is present in 37 (36.27%) of CRC samples. Additionally, the expression of LMP1 onco-protein of EBV was found to be correlated with Fascin expression/overexpression in the majority of CRC tissue samples, which are intermediate/high grade invasive carcinomas. Our data indicate that EBV is present in CRC and its presence is associated with more aggressive cancer phenotype. Consequently, future investigations are needed to expose the role of EBV in CRC initiation and progression.

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Gastric cancer is the fourth most common cancer and the second leading cause of cancer deaths worldwide. Additionally, it is well-known that metastatic cancer disease is a major cause of morbidity and mortality in cancer patients. Several investigations reported that HER-2 (ErbB-2 receptor) and Epstein-Barr virus (EBV) are important etiological factors in human gastric cancer, where either oncogene/oncovirus alone can derive a major event of cancer progression and metastasis via epithelial-mesenchymal transition (EMT). Herein, we discuss, for the first time, the possibility of HER-2/EBV-oncoproteins interaction in human gastric cancer initiation and/or progression.

Colorectal, colon and rectal, cancer is the third most common malignancy in both men and women worldwide. Colorectal carcinogenesis is a complex, multistep process implicating environmental and lifestyle factors in addition to gene mutation and viral infections. On the other hand, it is well established that human papillomaviruses (HPVs) infection play a crucial role in certain types of human carcinomas including cervical and head and neck (HN); as roughly 96% and 30% of these cancers are positive for high-risk HPVs, respectively. Moreover, it has been reported that the presence of high-risk HPVs is associated with vascular invasion, lymph node metastases, and tumor size in cervical and HN cancers. Recently, several investigations pointed-out that high-risk HPVs are present in around 70% of human colorectal cancers. Likewise, our group has demonstrated that E6/E7 oncoproteins of HPV type 16 convert noninvasive and nonmetastatic human cancer cells to invasive and metastatic form. Accordingly, it is evident that high-risk HPVs are present in human colorectal cancers where they could play an important role in the development of these malignancies. In this chapter, we will discuss the presence and role of high-risk HPVs in human colorectal carcinogenesis and metastasis; particularly, the interaction between E5 and E6/E7 oncoproteins of high-risk HPVs in colorectal malignancies, which has been linked with the initiation and progression of these tumors.