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The endogenous retrovirus (ERV) appeared in the vertebrate genome millions of years ago, but is now inactivated due to mutations such as deletions or nonsense mutations. After the mutation, ERV eventually became fixed in the genome in its endogenous form. In the case of human ERV (HERV), 98 000 ERV elements or fragments were inserted into the human genome, which is approximately 8% of the whole genome.1 HERV is defective and unable to replicate and only traces of the original viruses exist in the human genome.2 Even though HERVs have been reported to be inactive, there are several studies showing the relationship between HERVs and some diseases including cancers. Contreras-Galindo et al3 first showed that HERV-K genes are significantly upregulated in the plasma of lymphoma and breast cancer patients and that there are virus-like particles in the plasma of lymphoma patients. Many other studies have shown that HERV-K can be a good model for immunotherapeutic targets4 and is a biomarker of early-stage breast cancer.5 Additionally, there have been reports demonstrating that HERV-K is involved in breast cancer,4–6 prostate cancer,7 melanoma8 and ovarian cancer.9 ERV3-1 (HERV-R) is related to lymphoma10 and HERV-E is upregulated in urothelial carcinoma11 and colon cancer.12
We recently reported that the ERV3-1 (HERV-R) env protein is expressed in both adult human organs and tumours using a tissue microarray. We also compared the expression of ERV3-1 between normal and tumour tissues to study the relationship between ERV3-1 and tumour formation. ERV3-1 was highly expressed in certain types of tumours, including lung adenocarcinoma, renal cell carcinoma, papillary carcinoma, hepatocellular carcinoma and adenocarcinoma in the gastrointestinal tract.13 Although a tissue …
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