Background: Cancer is a significant and growing problem worldwide. While this increase may, in part, be\r\nattributed to increasing longevity, improved case notifications and risk-enhancing lifestyle (such as smoking, diet\r\nand obesity), hygiene-related factors resulting in immuno-regulatory failure may also play a major role and call for a\r\nrevision of vaccination strategies to protect against a range of cancers in addition to infections.\r\nDiscussion: Human endogenous retroviruses (HERVs) are a significant component of a wider family of\r\nretroelements that constitutes part of the human genome. They were originated by the integration of exogenous\r\nretroviruses into the human genome millions of years ago. HERVs are estimated to comprise about 8% of human\r\nDNA and are ubiquitous in somatic and germinal tissues.\r\nPhysiologic and pathologic processes are influenced by some biologically active HERV families. HERV antigens are\r\nonly expressed at low levels by the host, but in circumstances of inappropriate control their genes may initiate or\r\nmaintain pathological processes. Although the precise mechanism leading to abnormal HERVs gene expression has\r\nyet to be clearly elucidated, environmental factors seem to be involved by influencing the human immune system.\r\nHERV-K expression has been detected in different types of tumors.\r\nAmong the various human endogenous retroviral families, the K series was the latest acquired by the human\r\nspecies. Probably because of its relatively recent origin, the HERV-K is the most complete and biologically active\r\nfamily.\r\nThe abnormal expression of HERV-K seemingly triggers pathological processes leading to melanoma onset, but also\r\ncontributes to the morphological and functional cellular modifications implicated in melanoma maintenance and\r\nprogression.\r\nThe HERV-K-MEL antigen is encoded by a pseudo-gene incorporated in the HERV-K env-gene. HERV-K-MEL is\r\nsignificantly expressed in the majority of dysplastic and normal naevi, as well as other tumors like sarcoma,\r\nlymphoma, bladder and breast cancer. An amino acid sequence similar to HERV-K-MEL, recognized to cause a\r\nsignificant protective effect against melanoma, is shared by the antigenic determinants expressed by some vaccines\r\nsuch as BCG, vaccinia virus and the yellow fever virus.\r\nHERV-K are also reactivated in the majority of human breast cancers. Monoclonal and single-chain antibodies\r\nagainst the HERV-K Env protein recently proved capable of blocking the proliferation of human breast cancer cells\r\nin vitro, inhibiting tumor growth in mice bearing xenograft tumors\r\nSummary: A recent epidemiological study provided provisional evidence of how melanoma risk could possibly be\r\nreduced if the yellow fever virus vaccine (YFV) were received at least 10 years before, possibly preventing tumor\r\ninitiation rather than culling melanoma cells already compromised. Further research is recommended to confirm\r\nthe temporal pattern of this protection and eliminate/attenuate the potential role of relevant confounders as\r\nsocio-economic status and other vaccinations.\r\nIt appears also appropriate to examine the potential protective effect of YFV against other malignancies expressing\r\nhigh levels of HERV-K antigens, namely breast cancer, sarcoma, lymphoma and bladder cancer.\r\nTumor immune-therapy, as described for the monoclonal antibodies against breast cancer, is indeed considered\r\nmore complex and less advantageous than immune-prevention. Cellular immunity possibly triggered by vaccines as\r\nfor YFV might also be involved in anti-cancer response, in addition to humoral immunity..
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