Cancer immunotherapy turns viral

The holy grail of anticancer therapy is to selectively eradicate malignant cells while sparing their normal counterparts. Tremendous progresses have been made in this sense during the past decade, as demonstrated by the development and subsequent integration into the clinical routine of ever more effective and safe therapeutic agents. Among these, chemical inhibitors of oncogenic drivers such as vemurafenib (an inhibitor of mutated BRAF currently employed for the treatment of melanoma), and highly specific monoclonal antibodies such as trastuzumab (an ERBB2-targeting antibody nowadays used for the treatment of several ERBB2 solid tumors including breast carcinoma) have contributed to significantly decrease the side effects associated with antineoplastic regimens and, simultaneously, to increase their therapeutic potential. Thus, the introduction of targeted anticancer agents has considerably improved the life expectancy of (at least some subsets of) cancer patients. In most cases, however, the therapeutic benefits of this approach are paradoxically limited by its own specificity. Indeed, only a few tumor types, when not a single one, can be successfully treated with a highly specific chemoor immunotherapy, owing to the restricted expression pattern of the drug target. Moreover, cancer cells can adapt quite rapidly to a very specific selective pressure, such as that posed by targeted anticancer agents, by downregulating one (or a few) protein(s), a mechanism that also intervenes in the escape of tumor cells from immunosurveillance. Conversely, traditional chemotherapeutics—which are Cancer immunotherapy turns viral