The Double-Edged Role of Noncanonical Oncogenes and Tumor Suppressor Genes in Cancer Progression; An Oncojanus Function

Dear Colleagues,

Current research in oncology is uncovering diverse properties of genes involved in cancer development and progression. An increasing number of genes and proteins appear to play prominent roles in one or more of the hallmarks of cancer depicted by Hanahan and Weinberg. To further complicate the already intricate pathway deregulation occurring in cancer cells, many genes in tumorigenesis have opposite effects on cancer progression according to the context and even to the type of mutations that they acquire, not to mention the gene dosage. This field of genetic oncology is relatively novel and requires a revisiting of the canonical concepts of oncogene and tumor suppressor gene. The roles of autophagy genes; AMPK; isocitrate dehydrogenase; metabolic enzymes such as respiratory complex I; and even the well-known pleiotropic p53 ought to be gauged carefully in the balance between cancer promotion and inhibition. The Special Issue will collect contributions from experts in genes and proteins whose role in cancer progression has been ascertained, but remains controversial in terms of whether they play a pro- or an anti-tumorigenic role, likely depending on the genetic background, microenvironmental pressures, and stages of tumorigenesis. This is particularly true for genes that are involved in the reprogramming of cancer metabolism, although oncojanus features have been described for other genes as well. In this Special Issue, each contribution will deal specifically with one gene or with a family of closely related genes/proteins (for autophagy, for instance), and illustrate their dualistic role in cancer.

Prof. Giuseppe Gasparre
Prof. Anna Maria Porcelli
Guest Editors

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