Transient oncogenes.

A given cancer is produced by a unique combination of genetic alterations that target specific genes, most often leading to activation of oncogenes and inactivation of tumor suppressor genes. Traditional oncogenes, such as RasV12, are involved in maintaining pro-survival and proliferation signals activated in the cell. Several evidences suggest that cancer cells are addicted to oncogenes and that their inhibition has dramatic effects on cancer cells. Here, the hypothesis that oncogenes may be activated only transiently and that this short activation may be important for cancer formation by affecting the differentiation state of the cancer cells is presented. These "transient oncogenes" are overlooked in genomic or proteomic analysis due to their transient nature. Here we argue that transcription factors, such as the so called Yamanaka factors, capable of reprogramming cells to a less differentiated state, which normally happens to cancer cells, can function as transient oncogenes. Several published evidences are used to support the proposed hypothesis. Analysis and even targeting of this new class of oncogenes could have a great impact on cancer biology, treatment and, most importantly, prevention.