Perlmutter has since left Amgen and is now leading drug research at Merck. T-Vec is an oncolytic (cancer-killing) virus that started as a simple herpes virus (the kind that causes cold sores) but was genetically re-engineered in the lab to seek out and invade fast-growing cancer cells. The virus is designed to leave healthy cells, which don't divide as fast, alone. Once T-Vec invades a cancer cell, it does what viruses typically do, hijack the cell's replication mechanics and starts making lots and lots of copies of itself. All these viral copies cause the cancer cell to burst and die. On its own, this cell-bursting technique isn't enough to turn T-Vec into a viable cancer treatment, so two other alterations were made to the herpes virus. First, a gene was removed from the virus that typically makes it invisible to a patient's immune system. With that gene gone, a patient's immune system is alerted when T-Vec starts replicating and bursting cancer cells. Second, a gene was inserted into the virus to produce a protein called GM-CSF that puts the immune system into a state of high alert. Now, immune system can more easily find the modified herpes virus inside tumor cells and mount a vigorous attack. Doctors inject T-Vec directly into tumors unlike most cancer drugs that are administered orally (as a pill) or intravenously into a vein. In Jan. 2011, Perlmutter explained that BioVex wouldn't have been worth Amgen's investment if OncoVex proved capable of only eliminating tumors via direct injection. The tumor burden in advanced cancer patients, especially those with skin cancer, is too great to treat them effectively. T-Vec, however, appears to activate a patient's immune system enough to target and eliminate tumors that are not directed injected. This so-called off-target or systemic response is what grabbed Amgen's attention and ultimately led to the company's decision to acquire BioVex. Initial results from Amgen's T-Vec study were announced last March.-- Reported by Adam Feuerstein in Chicago. Follow Adam Feuerstein on Twitter.