All forms of pancreatic cancer are difficult to treat. Surgery is the only potential solution for the rare neuroendocrine variety, the type that Steve Jobs succumbed to, and we all know how ineffective that method still is. Adenocarcinoma, the more common variety that killed the likes of Patrick Swayze and Luciano Pavarotti, is no better a sentence, as anyone who does their own supermarket shopping knows from seeing the tabloids.

Most cases of pancreatic adenocarcinoma are caused by mutation in the so-called Kras gene that is active in the acinar cells. These are the cells that secrete the major digestive enzymes. An errant setting of a single bit (technically 2 bits for four base pair options) at the right spot in the Kras gene reconfigures the entire flow chart of the acinar cell to differentiate itself into a highly unstable ‘ductal’ type cell — those which line the secretory output ducts of the pancreas and feed into the gut.

Researchers at the Sanford-Burnham Institute in San Diego have now figured out a way to reprogram these rogue ductal cells back into obedient acinar cells. The way they did this was to overexpress a single master control gene known simply as E47 in an adenocarcinoma cell line obtained from mice. When they re-introduced the cells (now carrying megaloads of the E47) back into the mouse pancreas, they reverted back to the docile acinar cell type. Technically speaking, if you recall your high-school biology, the cells were said to be stalled in the G0/G1 growth phase of the putative cell cycle.

The obvious next step is to test tumor tissue from humans to find out whether E47 gives the same therapeutic effect in us. If it does, then there may be ways to induce the natural production of E47 with drugs, or introduce it directly by some other imaginative means. This E47 approach is but one among many parallel efforts to solve these particular diseases. To grasp the magnitude of the cancer research machine that now operates at large in the US and beyond, one need look no further than the table of contents of the journal Pancreas where this work was just published.

In it you see all kinds of new studies, each looking at their own pet protein or gene to address one problem or another. What makes E47 particularly enticing is that it happens to specifically bind to the DNA sequences controlling the genes that influence the growth and differentiation of these specific cell types. Those particularly attuned to the current pancreatic zeitgeist may note that the E47 saga is not even the only major pancreatic story now circulating in the news.

Other researchers have just shown that viruses can be used to treat pancreatic cancer, albeit in a slightly different way. If the use of viruses against cancer sounds slightly familiar to you, then you may have heard about the recent successes at Duke in using the polio virus to treat glioblastoma — the difficult to treat brain tumors we recently discussed here on ET. Reporting in the journal Nature Medicine, University of Ottawa scientists describe how they engineered the Maraba virus for use against pancreatic cancer cells.

While these kinds of treatments may still be years away from the clinic, they potentially offer a refreshing alternative to the current cancer drugs we use, which for the most part (perhaps with the exception of a few miracle medicines like Gleevec) are little more than pure poison.