Breakthrough Causes Cancer Cells to Turn Back into Normal Cells

Introduction of protein to pancreatic cancer cells causes them to revert back to normal.

Introduction of protein to pancreatic cancer cells causes them to revert back to normal.

A new approach to fighting cancer may allow for the transformation of cancerous cells back into normal cells.

A study published recently in the journal Pancreas showed that the introduction of a protein called E47 coaxes pancreatic cancer cells to revert toward normal cells. The researchers found E47 binds to specific DNA sequences, which controls genes that are involved in growth and differentiation.

"For the first time, we have shown that overexpression of a single gene can reduce the tumor-promoting potential of pancreatic adenocarcinoma cells and reprogram them toward their original cell type,” said lead author Pamela Itkin-Ansari, PhD, in a press release. “Thus, pancreatic cancer cells retain a genetic memory which we hope to exploit.”

For the study, the researchers generated human pancreatic ductal adenocarcinoma cell lines to produce greater than normal E47 levels. As a result, the increased levels of E47 caused cells to stall during the G0/G1 growth phase and differentiate back to an acinar cell phenotype.

In vivo studies found that the introduction of reprogrammed cancer cells into mice reduced the ability of the cancerous cells to form tumors, compared with untreated adenocarcinoma cells.

"Presently, pancreatic adenocarcinoma is treated with cytotoxic agents, yet the average survival for patients post-diagnosis is merely 6 months, and the improvements in therapies are measured in days," said Andrew M. Lowy, MD, co-chair of the National Cancer Institute Pancreatic Cancer Task Force, in a press release. "The finding that we can differentiate these cancer cells back to a non-threatening phenotype is encouraging. Indeed, there is a precedent for cell differentiation therapy in that the approach has been used to treat acute promyelocytic leukemia and some neuroblastomas successfully."

Researchers next plan to test primary patient-derived tumor tissue to evaluate if E47 can produce similar results.

"Additionally, we are screening for molecules -- potential drugs -- that can induce overexpression of E47,” Itkin-Ansari said.