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Pancreatic cancer tumors addicted to mutant Kras signaling for their growth and progression have a ready-made substitute to tap if they're ever forced to go cold-turkey on the mutant oncogene, according to a new study. 

The study noted that when mutant Kras to spur pancreatic cancer growth in mice were dialed up and then eventually shut it down, a group of recurrent tumors grew back independent of mutant Kras, relying on a difference oncogene.

"There's a great deal of effort under way trying to find ways to target Kras or some of the downstream targets that it activates," said co-lead author Haoqiang Ying, Ph.D., assistant professor of Molecular and Cellular Oncology in the press release. "It's important to understand how Kras-dependent tumors might evolve in response to targeted therapy."

Researchers also observed that some recurrent tumors were completely independent of mutant Kras, instead relying on signaling through another known oncogene called Yap1. 

"Pancreas cancer remains an intractable disease with limited therapeutic options," said senior author Ron DePinho, M.D., president and professor of Cancer Biology, in the press release. "Identifying and validating key targets in faithful model systems represents a critical first step in ultimately providing our patients with meaningful therapies."

Pancreatic ductal adenocarcinoma is one of the deadliest forms of cancer allowing just 6.7 percent of patients to survive for five years. Reports form National Cancer Institute suggest that an estimated 46,420 new cases will be diagnosed in 2014 and nearly 39,600 people will die of the disease. 

"The only gene amplified was Yap1, which made sense, because it's a known oncogene," said co-lead author Avnish Kapoor, Ph.D., a postdoctoral fellow in Genomic Medicine who conducted the analysis, in the press release. 

"With Kras turned off, Yap1 can recreate this transcription program involving cell cycle and DNA replication machinery that is normally controlled by Kras," Yao added.

The study has been published in the journal Cell.