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LIF Protein shows promise as target in pancreatic cancer

Accepted submission by RandomFactor at 2019-04-18 02:46:29 from the What is best in LIF? To crush your cancer, see it driven before you.... dept.
Science

SALK Institute researchers have discovered a potential therapeutic target for pancreatic cancer [sciencedaily.com].

Pancreatic cancer is often far advanced by the time it is discovered since it is often symptomless until after spreading throughout the body.

Additionally, tumor cells are encased in a "protective shield," a microenvironment conferring resistance to many cancer treatment drugs.

Silent, evasive, and very deadly.

pancreatic stellate cells -- resident cells typically dormant in normal tissue -- become activated and secrete proteins to form a shell around the tumor in an attempt to wall off and contain it. The activated stellate cells also secrete a signaling protein called LIF, which conveys stimulatory signals to tumor cells to drive pancreatic cancer development and progression. Results also suggest LIF may be a useful biomarker to help diagnose pancreatic cancer more quickly and efficiently.

Detection is a good step, but they didn't stop there

After pinpointing LIF as the critical communicator, the researchers wanted to better understand the function of LIF during pancreatic cancer progression to evaluate the protein as a potential therapeutic target. By observing the effects on tumor growth of blocking or destroying LIF (both render the protein nonfunctional) in a mouse model of pancreatic cancer, the researchers could examine how LIF affects tumor progression and response to treatment. Both techniques independently showed that without functional LIF signaling, tumor progression slowed down and responses to chemotherapeutic drugs used in treating human cancer (such as gemcitabine) were improved.

Early days as per usual, but it is about time some progress was made on this particular scourge. Earlier detection and improved responsiveness to treatment could move the needle towards survival.


Original Submission