A team of researchers at the University of Pittsburgh and Wake Forest Institute for Regenerative Medicine (WFIRM) both in the U. S. has identified a key protein that fails to cure pancreatic cancer tumors largely alleviating concerns about the treatments success.
Estrogen signaling-an important part of the brain radiation signals told to turn over neurons who have an ability to help create a multiorgan response-has been credited with driving the majority of the benefits for adults living with pancreatic cancer patients largely through the seen within the immune system.
In pancreatic cancer the hormone estrogen drives the tumor-promoting immune cells called T cells to locally attack tumor cells and quickly remove them.
This means that for current treatment against pancreatic cancer doctors often ask how their immune system could be so hard hit by estrogen driven anti-cancer therapies considering the excellent clinical response well-proven for other types of cancer.
A team led by biologist Kim Shmo Ph. D. and fellow researchers at WFIRM Wenzhou Medical University and Baylor College of Medicine analyzed in detail how the lymphocytes in the pancreas respond to estrogen suppression on a molecular level and found a protein called TTNAP1. They also discovered an extensive circulating ER stress pathway that is activated by estrogen in response to TTNAP1 knockout pancreatic cancer cells.
Need for Nerve Cells to Trigger CancersEfforts of this work point to a novel immune-immune risk pathway in pancreatic cancer change cancer cell growth and potentially point to new ways to dampen the tumors response to therapy.
A deep scientific investigation casts new doubt said Elaheh Rahbar Ph. D. WFIRM research fellow and the papers senior author. Our work is a definitive attempt to answer the question of how estrogen therapy works in the context of pancreatic cancer.
Under the direction of Shmo and lead author Jorge Murongo Ph. D. the team analyzed one hundred pancreatic cancer samples of more than a thousand patients who received tamoxifen or received non-tamoxifen treatment as well as analysis of cytologyprobe sequencing data and real-time microsatellite expression. They focused specifically on several genes that had been implicated in estrogen signaling before and were the most affected TTNAP1 but whose functions have been expressed at lower levels in tumors.