Health
Stress-resistant cells promote tumorigenesis in pancreatic cancer
Further experiments also showed that using integrin antagonists to block the ability of cells to utilize the fibronectin matrix reversed the stress tolerance advantage of LPAR4 expression. Therefore, the authors suggested that targeting the LPAR4 pathway or disrupting the fibronectin/integrin interaction may be effective in preventing pancreatic tumor growth, spread, and drug resistance. suggesting.
“Tumor-initiating cells can be thought of as being in a transient state induced by various stressors. Therefore, our clinical goal is to prevent oncogenic cells from entering this state.” Cheresh said. “Now that we have identified the pathway, we can evaluate all the different ways we can intervene.”
The researchers suggest that new drugs that target this pathway could be used as prophylaxis in patients at high risk of developing the disease, or to prevent new tumors from forming in cancer cases with a high likelihood of metastasis. Did.
Combining existing chemotherapies with new drugs that stress mature tumor cells could also mitigate the effects of drug resistance and make cancer treatment more effective, the authors say.
“Cancer treatment can feel like whack-a-mole, but if you have two or three hammers and you know where the next mole will appear, you can beat the game,” says Cheresh. said.
Co-authors include Taha Rakhshandehroo, Hiromi I. Wettersten, Alejandro Campos, Tami Von Schalscha, Shashi Jain, Ziqi Yu, Jiali Tan, Evangeline Moses, Betzaira G. Childers, Andrew M. Lowy, Sara M. Weis . San Diego.
This study was funded in part by the National Institutes of Health (Grants R01CA155620, R01CA045726, R35CA220512, K01OD030513, T32CA009523, T32OD017863, and T32HL086344) and the University of California Tobacco-Related Diseases Research Program (Grant T29FT0343).
Disclosure: Cheresh is a co-founder and investor of Alpha Beta Therapeutics, Inc. and a member of its scientific advisory board.
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