Pancreatic cancer has long been one of the deadliest forms of cancer, often spreading to other organs before it’s even detected.
A new study led by Cornell University may finally explain why this happens—and offer a promising new path for treatment.
The research focuses on pancreatic ductal adenocarcinoma, a particularly aggressive type of cancer. Despite the tumor being surrounded by a thick, fibrous tissue that should act as a protective shield, the cancer still manages to spread quickly and efficiently. This mystery has challenged scientists for years.
Published in the journal Molecular Cancer, the study reveals that a receptor called ALK7 plays a key role in helping cancer cells escape from the tumor and enter the bloodstream.
ALK7 does this in two ways: it activates one pathway that makes the cancer cells more mobile and another that produces enzymes that break down blood vessel walls. This combination gives the cancer both the ability to move and the means to invade new tissues.
“ALK7 gives pancreatic cancer cells both the engine to move and the tools to invade,” explained Esak Lee, lead author of the study and assistant professor at Cornell’s Meinig School of Biomedical Engineering.
There has been some confusion in past studies about whether ALK7 helps or stops cancer from spreading. But by using new lab techniques and organ-on-chip technology that mimics human blood vessels, the Cornell team was able to settle the debate.
Their tests on mice and chip-based models clearly showed that when ALK7 is blocked, cancer spread slows down significantly.
The organ-on-chip system used in this research is especially innovative. Created in Lee’s lab, it mimics the human tumor environment better than traditional animal models. This allowed researchers to look closely at whether ALK7 helps cancer cells break into the bloodstream (the start of spreading) or escape into other tissues (the later stage).
What they found was striking: when ALK7 was turned off, cancer cells could not enter blood vessels at all. But when the researchers placed cells directly into the vessels to mimic later-stage disease, the cells were able to spread. This means the best time to block ALK7 is at the very beginning—before the cancer enters the bloodstream.
“Once we miss this early opportunity to block ALK7 receptors, the cancer cells can freely circulate in the bloodstream and easily seed into other organs,” Lee said. “But if we can inhibit ALK7 at the cancer’s earliest and most vulnerable stage, we might see better outcomes for patients.”
The team believes this finding could have a major impact on how doctors treat not only pancreatic cancer but possibly other cancers too. Different types of tumors have unique environments, and studying them with organ-on-chip systems could reveal more useful targets like ALK7.
This study is a big step forward in understanding how deadly cancers like pancreatic ductal adenocarcinoma spread. With more research, it could lead to treatments that stop cancer before it has a chance to spread—improving survival rates and giving patients a better chance at recovery.
The study is published in Molecular Cancer.
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