Scientists solve an 80-year-old mystery of pancreatic cancer

In a new study, researchers have made a new discovery about how pancreatic cancer fuels its growth.

The finding may help explain how promising cancer drugs work—and for whom they will fail.

It also helps to answer an 80-year-old mystery: Why and how do cancers rewire cells to fuel themselves using a much more inefficient process?

Researchers hope the finding one day could help doctors determine which treatments will be most effective for patients so that they get the best outcomes.

The research was conducted by a team from the University of Virginia.

Pancreatic cancer is a very difficult disease. The survival for pancreatic cancer patients is very low compared to other tumors.

Scientists really trying to understand biology so that scientists and drug developers can be more informed as they try to tackle this disease.

Scientists previously have noted strange changes in the shape of mitochondria, the powerhouses of cells, in cancers driven by mutations in the RAS gene.

In the new study, the team wanted to understand what was occurring and how it affected pancreatic cancer’s growth.

They found that when the mutated RAS gene gets activated, it causes the mitochondria to fragment. This fragmentation supports the earliest shifts toward cancer’s new fueling process.

This was quite surprising because suddenly the mitochondria were playing a very unusual role. Their division was actually helping cancer establish itself.

The team also found this process could prove to be a weakness for cancer that doctors could exploit to help patients.

They found that blocking mitochondrial division in tumor samples largely prevented the tumors from growing. And when they did grow, the cancer cells gradually lost mitochondrial function.

This was bad for cancer, and the loss of mitochondria represents another weakness doctors could exploit.

The finding also may help explain the workings of several drugs in development, and it could help doctors understand which patients they will benefit.

The study is published in Cell Reports.

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