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Sugary disguise

Killing cancer cells is tricky business, partly because they can be hard to find. Those tricky cells are good at hiding, but researchers are on to them. It seems their “invisibility cloak” is made up of a sugary coating that can now be detected.

The study, published in Science, shows that leukemia cells coat themselves in a slippery, sugar-coated protein called CD43. This shield makes it difficult for the body’s immune system to grab and destroy them.

When researchers removed the CD43, they found that immune cells were suddenly more adept at doing their job.

The sugar coating acts both as a barrier and a disguise — cancer cells are harder to reach, and the signals received by cells like macrophages, the body’s cleaning crew, says “don’t attack me.” This combination is what scientists are referring to as a glyco-immune barrier.

Notably, the barrier isn’t evading only one type of immune cell, it also interferes with natural killer cells and T cells, which are instrumental in fighting cancer.

The next step is for scientists is to figure out a way to strip away this sugary cloak at scale, which could make existing cancer treatments like immunotherapy more effective.

More like this: Cancer can run, but it can no longer hide

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Sweat versus cancer

Research tells us that exercise is a great way to “>boost immunity. With this in mind, a small study published in the Journal of Sport and Health Science found some promising results in a group of people with esophageal cancer who exercised during chemotherapy.

Half of the participants were given a mix of cardiovascular and strength-training exercises to complete over the course of 16 weeks. The other half of the group received regular, standard care without exercise programs.

The patients who maintained the exercise program proved to have more cancer-fighting immune cells (CD8+T cells and natural killer cells) in their tumors.

They also had more tertiary lymphoid structures. Normally, the immune system works out of larger centers like the lymph nodes, but these “hubs” are like command centers that set themselves up when and where danger, like a growing tumor, is detected. These are important because they set up more localized attacks.

Though the tumors didn’t shrink in size and survival rates did not alter, results are promising. The scientists say further research is required to see whether such an immune activation will lead to enhanced longer-term outcomes.

In the interim, staying active during chemotherapy might assist your body in rallying its internal troops.

More like this: Cancer can run but it can no longer hide

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Enzymes caught in the act

A protein that is not functioning the way it should could be the catalyst for an array of medical conditions like cancer and autoimmune diseases. So it makes sense that identifying and understanding what’s wrong with the protein can help develop treatments.

A recent study published in PNAS produced a breakthrough image of a powerful enzyme (a type of protein) involved in the body’s immune response that may offer a key route to how we treat these diseases.

The research team used cryo-electron microscopy, kind of like a camera for things at the molecular level, to look at the structure of ADAM17. This protein behaves like a pair of molecular scissors, removing other proteins off the cell to send important signals. ADAM17 needs a helper protein called iRhom2 to maintain stability and act as an action guide.

The researchers were able to work out how these two proteins fit together and how an antibody called MEDI3622 can plug ADAM17’s active site, keeping it from turning on. But they also found the solution — a hidden control switch of sorts in the iRhom2 protein that helps to connect signals from inside the cell to what’s going on outside.

Understanding these new functions may help in the design of more precise drugs that shut down ADAM17 when it’s misbehaving, without causing unwanted side effects, offering a clearer path to targeting inflammation at its root.

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Cancer can run, but it can no
longer hide

Envision cancer sneaking around your immune system by feeding certain cells fatty snacks that make them too sleepy or bossy to help.

That’s what liver cancer does — it hijacks your body’s immune response by jamming immune cells full of fat, turning some into lazy pushovers (called exhausted T cells) and others into overbearing peacekeepers (Tregs) that tell patrolling cancer-killing cells to back off.

But scientists have a new trick up their sleeve to outmaneuver the fatty snack giving — a lab-made antibody called PLT012. It blocks a protein called CD36, which acts like a fatty-acid vacuum cleaner for these sneaky immune cells. When PLT012 steps in, it cuts off the fat supply, helping the immune system to snap out of its slump and start attacking cancer cells again.

In mice — even the tough-to-treat ones — and in human liver-cancer samples in the lab, PLT012 not only boosts cancer-killing immune cells, it also works well alongside other cancer treatments. More notably, it holds strong in high-fat environments that normally limit the effectiveness of treatments.

PLT012 is shaping up to be a potential game changer in liver cancer treatment by targeting the tumor’s tricks and offering the immune system a second wind.

The paper was published in Cancer Discovery.

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A step forward in targeting tumors

Current immunotherapies often struggle against hard-to-treat tumors with low mutation rates and high variability.

They are hard to target effectively, but new research published in Nature introduces a promising approach by targeting tumor-wide neoantigens — abnormal proteins created due to errors in RNA splicing.

The researchers found that these public neoantigens are common across multiple cancer types, including those more difficult to treat. By mapping RNA splicing patterns
RNA splicing patterns, they identified specific abnormal proteins that are consistently presented by cancer cells and recognized by the immune system.

Targeting these neoantigens could offer a more universal and stable target. This approach could lead to immunotherapies that work across different cancer types, potentially improving outcomes for patients with hard-to-treat tumors.

More on this topic: Launching medical research