Breast Cancer Little Silver, NJ

Molecule Shows Promise in Blocking Tumor Growth

Cancer is a sneaky customer. One of its underhanded ways is to trick the body’s immune system into not attacking it, or to even help it grow.

But a team of scientists seems to have found a way to use immunotherapy to pull the rug on this deception of cancer cells. Their study was reported in the journal Nature Communications.

How cancer uses the body to grow

Our myeloid cells are key weapons in our immune system’s response to invaders. Myeloid cells are crucial in the body’s standard immune response, but also its adaptive response to a wide range of pathogens.

That’s where cancer is tricky. Myeloid cells should be actively attacking all invaders, of which cancerous cells would be foremost. But the cancer cells trick the myeloid cells into believing that the cancer cells are not invaders, but are actually a part of the body that something has damaged. They make the myeloid cells believe they don’t need to be destroyed, but they need to be repaired. When this happens the myeloid cells actually help the cancer cells divide and grow.

This process wasn’t understood, but new research from a joint team from the Department of Internal Medicine at Rush Medical College in Chicago, Illinois and the Moores Cancer Center at the University of California in San Diego seems to have unlocked the cancer trick and found a way to subvert it.

Protein is the key

In the study, the teams used genetically modified mice to get to the bottom of how the cancer cells trick the myeloid cells. In the mice, they found a protein called CB11b was needed to help the myeloid cells transform into a sub-type called M1 macrophages. M1 macrophages will attack and kill tumor cells.

But cancer cells interfere with the activity of CD11b, so instead of becoming helpful, destroyer M1 macrophages, the myeloid cells become M2 macrophages. Instead of attacking and suppressing the growth of the cancer cells, these M2 macrophages boost them. The M2 macrophages do this by keeping the immune T cells away (they are crucial for fighting disease) and by secreting growth factors that fuel the cancerous cells with new blood vessels, helping them grow. Double whammy.

Other research has shown how effective T cells can be in controlling tumor growth, so when it was discovered that the M2 macrophages were actually blocking T cells and promoting tumor growth that opened eyes.

So, the goal was to help the CD11b protein to keep on task and stop the myeloid cells from changing into M2 macrophages.

Protein keeps CD11b active

To isolate the role of CD11b, the scientists studied mice without CD11b. In these mice, transplanted tumors grew much faster and larger. Also the majority of myeloid cells had changed into M2 macrophages.

Next, the teams developed and used a new molecule, called Leukadherin-1 (LA-1) to boost the activity of CD11b and placed it in mice. This protein drastically reduced tumors in the mice receiving treatment. They also engineered other mice with a mutation that made the CD11b stay active all the time. Like the mice given the CD11b, the tumors in the engineered mice shrank dramatically.

This proves that activating CD11b is a valid new goal in cancer immunotherapy. To do so, LA-1 could be a promising new drug, although this research is only in the beginning stages.

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