Scientists find site of placebo effect in brain

Hello Health Rounds readers! Today we highlight three early experimental findings: a fascinating discovery that may help explain the placebo effect, which causes people to respond to fake drugs, and two discoveries that could lead to treatments for keeping breast cancer tumors from growing and colon cancer from spreading to the liver.

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Neuroscientists have discovered a key piece of a puzzle to explain the placebo effect in which individuals appear to respond and feel better after receiving a fake pill or treatment, according to a report published on Wednesday in Nature.

Studying mice, the researchers found that when the animals are expecting pain relief, neurons and synapses along a pain control pathway in the brain are activated even when no medication has been given.

The pathway runs from the cingulate cortex in the front of the brain, through the pons region of the brainstem, to the cerebellum in the back of the brain.

“That neurons in our cerebral cortex communicate with the pons and cerebellum to adjust pain thresholds based on our expectations is both completely unexpected… and incredibly exciting,” study leader Greg Scherrer of the University of North Carolina said in a statement.

The pathway contains “an extraordinary abundance” of proteins called opioid receptors that play a role in pain control, Scherrer said.

Blocking the pathway interrupted the placebo effect, and activating the pathway caused pain relief even in animals that had not been trained to expect it, he added.

“Our results open the possibility of activating this pathway through other therapeutic means, such as drugs or neurostimulation methods to treat pain,” Scherrer said.

Lab experiments on tissue samples from more than 1,500 patients suggest drugs from a class known as sodium channel blockers might help keep breast cancer at bay during the interval between diagnosis and surgery, researchers said.

The drugs have been shown in earlier test tube experiments to keep breast cancers from growing, but how they achieve that effect has not been clear.

By blocking sodium from entering the cancer cells, the drugs cut off a process that enables the cells to move out of the tumor, the researchers found.

When sodium enters the cell, the cell pumps out lactic acid, causing the local area to become more acidic. That increases the activities of enzymes that digest the material that fills the spaces between cells, freeing up room for cancer cells to spread and move out of the tumor, the researchers reported on Thursday in Oncogene.

They also found that human breast cancer tumors with more channels for sodium entry were more likely to metastasize, or spread.

The drugs still need to be tested in clinical trials to see whether targeting sodium channels in breast cancer tumors would be effective in patients.

The drugs are already used to treat conditions such as epilepsy, nerve pain, and heart rhythm disturbances, “so there is a possibility that a drug which already has a good safety profile could be repurposed for breast cancer patients on the waiting list for surgery,” study leader Will Brackenbury from the University of York in the UK said in a statement.

Commercially available sodium blockers include Tegretol (carbamazepine) from Novartis and Dilantin (phenytoin) from Viatris.

Researchers have discovered how colorectal cancer cells manage to attach themselves so effectively to liver cells, according to a report published on Wednesday in Nature.

When colorectal cancers spread to other organs, the liver is usually the first target. Liver metastases affect up to 60% of colorectal cancer patients and are often fatal, earlier studies have shown.

In lab experiments, investigators found that proteins on the surfaces of the colorectal cancer cells and the liver cells bind together in a way that changes the cancer cells and allows them to colonize in the liver.

More specifically, when liver cells traveling in the bloodstream have a protein called Plexin-B2 and the colorectal cancer cells have proteins from the semaphorin family, the colorectal cancer cells can attach themselves to the liver cells.

Further tests have shown that plexin also encourages the formation of metastases in melanoma and pancreatic cancer, the researchers said.

If new treatments can be developed to inhibit the crucial interaction between plexin and semaphorin, it may be possible to prevent these cancers from establishing new tumors, the researchers said in a statement.

This newsletter was edited by Bill Berkrot; additional reporting by Shawana Alleyne-Morris.

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