Once in the brain, skin cancer cells produce Alzheimer's protein: study

The amyloid beta protein that is seen in some cognitive diseases may help cancer spread.

Chris Arnold 3 minute read March 11, 2022
Brain neuro growth on black

Alzheimer’s disease, is believed to be the result of the accumulation of certain proteins in the brain that leads to the slow death of neurons. GETTY

A protein that builds up in the brains of Alzheimer’s patients could be causing skin cancer cells to spread easier once they reach the brain. 

A study out of the New York University Grossman School of Medicine published in the journal Cancer Discovery says the protein amyloid beta could be responsible.  

Researchers chose to focus on melanoma — a type of skin cancer that can also occur in the mouth and eyes — because it spreads to the brain in 40 per cent of patients in stage 4 of the disease, the highest rate among common cancer types. 

Cancer unnoticed

The team also found cancer cells that secreted the amyloid beta protein slowed the immune response that would normally recognize cancer cells as harmful, and attempt to attack. The theory is that the amyloid beta moves brain immune cells into an infectious fade mode, which heals tissue, but allows the cancer to go unnoticed by the body. 

To monitor how these cells and proteins interacted with one another, the researchers used 24 human samples of brain and non-brain cancer metastases — essentially cancer that has grown or spread. The team was able to show that melanoma cells from the brain are, in fact, producing the proteins related to various cognitive diseases including Alzheimer’s, Parkinson’s, and Huntington’s.

Further experiments showed that the melanoma cells that lacked amyloid beta proteins were not able to grow due to an immune attack during the period where they would usually form cell colonies. 

The original batch of data led researchers to believe that the cancer cells produced the protein in patients’ brains for their own survival. Once the gene responsible for amyloid precursor protein — which becomes amyloid beta — was removed in cancer cells injected into the hearts of mice, the volume of cancer cells detected in the mice’s brains decreased.

“Our study reveals an unexpected role for tumour-secreted amyloid beta in promoting the survival of melanoma brain metastases, and suggests a new way to counter it,” senior author of the study Eva M. Hernado-Monge said in a statement

The scientists also found that amyloid beta released by cancer cells changed the gene expression in brain cells that assist neurons — which are the cells responsible for carrying messages and signals throughout the brain. 

The team also discovered that amyloid beta released by cancer cells are actually more resilient to microglia, a type of cell that makes up about 15 per cent of all brain cells. Microglia typically clears away amyloid beta, according to a 2013 study from researchers at the University of California, Los Angeles. 

The researchers think it’s possible that amyloid beta released by melanoma cells are being influenced to stop destroying them. 

“The field has already developed treatments that have been shown in clinical trials to potently and safely reduce amyloid beta levels, but that fail to counter Alzheimer’s disease for reasons unknown,” Kevin Kelfman, one of the study authors said. “With this in mind, our team is already evaluating whether repurposed, tested anti–amyloid beta antibodies could prevent or reduce brain metastases in animal studies. Another next step is combining immunotherapies, including checkpoint inhibitors, and anti–amyloid beta therapies to ensure they can be used safely together.”


Chris Arnold is a Toronto-based writer.

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