Israeli researchers find way to block melanoma cells from spreading to brain

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JERUSALEM, Aug. 19 (Xinhua) -- A new Israeli research shows how melanoma metastases manage to spread to the brain, and develops a method to neutralize this mechanism, the Tel Aviv University (TAU) reported Monday.

The method may block the deadly spread of brain metastases in patients with the violent cancer.

Brain metastases are among the deadliest tumor metastases, with a median survival time of less than a year, and the incidence of brain metastasis is rising.

The new research, published in the journal Cell Report, focused on melanoma brain metastasis because it is the deadliest skin cancer due to its high rate of metastasis, frequently to the brain.

The TAU scientists utilized a mouse model of spontaneous melanoma brain metastasis to study the interactions of melanoma tumors within the brain microenvironment.

They discovered that melanoma brain metastasis is facilitated by the takeover of a physiological inflammatory pathway by astrocytes, the brain cells that maintain a protected environment in the brain.

In addition, astrocytes respond to tissue damage in the brain by instigating an inflammatory and tissue repair response to contain the damage, secreting inflammatory factors that recruit immune cells.

The researchers discovered that tumor cells recruit these inflammatory factors to "hijack" their way to the brain.

The team identified a specific factor that mediates their attraction to the brain and showed that brain metastasizing melanoma cells express the receptor for the inflammatory factor, which is how they respond to this signal.

Significantly, when the researchers used genetic tools to inhibit the expression of the receptor on melanoma cells, they successfully blocked the ability of tumor cells to respond to astrocyte signaling, and the development of brain metastases was significantly inhibited.

Next, the scientists validated their results in the brain metastases of patients who had undergone brain surgery and found that the identical mechanism is operative in humans. Enditem

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