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Researchers at Tel Aviv University believe they have found a "pathway" that allows melanoma cells to spread to the brain and may have found a way to prevent this from happening.
The study was conducted in mice, but was also validated on samples of human brain tissue where melanoma had spread, the researchers said.
"Melanoma is the most deadly skin cancer because of its high rate of metastasis, often to the brain," said Professor Neta Erez of the Department of Pathology at Tack Medical School, TAC, lead author of the 39; study.
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"The prognosis of patients with brain metastases is very dark," said Erez.
Photo of the Tel Aviv University Research Team, from left to right: Malak Amer, Professor Neta Erez, and Dr. Hila Doron (Tamar Shami)
Patients died of metastases in other parts of the body before they were spotted in the brain. However, thanks to improved treatments and longevity of patients, "the incidence of diagnosed brain metastases is increasing. Understanding how and why brain metastases occur is an urgent challenge for cancer researchers today, "Erez said.
The researchers sought to know how these cells spread in the brain and how this transmission could be stopped. In their work, they took mice with spontaneous brain melanoma metastases and studied how they reacted with the brain.
Astrocytes are among the most abundant cells in brain tissue. Their role is to protect the brain and maintain its function through tissue repair. If astrocytic cells detect tissue damage, such as a stroke, they trigger an alarm and begin to secrete inflammatory factors that attract immune cells to the brain.
"We discovered that these melanoma cells could activate these inflammatory pathways leading to the brain, and then divert that path," Erez said during a phone interview. "They trigger inflammatory secretions, then take advantage of this pathway that helps them to enter the brain."
When researchers used genetic manipulations to neutralize melanoma cell receptors, they successfully blocked the ability of tumor cells to respond to astrocyte signaling. "The development of brain metastases was significantly inhibited," said the university in a statement.
The research, emphasized Erez, was performed on mice and not on humans. But the researchers validated their findings in brain metastases of brain operated patients. They found that in humans, astrocyte cells expressed the same inflammatory factor – called CXCL10 – and that human tumor cells also expressed the same receptor, CXCR3, as mice.
"This suggests that the identical mechanism works in humans," the statement said.
"Our findings suggest that blocking this signaling pathway could prevent brain metastases," said Erez. "The CXCL10-CXCR3 axis could be a potential therapeutic target for the prevention of brain metastases of melanoma."
The researchers are currently studying what could be the trigger for brain inflammation, which promotes metastasis.
The research, published in Cell Reports on August 13, was led by TAU graduate students, Dr. Hila Doron and Dr. Malak Amer, in collaboration with Professor Ronit Satchi-Fainaro, also from the TAU Faculty of Medicine in Sackler.
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