Scientists came up with a breakthrough discovery in the field of research and development of cancer drugs. A way to prevent cancer cells from entering the blood.
Just recently, news of a groundbreaking discovery appeared on the Internet and social networks. It was earned by scientists from Israel, from the Bar Ilan University research team. They managed to create a peptide that prevents cancer cells from penetrating the blood and spreading further into the body through the blood. On this basis, scientists are now trying to produce the first preventive drug in the world, which would be designed to stop secondary tumors. In research on mice with breast cancer, the drug's alleged active ingredient proved more than 90% effective.
Research shows that the peptide successfully prevented the formation of metastases in mice, thus preventing the spread of diseased cells that can cause secondary tumors. It is the dissemination of cancer cells from the primary tumor to distant body tissues and organs that is the main cause of death in a large percentage of cancer patients, Nature reports.
Cells of solid tumors can through the so-called invadopodia, foot-shaped cytoskeletal structures that protrude from their surface, penetrate the basement membrane. Invadopodia allow cells to push their way through tissue. In this way, cancer cells can enter the blood vessels and form metastases in other distant tissues and organs. However, the process only happens when the invadopodia are activated by the association of the 2 proteins.
Prof. Jordan Chill, co-author of the mentioned research study, said that the Bar Ilan team's breakthrough lies in finding a peptide that stops this protein interaction. "We believe that this can prevent the activation of the invadopodia and therefore inhibit metastasis. I expect that it could be used in addition to chemotherapy or other treatments that kill cancer cells," he said.
In breast cancer, the non-receptor tyrosine kinase Pyk2 is highly expressed. It mediates the formation and function of invadopodia through interaction with the factor supporting actin nucleation, the protein cortactin. The researchers designed a peptide inhibitor that inhibits the interaction between Pyk2 and cortactin in invadopodia. Pyk2-PRR2 peptide blocks spontaneous lung metastasis in immunocompetent mice and reduces invasiveness of MMP-dependent tumor cells. Mice with breast cancer that received the peptide were at least 90% less likely to develop secondary tumors than the control group.
Although the research study focused specifically on breast cancer, the research team believes that the peptide will be effective on all solid tumors. They therefore expect effects on other types of cancer than just blood, bone marrow or lymph node cancer.
Previous research shows that 12% of patients diagnosed with breast cancer develop metastatic disease. Chemotherapy is used to "kill"as many cancer cells as possible, but it does little to prevent the cells that "survive" from becoming active again.
"Our advance is very exciting, as today there are no drugs in production that prevent metastasis, [or] in other words exist especially to stop cancer from spreading," said Dr. Hava Gil-Henn, co-author of the study.
According to the particular research study, the findings shed favorable light on the specific molecular interactions between Pyk2 and cortactin and may lead to the development of new strategies to prevent the spread of primary breast tumors that were predicted to be highly metastatic at the time of diagnosis and secondary tumors, which have already spread to other parts of the body.
"Most drugs are focused on shrinking tumors once they develop. We are taking a preventative approach, which could save many from a second illness and save many lives," says the co-author.
Professor Chill also said another challenge was to develop the peptide into a drug with delivery mechanisms that could deliver it to a specific area in the human body. “So far we have the arrowhead of the missile; now we need to develop the whole missile,” he said.
The Times of Israel, 2023
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