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Synthetic lethality refers to the phenomenon that the simultaneous inactivation of two non-lethal genes leads to cell death. If a specific gene is found to be inactivated in a tumor, then it can specifically kill cancer cells without damaging healthy cells by inhibiting its synthetic lethal partner with drugs. Such a strategy is expected to achieve more effective and less effective personalized cancer treatment, and is a new direction for anticancer drug research.
In recent decades, people have high hopes for synthetic death, but its potential has not been fully explored. A group of researchers from the University of California, San Diego, recently adopted a multi-species approach to develop a cancer treatment. Synthetic lethal interaction technology. The findings were published in the Molecular Cell magazine.
First, researchers screened more than 160,000 interactions in yeast that interact with human tumor suppressor gene (TSG) orthologs and encode drug genes that target multiple genotoxic environments. . Based on these signals, the researchers evaluated thousands of TSG drug combinations in HeLa cells and found a conserved synthetic lethal interaction network.
Later, the researchers analyzed the network and found that the stability of interaction between the cross-environment and shared gene functions can increase the probability of observable interactions in human cancer cells. Using this approach, the researchers found a preferred TSG drug combination approach in the future and validated these interactions based on cell, or patient survival.
Synthetic lethal methods can target a range of cellular defects, including DNA repair, cell cycle control, and metabolic changes, as well as targeting the interaction of tumor cells with normal cells surrounding them.
Previously, researchers at the Moffitt Cancer Center have used synthetic lethal methods to treat breast cancer patients with BRCA1 and BRCA2 mutations. BRCA1 plays an important role in repairing damaged DNA, while women with BRCA1 or BRCA2 mutations often develop breast cancer. The risk of ovarian cancer is higher because the body cells cannot perform proper DNA repair. This suggests that BCRA-mutated breast cancer cells may be quite sensitive to drugs targeting DNA. Laboratory studies have shown that targeting another DNA repair protein, PARP, can effectively kill BCRA-mutated cancer cells. Some PARP inhibitors are being tested clinically for breast cancer patients, and early trial results are very good.
Synthetic lethal studies, in addition to helping to personalize cancer treatments, can also help people tap into the anticancer potential of other disease drugs. For example, researchers at TelAviv University have developed a new algorithm for identifying synthetic lethal interactions. By analyzing the genetic and molecular data (copy number, DNA sequencing, gene expression, shRNA, etc.) of cancer clinical samples, they comprehensively identified synthetic lethal genes in cancer cells and generated a core network of cancer synthesis death. Studies have shown that such networks can predict the importance of genes, cell-to-drug responses, and patient outcomes. (Original: A Network of Conserved Synthetic LethalInte ractions for Exploration of Precision Cancer Therapy)
US research and development of synthetic lethal technology to help precision cancer treatment
[China Pharmaceutical Network Technology News] Recently, researchers from the University of California, San Diego, etc. developed a synthetic lethal interaction technology related to cancer treatment. It is understood that in addition to helping to personalize cancer treatment, synthetic lethal research can also help people tap the anti-cancer potential of other disease drugs.