Researchers from the University of Seville at the Andalusian Center for Molecular Biology and Medicine regenerative (Capimer) They discovered a new security vulnerability in breast cancer. Some proteins have a known ability to expand as in “single-strand DNA gaps,” and this process is “crucial” for their subsequent repair. the Progress This study was compiled in a study published in the prestigious journal Nucleic Acids Research, as reported by the University of Seville in a press release.
The absence of these proteins prevents the repair of these “gaps,” which spontaneously accumulate in cancer cells deficient in the BRCA1 gene, leading to a loss of cell viability. To compensate for this problem, tumors associated with BRCA1 mutations need to accumulate more of these proteins.
Therefore, these discoveries raise the possibility of developing drugs capable of inactivating these proteins. com Therapeutic targets in the treatment of BRCA1-deficient breast tumors. Since these cases represent between five and ten percent of the millions of new breast cancer cases diagnosed worldwide each year, these treatments could benefit a large number of patients.
The genetic information contained in DNA is constantly exposed to various sources of stress, both internal and external. A particularly complex situation raisins When our DNA is copied, a process called replication, the machinery responsible for doing so must face many obstacles. Among them, damaged DNA stands out, which has undergone some physical or chemical changes due to the action of internal or external factors.
When the presence of these obstacles is high, what is called “stress” occurs. com. replicatetiu“, that is, multiplying under the unfavorable conditions that are characteristic of cancer cells. To complete genome duplication in the presence of damaged DNA, our cells have evolved a series of mechanisms that allow them to tolerate this Danny.
One such mechanism involves stopping the transcription machinery when it encounters an obstacle and restarting DNA synthesis after a few nucleotides, leaving behind an untranscribed piece of DNA called a “simple DNA gap” or ssDNA gap. These “gaps” must later be filled in for the DNA copy to be completed.
It has recently been discovered that the presence of these “gaps” represents a weakness in cancer cells. For example, mutations in the BRCA1 and BRCA2 genes, which are associated with hereditary breast cancer, also cause the accumulation of these “gaps.” In addition, therapies currently used to treat tumors with these genetic mutations BarcaIncreased formation of these “gaps”. Therefore, their formation and/or repair represents a potential therapeutic target for the treatment of breast tumors.
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