Leukemia cells from patients suffering from chronic myeloid leukemia, especially in the advanced stage, lack one of the proteins: the famous BRCA1. Importantly, the protein is not present even if the patient carries the proper, not mutated gene responsible for BRCA1 production. Scientists from the Nencki Institute, Warsaw, Poland, showed that BRCA1 deficiencies in case when the gene is functional are caused by defects in the protein synthesis process. Such discovery not only explains the mechanism which supports leukemia development, but also uncovers its weakness. Results of this project performed in collaboration with the group of Prof. Tomasz Skorski from the Temple University School of Medicine in Philadelphia might lead to improvement of diagnostics in leukemia and in the future it might benefit in development of better, more efficient therapies leading to cure of patients. Chronic Myeliod Leukemia (CML) is diagnosed in about 25% of adult leukemia patients. The disease is caused by the translocation between chromosomes 9 and 22. This leads to generation of the fusion chromosome, known as Philadelphia chromosome, and a new fusion gene coding a new protein: BCR-ABL1 kinase. The presence of BCR-ABL1 kinase results in activation of signaling pathways, which promote and are responsible for development of chronic myeloid leukemia. Therapeutic regimes routinely used in CML usually do not cure patients. They allow to control the chronic phase of the disease and delay advanced phases, however they do not protect from resistance. Therapies based on the synthetic lethality open new possibilities to develop novel, personalized therapies, which can eliminate leukemia cells, including the leukemia stem cells, which are responsible for disease relapse and malignant progression

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