Chronic Lymphatic Leukemia (CLL) is the most common type of leukemia in adults in the West. It mainly affects elderly patients and its incidence is expected to increase due to the progressive increase in life expectancy in our society. Today is an incurable disease, with a development that can be indolent or more aggressive. Knowing the molecular cause of this disease is essential to develop healing therapies.

Researchers of the group of hematological neoplasms and transplantation of hematopoietic progenitors of IDIVAL, led by Dr. Carlos Pipaón of the Molecular Hematology Laboratory (HEMMOL), have discovered that high levels of expression of the FANCA gene, involved in DNA repair, constitute a marker of worse prognosis in CLL. In the recently published work in the FASEB Journal (https://doi.org/10.1096/fj.201802439RR), also signed by the predoctoral student Sara Bravo, Dr. Lucrecia Yáñez and Dr. Íñigo Romón from the Hematology Service, analyzed the expression of this type of genes in samples of several hundred of patients of the hospital. This marker is associated with other factors of poor prognosis such as the deletion of the long arm of chromosome 11 and with a time from diagnosis to the shortest treatment. The group has investigated the molecular basis of this worse prognosis and has discovered that FANCA collaborates in the degradation of the p53 protein, involved in the protection of the genome and the response to chemotherapeutic agents, which leads to a greater proliferation of B lymphocytes of the CLL. The work reveals the importance that cellular processes that modify the function of proteins can have on the development and treatment of pathologies in which a genetic cause has not been identified.

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