Researchers reveal the origin of common pediatric leukemia

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Agencies AprilThe team led by Óscar Molina, researcher in the Stem Cells, Developmental Biology and Immunotherapy group at the Josep Carreras Leukemia Research Institute , has discovered the pathophysiological mechanisms related to hyperdiploidy in pediatric B-ALL. To carry out the study, published in the journal 'Blood', the experts hypothesized that the origin of these mechanisms could occur at the moment when the cell divides: mitosis, a cellular process that controls the equitable distribution of the genetic material, already duplicated and previously compacted in the chromosomes, and distributes them into two 'newborn' cells . «We already knew that hyperdiploidy of this type of leukemia arises in a B cell progenitor in the uterus.

However, the molecular mechanisms remained an enigma. We observed what was happening right at the time of chromosome segregation in hyperdiploid B-ALL to find an explanation for this oncogenic process," explained Molina. by Taboola Sponsored links you may like Unsold Prefabricated Cabins Sell For Almost Nothing! (Take A Look) Unsold Prefabricated Cabins Singapore Phone Number List Thank you for watching The researchers used a large cohort of primary pediatric B-ALL samples from 54 patients, finding that three key processes and factors for proper chromosome segregation during cell division were damaged or inhibited in hyperdiploid cells. Furthermore, they found that the artificial interruption of these processes in blood cells with normal chromosome numbers generated hyperdiploid cells similar to those in B-ALL samples.



These players are the condensin protein complex, responsible for helping to properly condense genetic material into chromosomes; the aurora B kinase protein, responsible for the chromosomes joining together correctly so that they end up going to the opposite poles of the cell that divides into two. What's more, dysfunctions have also been seen in the cellular control point of this last process (known as SAC). With these findings, the team has revealed the molecular mechanisms that are altered in this common type of pediatric blood cancer. 'The next steps would be to study whether other subtypes of B-ALL with abnormal chromosome numbers, such as hypodiploid B-ALL, which is a very aggressive subtype of pediatric blood cancer, share a common molecular mechanism. These studies will allow the generation of the first in vivo preclinical models of leukemias with abnormal chromosome numbers, crucial to understanding their origin and growth.