Acute lymphoblastic leukemia (ALL) is the most common cancer in children. This tumor is characterized by the uncontrolled growth of lymphoblasts, immature cells that are the precursors of lymphocytes, a type of white blood cell. Its abnormal multiplication affects the manufacture of different blood cells, such as red blood cells, platelets or red blood cells, for example, which can cause hemorrhages and anemia and promote infections; they can also infiltrate organs and other tissues.
Broadly speaking, there are two major varieties of this disease, B-ALL and T-ALL, named for the type of leukocyte that is affected. The latter, known as T-cell acute lymphoblastic leukemia, accounts for approximately 10-15% of pediatric ALL and about 25% of adult ALL. In essence, it is an aggressive tumor that, if left untreated, progresses rapidly . In fact, although in recent years it has been observed that the application of chemotherapy intensively improves the prognosis of those affected, it is not unusual for them to relapse.
Well, a team of researchers coordinated by María Luisa Toribio, an expert from the Severo Ochoa Molecular Biology Center – a mixed body between the Higher Council for Scientific Research (CSIC) and the Autonomous University of Madrid (UAM) -, has presented a an ‘in vivo’ model of the disease that, in the future, will make it possible to collect key information about its origin and how it develops.
New weapons against disease
In a statement, these scientists explain that for this, they started from a healthy cell, a biomedical milestone that, in their opinion, will help to find more effective therapies. “This model has made it possible to identify a protein necessary at the beginning of the generation of leukemia that, in addition, is subsequently involved in its spread”, indicates María Luisa Toribio. The use of monoclonal antibodies –a type of immunotherapy designed to attack specific proteins of cancer cells– against this molecule, which bears the name of CD44, has also shown that it plays a relevant role in the interactions that occur between the aforementioned preleukemic cells and bone marrow. Apparently, this phenomenon is essential for the activity of the leukemia initiating cells and the progression of the disease to be maintained.
Toribio and his team emphasize that to combat this disease it is urgent to develop new therapeutic strategies that allow the safe elimination of the cells that cause leukemia and that are responsible for the aforementioned relapses. In this sense, this biologist points out that this work, published in The Journal of Clinical Investigation , represents a great advance in the knowledge of the pathogenesis of this type of leukemia, which, over time, could improve life expectancy from the patients.
Reference: The NOTCH1 / CD44 axis drives pathogenesis in a T cell acute lymphoblastic leukemia model . María Luisa Toribio et al. The Journal of Clinical Investigation . DOI: 10.1172 / JCI92981
Image: The thymus is the organ where the transformation process of the cells that generate acute T-cell leukemia begins. CSIC
