Skip to main content
31/08/2011

Discovered how works a key protein that could be target for new treatments for CLL

2011_0276_2011_0276_IMATGE

31/08/2011

A recent study of Vall d'Hebron Research Institute (VHIR) has shown the mechanism that explains why the presence of a protein -ZAP-70- determines the prognosis of chronic lymphocytic leukemia (the most common among adults in the western world) and has given its key role as a potential therapeutic target for this disease when it progresses.This finding, led by the research group in Experimental Hematology at VHIR was published in the latest edition of the prestigious journal Blood and is a step toward understanding the disease, while opening the door to possible new treatments. "Our study clearly establishes the importance of ZAP-70 protein as a marker that distinguishes patients with poor prognosis from those with a more favorable and states that the cause of this difference is the presence of adhesion molecules on the membrane of the cells responsible for the more rapid spread of this type of leukemia", says Dr. Francesc Bosch, head of that group and coordinator of the research. "The study also determines both the possibility that this protein may be a clear target for drug design and the usefulness of using monoclonal antibodies against these adhesion molecules present in the cell membrane and help to slow the progression of the disease". concludes Dr. Bosch.Chronic lymphocytic leukemia (CLL) is typical of older adults, usually 65 to 70 years, and most cases are detected incidentally on routine analytical, in which appears a large number of lymphocytes. After careful diagnosis by the hematologist, 80% of the LLC do not require chemotherapy until many years pass and the disease progresses. Even some patients may not require treatment and will only ever need to be monitored closely, while the other 20% of cases they will need chemotherapy, mainly due to the clinical characteristics of the disease.

A recent study of Vall d'Hebron Research Institute (VHIR) has shown the mechanism that explains why the presence of a protein -ZAP-70- determines the prognosis of chronic lymphocytic leukemia (the most common among adults in the western world) and has given its key role as a potential therapeutic target for this disease when it progresses.This finding, led by the research group in Experimental Hematology at VHIR was published in the latest edition of the prestigious journal Blood and is a step toward understanding the disease, while opening the door to possible new treatments. "Our study clearly establishes the importance of ZAP-70 protein as a marker that distinguishes patients with poor prognosis from those with a more favorable and states that the cause of this difference is the presence of adhesion molecules on the membrane of the cells responsible for the more rapid spread of this type of leukemia", says Dr. Francesc Bosch, head of that group and coordinator of the research. "The study also determines both the possibility that this protein may be a clear target for drug design and the usefulness of using monoclonal antibodies against these adhesion molecules present in the cell membrane and help to slow the progression of the disease". concludes Dr. Bosch.Chronic lymphocytic leukemia (CLL) is typical of older adults, usually 65 to 70 years, and most cases are detected incidentally on routine analytical, in which appears a large number of lymphocytes. After careful diagnosis by the hematologist, 80% of the LLC do not require chemotherapy until many years pass and the disease progresses. Even some patients may not require treatment and will only ever need to be monitored closely, while the other 20% of cases they will need chemotherapy, mainly due to the clinical characteristics of the disease.

Subscribe to our newsletters and be part of the Campus life

We are a world-leading healthcare complex where healthcare, research, teaching and innovation go hand in hand.

This question is for testing whether or not you are a human visitor and to prevent automated spam submissions.