Cause of the discovered burkitt Lymphoma
Cause of the discovered burkitt Lymphoma
Burkitt lymphoma is a form of lymphoma non Hodgkin extremely fast which comes from a subset of white blood cells called lymphocytes B of the immune system. Now, researchers of the Max Delbrück Center for Molecular Medicine (MDC) Berlin-Buch discovered a component essential that converts the immune cells in malignant lymphoma cells.
According to Dr. Sandrine Sander and Professor Klaus Rajewsky, Burkitt Lymphoma comes from the germinal centers of Lymphoid organs (Peyer plates in the small intestine, the spleen and lymph nodes). By the germinal Center reaction is triggered by B cells when antigens are detected. Once the reaction happens, B cells modify their DNA causing a very specific antibody against the Antigen response.
(BCR) B cell receptor plays an essential role in the reaction process. To fully recognize the Antigen and to trigger an appropriate immune response, the segments of DNA coding for the antibodies must be changed and rearranged. This complicated process of DNA breaks can occur and repair mechanisms that may lead to errors may cause genetic mutations related to the development of cancer.
In Burkitt Lymphoma, DNA repair errors cause the translocation of the oncogene c - MYC, a gene that controls cell division. C - MYC translocation is that the affected cells divide of unregulated manner and the overexpression of c - MYC leads a massive death of cells. As a result, only c - MYC deregulation cannot convert normal cells into cancer cells. In Burkitt Lymphoma, the induction of apoptosis of high c - MYC expression must be overcome by additional mutations preventing cell death.
In a recent study, Professor Rejewsky and his team showed that the enzyme PI3K is vital if mature B cells to survive. PI3K stimulates a way of signaling that controls cell growth and challenging programmed cell death.
Dr. Sander and Professor Rajewsky based their study on these results. They examined the interaction of c - MYC and PI3K in tumorigenesis of mouse. The team showed that PI3K is an essential component of the development of Burkitt lymphoma. They found that PI3K allows c - MYC to transform the germinal Center B lymphocytes in lymphoma cells which divide continuously and avoid apoptosis.
However, the researchers believe that other genetic mutations play a role in the lymphomagenese of Burkitt, because all B cells coexist, c - MYC and PI3K turns into a lymphoma cell. Such aberrations may be identified in their mouse model. In addition, a study by Dr. Louis Staudt of the National Cancer Institute, Bethesda, Maryland, United States, showed that patients with Burkitt's lymphoma, carry genetic mutations that resemble those of the mouse.







0 comments:
Post a Comment