Full text
| |
| Author(s): |
Welbert de Oliveira Pereira
Total Authors: 1
|
| Document type: | Doctoral Thesis |
| Press: | São Paulo. |
| Institution: | Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) |
| Defense date: | 2011-11-04 |
| Examining board members: |
Joao Gustavo Pessini Amarante Mendes;
Jose Alexandre Marzagao Barbuto;
Andre Luiz Vettore de Oliveira;
Glaucia Maria Machado Santelli;
João Paulo de Biaso Viola
|
| Advisor: | Joao Gustavo Pessini Amarante Mendes |
| Abstract | |
Bcr-Abl is the tyrosine kinase (TK) responsible for causing Chronic Myeloid Leukemia (CML). This fusion protein up- and down-regulates several genes and pathways, producing a strong resistance to apoptosis and a blockage of cell maturation in the hematopoietic compartment. The last follow-up studies provided that only 50% of the patients treated with second generation achieve complete remission, what means that one-half of these patients needs something better. Wiskott Aldrich Syndrome Protein (WASP) is an essential gene for the proper development and function of the hematopoietic cells. In the light of this background, we decided to investigate if WASP could have some role or relevance in the CML context. In conclusion, Bcr-Abl suppresses WASP expression by an epigenetic mechanism. The re-expression of WASP makes the CML cells more susceptible to apoptosis and contribute to respond to Imatinib. We suggest that recovery of WASP expression should be discussed as a new and additional strategy for CML therapy. (AU) | |