Molecular mechanisms of glucocorticoid resistance in childhood acute lymphoblastic leukemia
Acute lymphoblastic leukemia (ALL) is the most common form of cancer in children, with 110 – 120 newly diagnosed children in the Netherlands each year. ALL is a haematological malignancy of lymphoid precursor cells and can be divided into two sub-groups: B-cell precursor ALL and T-cell precursor ALL. These two subgroups can be differentiated using light microscopy (morphology and cytochemical staining) and immunophenotypic classifi cation. More recently, other subgroups have been identifi ed based on genetic abnormalities in the leukemic cells such as chromosomal translocations (BCR-ABL, TEL-AML1, E2A-PBX1, MLLgene rearranged) and chromosome copy number (hyperdiploidy). Both a favorable (TEL-AML1, hyperdiploidy) and unfavorable (BCR-ABL, MLL-gene rearranged ALL) prognosis have been linked to these genetic subtypes. The prognosis for children with ALL has increased signifi cantly over the past 35 years, with a 5-year eventfree survival of 75-80% in most current treatment protocols. (Figure 1) However, still 20-25% of the children relapses, with a signifi cantly worse prognosis for survival. In most international treatment protocols, patients are divided into three risk-groups, i.e. standard risk, intermediate risk and poor risk.
|Keywords||acute leukemia, leukemia|
|Promotor||Pieters, R. (Rob)|
|Sponsor||Amgen B.V. , Merck Sharp & Dohme B.V. , Novartis Oncology , Pfizer B.V. , Pieters, Prof. Dr. R. (promotor) , Sanofi Aventis , Zambon Nederland B.V.|
Tissing, W.J.E.. (2006, April 27). Molecular mechanisms of glucocorticoid resistance in childhood acute lymphoblastic leukemia. Retrieved from http://hdl.handle.net/1765/10479