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Chronic Lymphocytic Leukemia |
1 Hematopathology Section, Department of Pathology
2 Genomics Unit and
3 Department of Hematology, Hospital Clínic, Institut dInvestigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain
Correspondence: Elias Campo, Hematopathology Unit, Hospital Clínic, Villarroel 170, 08036 Barcelona, Spain. E-mail: ecampo{at}clinic.ub.es
The biologic mechanisms involved in the clinical progression from early stages of patients with chronic lymphocytic leukemia (CLL) are not well known. We investigated sequential samples from 16 untreated CLL patients obtained at diagnosis in early stage and after progression before treatment. One patient had a p16 INK4a homozygous deletion at diagnosis and progression, and 3 patients acquired a p53 mutation, gains of 5q21-q23 and 11pter-p14, and a gain of chromosome 12 respectively, during the progression of the disease. Gene expression profile analysis showed a significant modulation of 58 genes with a particular downregulation of genes that are inhibitors of cell adhesion and motility.
Key words: chronic lymphocytic leukemia, progression, microarrays, comparative genomic hybridization.
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