Gene expression profile and genomic changes in disease progression of early-stage chronic lymphocytic leukemia.
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.
Fernàndez
Verònica
V
Hematopathology Section, Department of Pathology, Hospital Clínic, Institut d'Investigacions Biomèdiques August Pi i Sunyer (IDIBAPS), University of Barcelona, Barcelona, Spain.
Jares
Pedro
P
Salaverria
Itziar
I
Giné
Eva
E
Beà
Sílvia
S
Aymerich
Marta
M
Colomer
Dolors
D
Villamor
Neus
N
Bosch
Francesc
F
Montserrat
Emili
E
Campo
Elias
E
D000368:Aged; D000369:Aged, 80 and over; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000378:metabolism; D018450:Disease Progression; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic; D016158:Genes, p53 / Q000235:genetics; D016678:Genome; D006801:Humans; D015451:Leukemia, Lymphocytic, Chronic, B-Cell / Q000175:diagnosis* / Q000235:genetics* / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D009693:Nucleic Acid Hybridization; D020411:Oligonucleotide Array Sequence Analysis
D019941:Cyclin-Dependent Kinase Inhibitor p16