Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 100, Issue 5, Pages 1061-1070Publisher
FEDERATION AMER SOC EXP BIOL
DOI: 10.1189/jlb.2AB0715-301R
Keywords
signal transduction; lymphocyte; HSP70; Smac/DIABLO
Categories
Funding
- Ministero dell'Istruzione dell'Universita e della Ricerca (PRIN)
- Ministero dell'Istruzione dell'Universita e della Ricerca (FIRB)
- Associazione Italiana per la Ricerca sul Cancro (AIRC project) [15397]
- Fondazione CARIPARO-Progetto Pediatria
- AIRC regional project
- Fondazione Cariparo and Cariverona, Regione Veneto on Chronic Lymphocytic Leukemia
- AIRC [15397]
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B cell chronic lymphocytic leukemia (CLL) is characterized by the accumulation of B lymphocytes from proliferative activity and apoptosis resistance. The increased awareness of the importance of B cell receptor signaling in CLL has raised new opportunities for targeted intervention. Herein, we describe a study performed with the high-throughput RPPA (reverse phase protein array) technique, which allowed us to simultaneously study different molecules in a large series of patients. We analyzed B lymphocytes from 57 patients with CLL and 11 healthy subjects. Different pathways were assessed for activation/expression of key signaling proteins. Data obtained were validated by Western blotting and confocal microscopy. The RPPA investigation and its validation, identified 3 series of proteins: 1) molecules whose expression levels reached statistically significant differences in CLL vs. healthy controls (HSP70, Smac/DIABLO, cleaved PARP, and cleaved caspase-6); 2) proteins with a positive trend of difference in CLL vs. healthy controls (HS1, gamma-tubulin, PKC alpha/beta-II Thr-638/641, p38 MAPK Thr-180/Tyr-182, NF-kappa B Ser-536, Bcl2 Ser-70 and Src Tyr-527); and 3) molecules differentially expressed in patients with IGHV mutations vs. those without mutations (ZAP70, PKC-zeta lambda, Thr-410/403, and CD45). This study identified some molecules, particularly those involved in apoptosis control, which could be considered for further studies to design new therapeutic strategies in CLL.
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