Publication details
FGF-2 abnormalities in B cell chronic lymphocytic and chronic myeloid leukemias
| Authors | |
|---|---|
| Year of publication | 2001 |
| Type | Article in Periodical |
| Magazine / Source | Leukemia |
| MU Faculty or unit | |
| Citation | |
| Doi | http://dx.doi.org/10.1038/sj.leu.2402012 |
| Field | Physiology |
| Keywords | AUG-INITIATED FORMS; FACTOR BFGF; IMMUNOGLOBULIN DOMAIN; |
| Description | An elevated level of fibroblast growth factor-2 (FGF-P) in peripheral blood is considered to play a role in regulating the growth of leukemia cells. Here, we show that the level of plasma FGF-P is increased in 54% of B cell chronic lymphocytic leukemias (B-CLL) and in 44% of chronic myeloid leukemias (CML), Notably, white blood cells (WBCs) from B-CLL patients contain 18, 22 and 24 kDa isoforms of FGF-2 whereas WBCs from CML patients contain only the 24 kDa isoform, Furthermore, as cultured B-CLL WBCs release 18 kDa FGF-2 into the medium, they constitute a potential source of FGF-2 in the blood. In a receptor binding assay, I-125-FGF-2 binds weakly to B-CLL WBCs, whereas the ligand binds more strongly to CML WBCs, Correspondingly, FGF-2 is unable to activate mitogen-activated protein kinase kinase (MEK) and its substrate, extracellular signal-regulated kinase (ERK), in B-CLL cells, whereas phosphorylation of both these cell growth-related kinases increases following treatment of CML WBCs, We conclude that B-CLL WBCs secrete FGF-P with no apparent autocrine actions. In contrast, WBCs in CML bind FGF-2 provided by other FGF2-hyperproducing cells and activate the MEK/ERK kinase cascade, possibly to modulate cell growth. |