FGF-2 abnormalities in B cell chronic lymphocytic and chronic myeloid leukemias

Varování

Publikace nespadá pod Lékařskou fakultu, ale pod Přírodovědeckou fakultu. Oficiální stránka publikace je na webu muni.cz.

Autoři	KREJČÍ Pavel DVORÁKOVÁ D. KRAHULCOVÁ E. PACHERNÍK Jiří MAYER Jiří HAMPL Aleš DVOŘÁK Petr
Rok publikování	2001
Druh	Článek v odborném periodiku
Časopis / Zdroj	Leukemia
Fakulta / Pracoviště MU	Přírodovědecká fakulta
Citace
Doi	http://dx.doi.org/10.1038/sj.leu.2402012
Obor	Fyziologie
Klíčová slova	AUG-INITIATED FORMS; FACTOR BFGF; IMMUNOGLOBULIN DOMAIN;
Popis	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.