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@article{971692,
author = {Krejčí, Pavel and Dvoráková, D. and Krahulcová, E. and Pacherník, Jiří and Mayer, Jiří and Hampl, Aleš and Dvořák, Petr},
article_location = {London : England},
article_number = {2},
doi = {http://dx.doi.org/10.1038/sj.leu.2402012},
keywords = {AUG-INITIATED FORMS; FACTOR BFGF; IMMUNOGLOBULIN DOMAIN;},
language = {eng},
issn = {0887-6924},
journal = {Leukemia},
title = {FGF-2 abnormalities in B cell chronic lymphocytic and chronic myeloid leukemias},
volume = {15},
year = {2001}
}
TY - JOUR
ID - 971692
AU - Krejčí, Pavel - Dvoráková, D. - Krahulcová, E. - Pacherník, Jiří - Mayer, Jiří - Hampl, Aleš - Dvořák, Petr
PY - 2001
TI - FGF-2 abnormalities in B cell chronic lymphocytic and chronic myeloid leukemias
JF - Leukemia
VL - 15
IS - 2
SP - 228-237
EP - 228-237
PB - Nature Publishing Group, Specialist Jour
SN - 08876924
KW - AUG-INITIATED FORMS
KW - FACTOR BFGF
KW - IMMUNOGLOBULIN DOMAIN;
N2 - 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.
ER -
KREJČÍ, Pavel, D. DVORÁKOVÁ, E. KRAHULCOVÁ, Jiří PACHERNÍK, Jiří MAYER, Aleš HAMPL a Petr DVOŘÁK. FGF-2 abnormalities in B cell chronic lymphocytic and chronic myeloid leukemias. \textit{Leukemia}. London : England: Nature Publishing Group, Specialist Jour, 2001, roč.~15, č.~2, s.~228-237. ISSN~0887-6924. Dostupné z: https://dx.doi.org/10.1038/sj.leu.2402012.
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