نتایج جستجو برای: kit

تعداد نتایج: 29127  

Journal: :The Journal of Experimental Medicine 1998
Gorazd Krosl Gang He Martin Lefrancois Frédéric Charron Paul-Henri Roméo Paul Jolicoeur Ilan R. Kirsch Mona Nemer Trang Hoang

In normal hemopoietic cells that are dependent on specific growth factors for cell survival, the expression of the basic helix-loop-helix transcription factor SCL/Tal1 correlates with that of c-Kit, the receptor for Steel factor (SF) or stem cell factor. To address the possibility that SCL may function upstream of c-kit, we sought to modulate endogenous SCL function in the CD34(+) hemopoietic c...

Journal: :Clinical chemistry 1983
L F Blight G H White

We have evaluated two commercially available 125I radioimmunoassay kits (Diagnostic Products Corp., DPC; and Radioassay Systems Laboratories, RSL) for measurement of serum or plasma progesterone, to determine their suitability for use in in vitro fertilization programs. Both kits were suitably rapid for program requirements. Results by both were linear with concentration up to 60 nmol/L, and bo...

2017
Katarina Lyberg Hani Abdulkadir Ali Jennine Grootens Matilda Kjellander Malin Tirfing Michel Arock Hans Hägglund Gunnar Nilsson Johanna Ungerstedt

Systemic mastocytosis (SM) is a clonal bone marrow disorder, where therapeutical options are limited. Over 90% of the patients carry the D816V point mutation in the KIT receptor that renders this receptor constitutively active. We assessed the sensitivity of primary mast cells (MC) and mast cell lines HMC1.2 (D816V mutated), ROSA (KIT WT) and ROSA (KIT D816V) cells to histone deacetylase inhibi...

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 2008
Séverine Tabone-Eglinger Frédéric Subra Hiba El Sayadi Laurent Alberti Eric Tabone Jean-Philippe Michot Nathalie Théou-Anton Antoinette Lemoine Jean-Yves Blay Jean-François Emile

PURPOSE Gastrointestinal stromal tumors (GIST) are frequently associated with gain-of-function mutations of KIT, which can be inhibited by imatinib both in vitro and in vivo. The survival of patients with GIST, following imatinib therapy, has been correlated with the nature of mutations but not with KIT expression. EXPERIMENTAL DESIGN Subcellular localization, activation, and trafficking of t...

Journal: :Clinical cancer research : an official journal of the American Association for Cancer Research 2003
Nancy K Pryer Leslie B Lee Regina Zadovaskaya Xiaoming Yu Juthamas Sukbuntherng Julie M Cherrington Cheryl A London

PURPOSE The purpose of this study was to evaluate the effect of the receptor tyrosine kinase inhibitor SU11654 on the activity of its molecular target KIT in canine mast cell tumors (MCT) and correlate target inhibition with mutational status of the c-kit juxtamembrane domain and SU11654 plasma concentration. EXPERIMENTAL DESIGN Tumor biopsies were obtained from dogs with advanced MCTs before...

Journal: :Journal of clinical oncology : official journal of the American Society of Clinical Oncology 2003
Michael C Heinrich Christopher L Corless George D Demetri Charles D Blanke Margaret von Mehren Heikki Joensuu Laura S McGreevey Chang-Jie Chen Annick D Van den Abbeele Brian J Druker Beate Kiese Burton Eisenberg Peter J Roberts Samuel Singer Christopher D M Fletcher Sandra Silberman Sasa Dimitrijevic Jonathan A Fletcher

PURPOSE Most gastrointestinal stromal tumors (GISTs) express constitutively activated mutant isoforms of KIT or kinase platelet-derived growth factor receptor alpha (PDGFRA) that are potential therapeutic targets for imatinib mesylate. The relationship between mutations in these kinases and clinical response to imatinib was examined in a group of patients with advanced GIST. PATIENTS AND METH...

Journal: :Blood 1996
T Tsujimura M Morimoto K Hashimoto Y Moriyama H Kitayama Y Matsuzawa Y Kitamura Y Kanakura

A peculiar point mutation results in constitutive activation of c-kit receptor tyrosine kinase (KIT) in three different tumor mast cell lines; ie, the HMC-1, P-815, and RBL-2H3. Because constitutive activation of KIT was also observed in the FMA3 mouse mastocytoma cell line, we investigated the molecular mechanism. Sequencing of the whole coding region of the c-kit showed that the point mutatio...

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