Effects of imatinib vary with the types of KIT-mutation in gastrointestinal stromal tumor cell lines

2005 ◽  
Author(s):  
Kazuhiro Noma ◽  
Yoshio Naomoto ◽  
Mehmet Gunduz ◽  
Junji Matsuoka ◽  
Tomoki Yamatsuji ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Gastrointestinal Stromal Tumor ◽  
Cell Lines ◽  
Stromal Tumor ◽  
Tumor Cell Lines ◽  
Kit Mutation

scholarly journals Potentiation of imatinib by cilostazol in sensitive and resistant gastrointestinal stromal tumor cell lines involves YAP inhibition

Oncotarget ◽  
2019 ◽  
Vol 10 (19) ◽  
pp. 1798-1811 ◽  
Author(s):  
Pierre Vandenberghe ◽  
Marine Delvaux ◽  
Perrine Hagué ◽  
Christophe Erneux ◽  
Jean-Marie Vanderwinden
Keyword(s):  
Tumor Cell ◽  
Gastrointestinal Stromal Tumor ◽  
Cell Lines ◽  
Stromal Tumor ◽  
Tumor Cell Lines

Targeting Gastrointestinal Stromal Tumor with 68Ga-Labeled Peptides: An In Vitro Study on Gastrointestinal Stromal Tumor-Cell Lines

2016 ◽  
Vol 31 (8) ◽  
pp. 302-310 ◽  
Author(s):  
Achim Paulmichl ◽  
Dominik Summer ◽  
Claudia Manzl ◽  
Christine Rangger ◽  
Francesca Orlandi ◽  
...  
Keyword(s):  
Tumor Cell ◽  
Gastrointestinal Stromal Tumor ◽  
Cell Lines ◽  
In Vitro Study ◽  
Vitro Study ◽  
Stromal Tumor ◽  
Tumor Cell Lines

Cellular Uptake of the Tyrosine Kinase Inhibitors Imatinib and AMN107 in Gastrointestinal Stromal Tumor Cell Lines

Pharmacology ◽  
2006 ◽  
Vol 77 (1) ◽  
pp. 11-16 ◽  
Author(s):  
Hans Prenen ◽  
Gunther Guetens ◽  
Gert de Boeck ◽  
Maria Debiec-Rychter ◽  
Paul Manley ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Tumor Cell ◽  
Gastrointestinal Stromal Tumor ◽  
Tyrosine Kinase Inhibitors ◽  
Cell Lines ◽  
Cellular Uptake ◽  
Kinase Inhibitors ◽  
Stromal Tumor ◽  
Tumor Cell Lines

scholarly journals Combined Inhibition of AKT and KIT Restores Expression of Programmed Cell Death 4 (PDCD4) in Gastrointestinal Stromal Tumor

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3699
Author(s):  
Marya Kozinova ◽  
Shalina Joshi ◽  
Shuai Ye ◽  
Martin G. Belinsky ◽  
Dinara Sharipova ◽  
...  
Keyword(s):  
Cell Death ◽  
Gastrointestinal Stromal Tumor ◽  
Cell Lines ◽  
Synergistic Effects ◽  
Single Agent ◽  
Xenograft Model ◽  
Stromal Tumor ◽  
In Vivo Studies ◽  
Preclinical Model ◽  
Kit Mutation

The majority of gastrointestinal stromal tumor (GIST) patients develop resistance to the first-line KIT inhibitor, imatinib mesylate (IM), through acquisition of secondary mutations in KIT or bypass signaling pathway activation. In addition to KIT, AKT is a relevant target for inhibition, since the PI3K/AKT pathway is crucial for IM-resistant GIST survival. We evaluated the activity of a novel pan-AKT inhibitor, MK-4440 (formerly ARQ 751), as monotherapy and in combination with IM in GIST cell lines and preclinical models with varying IM sensitivities. Dual inhibition of KIT and AKT demonstrated synergistic effects in IM-sensitive and -resistant GIST cell lines. Proteomic analyses revealed upregulation of the tumor suppressor, PDCD4, in combination treated cells. Enhanced PDCD4 expression correlated to increased cell death. In vivo studies revealed superior efficacy of MK-4440/IM combination in an IM-sensitive preclinical model of GIST compared with either single agent. The combination demonstrated limited efficacy in two IM-resistant models, including a GIST patient-derived xenograft model possessing an exon 9 KIT mutation. These studies provide strong rationale for further use of AKT inhibition in combination with IM in primary GIST; however, alternative agents will need to be tested in combination with AKT inhibition in the resistant setting.

Interaction of Human Tumor Cells with Human Platelets and the Coagulation System

1983 ◽  
Vol 50 (03) ◽  
pp. 726-730 ◽  
Author(s):  
Hamid Al-Mondhiry ◽  
Virginia McGarvey ◽  
Kim Leitzel
Keyword(s):  
Tumor Cell ◽  
Tumor Cells ◽  
Cell Lines ◽  
Human Tumor ◽  
Human Platelets ◽  
Factor Vii ◽  
Coagulation System ◽  
Breast Adenocarcinoma ◽  
Activate Factor ◽  
Tumor Cell Lines

SummaryThis paper reports studies on the interaction between human platelets, the plasma coagulation system, and two human tumor cell lines grown in tissue culture: Melanoma and breast adenocarcinoma. The interaction was monitored through the use of 125I- labelled fibrinogen, which measures both thrombin activity generated by cell-plasma interaction and fibrin/fibrinogen binding to platelets and tumor cells. Each tumor cell line activates both the platelets and the coagulation system simultaneously resulting in the generation of thrombin or thrombin-like activity. The melanoma cells activate the coagulation system through “the extrinsic pathway” with a tissue factor-like effect on factor VII, but the breast tumor seems to activate factor X directly. Both tumor cell lines activate platelets to “make available” a platelet- derived procoagulant material necessary for the conversion of prothrombin to thrombin. The tumor-derived procoagulant activity and the platelet aggregating potential of cells do not seem to be inter-related, and they are not specific to malignant cells.

Differential Increases in Glutathione S-Transferase Activities in a Range of Multidrug-Resistant Human Tumor Cell Lines

1989 ◽  
Vol 1 (6) ◽  
pp. 359-365 ◽  
Author(s):  
Richard D. H. Whelan ◽  
Louise K. Hosking ◽  
Alan J. Townsend ◽  
Kenneth H. Cowan ◽  
Bridget T. Hill
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Human Tumor ◽  
Multidrug Resistant ◽  
Tumor Cell Lines ◽  
Glutathione S Transferase ◽  
Human Tumor Cell ◽  
Human Tumor Cell Lines

Cytotoxic Activities of Red Algae Collected from Jeju Island Against Four Tumor Cell Lines

2006 ◽  
Vol 11 (3) ◽  
pp. 177-183 ◽  
Author(s):  
Kil-Nam Kim ◽  
Ki-Wan Lee ◽  
Choon-Bok Song ◽  
Chang-Bum Ahn ◽  
You-Jin Jeon
Keyword(s):  
Tumor Cell ◽  
Cell Lines ◽  
Red Algae ◽  
Jeju Island ◽  
Cytotoxic Activities ◽  
Tumor Cell Lines
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