Multitargeted receptor tyrosine kinase inhibition: An antiangiogenic strategy in non-small cell lung cancer

2011 ◽  
Vol 37 (8) ◽  
pp. 611-617 ◽  
Author(s):  
Mark A. Socinski
Keyword(s):  
Lung Cancer ◽  
Tyrosine Kinase ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Receptor Tyrosine Kinase ◽  
Small Cell ◽  
Small Cell Lung ◽  
Kinase Inhibition ◽  
Tyrosine Kinase Inhibition

scholarly journals Functional Analyses of Mutations in Receptor Tyrosine Kinase Genes in Non–Small Cell Lung Cancer: Double-Edged Sword of DDR2

2016 ◽  
Vol 22 (14) ◽  
pp. 3663-3671 ◽  
Author(s):  
Masato Terashima ◽  
Yosuke Togashi ◽  
Katsuaki Sato ◽  
Hiroshi Mizuuchi ◽  
Kazuko Sakai ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tyrosine Kinase ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Receptor Tyrosine Kinase ◽  
Small Cell ◽  
Small Cell Lung ◽  
Functional Analyses

scholarly journals Receptor Tyrosine Kinase and p16/CDKN2 Expression in a Case of Tripe Palms Associated with Non-Small-Cell Lung Cancer

Dermatology ◽  
1999 ◽  
Vol 199 (4) ◽  
pp. 290-295 ◽  
Author(s):  
G. Krähn ◽  
K.M. Greulich ◽  
G. Bezold ◽  
C. Dieterle ◽  
H. Wolff ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Tyrosine Kinase ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Receptor Tyrosine Kinase ◽  
Small Cell ◽  
Small Cell Lung

Activation of HGF/c-Met pathway contributes to the reactive oxygen species generation and motility of small cell lung cancer cells

2007 ◽  
Vol 292 (6) ◽  
pp. L1488-L1494 ◽  
Author(s):  
Ramasamy Jagadeeswaran ◽  
Sujatha Jagadeeswaran ◽  
Vytas P. Bindokas ◽  
Ravi Salgia
Keyword(s):  
Lung Cancer ◽  
Reactive Oxygen Species ◽  
Tyrosine Kinase ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Receptor Tyrosine Kinase ◽  
Small Cell ◽  
Oxygen Species ◽  
Small Cell Lung ◽  
Met Receptor Tyrosine Kinase

Small cell lung cancer (SCLC) is a difficult disease to treat and sometimes has overexpression or mutation of c-Met receptor tyrosine kinase. The effects of c-Met/hepatocyte growth factor (c-Met/HGF, ligand for c-Met) on activation of reactive oxygen species (ROS) was determined. HGF stimulation of c-Met-overexpressing H69 SCLC cells (40 ng/ml, 15 min) resulted in an increase of ROS, measured with fluorescent probe 2′-7′-dichlorofluorescein diacetate (DCFH-DA) or dihydroethidine (DHE) but not in c-Met-null H446 cells. ROS was increased in juxtamembrane (JM)-mutated variants (R988C and T1010I) of c-Met compared with wild-type c-Met-expressing cells. ROS was significantly inhibited by preincubation of SCLC cells with pyrrolidine dithiocarbamate (PDTC, 100 μM) and/or SU11274 (small molecule c-Met tyrosine kinase inhibitor, 2 μM) for 3 h. PDTC and SU11274 also abrogated the HGF proliferative signal and cell motility in a cooperative fashion. H2O2 treatment of SCLC cells (over 15 min) led to phosphorylation of c-Met receptor tyrosine kinase and further upregulated downstream phosphorylation of phospho-AKT, ERK1/2, and paxillin in a dose-dependent manner (125 μM to 500 μM). c-Met is an important target in lung cancer, and the pathways responsible for ROS generation together may provide novel therapeutic intervention.

scholarly journals RADI-19. The Incidence of New Brain Metastases in Patients with Non-Small Cell Lung Cancer Following Discontinuation of Systemic Therapy

2021 ◽  
Vol 3 (Supplement_3) ◽  
pp. iii22-iii22
Author(s):  
Dennis London ◽  
Dev Patel ◽  
Bernadine Donahue ◽  
Ralph Navarro ◽  
Jason Gurewitz ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Brain Metastases ◽  
Tyrosine Kinase ◽  
Small Cell Lung Cancer ◽  
Cell Lung Cancer ◽  
Receptor Tyrosine Kinase ◽  
Systemic Therapy ◽  
Cox Regression ◽  
Small Cell ◽  
Small Cell Lung

Abstract Purpose Patients with non-small cell lung cancer (NSCLC) metastatic to the brain increasingly are living longer due to improvements in systemic therapy and local modalities. The risk of new brain metastases when these patients stop systemic therapy is unknown. Recognizing patterns of new tumor occurrence is necessary to determine the frequency of follow-up and the need for further treatment. Methods We included patients in a prospective registry who had non-small cell lung cancer (NSCLC) brain metastases, discontinued systemic therapy for at least 90 days, and underwent active surveillance. 63 patients with 73 off-periods were studied. The risk factors for the development of new tumors were determined using Cox regression and multi-state Markov modeling. Results The median time to new brain metastases off systemic therapy was 16.0 months. The probability of developing an additional new tumor at 6, 12, and 18 months was 26%, 40%, and 53%, respectively. There were no additional new tumors 22 months after stopping therapy. Patients who discontinued therapy due to intolerance or progression of the disease and those with mutations in RAS or receptor tyrosine kinase pathways (e.g. KRAS, EGFR) were more likely to develop new tumors (HR: 2.21, 95% CI: 1.25–3.91, p=6.3 x 10–3; HR: 2.03, 95% CI: 1.09–3.77, p=0.026, respectively). Conclusion The rate of new brain metastases from NSCLC in patients off systemic therapy decreases over time and is uncommon 2 years after cessation of cancer therapy. Patients who stop therapy due to toxicity or who have RAS or receptor tyrosine kinase pathway mutations have a higher rate of new metastases and should be followed more closely.

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