scholarly journals Numerical Computation of Signal Stimulation from Ligand-EGFR Binding During Invadopodia Formation

MATEMATIKA ◽  
2019 ◽  
Vol 35 (4) ◽  
pp. 139-148
Author(s):  
Noorehan Yaacob ◽  
Nur Azura Noor Azhuan ◽  
Sharidan Shafie ◽  
Mohd Ariff Admon
Keyword(s):  
Cell Membrane ◽  
Dirichlet Boundary ◽  
Boundary Surface ◽  
Growth Factor Receptor ◽  
Extrapolation Methods ◽  
Subcellular Membrane ◽  
Level Set Function ◽  
Epidermal Growth ◽  
Set Function ◽  
Invadopodia Formation

Invadopodia are finger-like protrusions located at subcellular membrane which can lead to cancer cell invasion. The formation of invadopodia involves several steps such as actin polymerizations, degradation of extracellular matrix which produce ligand and signal stimulation that is occurred from the binding of ligand with epidermal growth factor receptor. In this paper, a mathematical model of signal transduction is investigated. Both signal and ligand are represented by Laplace equation with Dirichlet boundary condition for each region. The cell membrane is treated as free boundary surface to separate any activity that occurred in intracellular and extracellular regions. The motion of the interface is taken as gradient of  nterior signal and the cell membrane is set as zero level set function. The problem is solved numerically using finite difference scheme of upwind, interpolation and extrapolation methods. The results showed that the formation of invadopodia is formed when protrusions exist on the cell membrane.

scholarly journals Epidermal growth factor receptor overexpression in resected pancreatic cancer.

2011 ◽  
Vol 29 (4_suppl) ◽  
pp. 317-317
Author(s):  
A. Mahipal ◽  
M. J. McDonald ◽  
A. Witkiewicz ◽  
B. I. Carr
Keyword(s):  
Pancreatic Cancer ◽  
Epidermal Growth Factor Receptor ◽  
Lymph Node ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Membrane ◽  
Growth Factor Receptor ◽  
Membrane Staining ◽  
Egfr Expression ◽  
Epidermal Growth

317 Background: The effect of overexpression of epidermal growth factor receptor (EGFR) in pancreatic carcinoma is uncertain. In this study, we examine the association between EGFR overexpression (membrane and cytoplasmic) and histopathologic features and clinical outcomes in patients post resection. Methods: Seventy three patients underwent curative resection for pancreatic cancer from 4/08 to 4/10. Tumor EGFR expression was determined immunohistochemically using EGFR pharmDxTM kit. Cytoplasmic overexpression was considered positive if EGFR expression was seen in the cytoplasm in ≥10% of cells. Cell membrane staining scores were assigned: 0 (no membrane staining), 1+ (incomplete membrane staining in ≥ 10% of cells, 2+ (complete weak/moderate membrane staining in ≥ 10% of cells) and 3+ (complete heavy staining in ≥ 10% of cells). A score of 2+ and 3+ were considered as membrane overexpression. Comparisons between EGFR overexpression and clinicopathologic features were assessed by chi-square test with p-value < 0.05 as statistically significant. Proportional hazard regression was used to estimate progression free survival and overall survival. Results: Out of 73 patients, 43 (59%) and 50 (68%) patients had membrane and cytoplasmic EGFR overexpression respectively. AJCC stages were: stage I: 8, stage II: 63, stage III: 1 and stage IV: 1 patient. There was statistically significant correlation between cell membrane EGFR overexpression and lymph node positivity (p=0.04). Membrane EGFR overexpression was not significantly associated with local invasion, margin positivity, vascular invasion, perineural invasion, histologic grade or stage. Cytoplasmic EFGR overexpression was significantly associated with margin positivity (p=0.01) only. The hazard ratios (95% CI) for PFS and OS in patients with membrane EGFR overexpression was 1.37 (0.72-2.60) and 1.27 (0.62-2.61) respectively. The corresponding values for patients with cytoplasmic overexpression were 1.65 (0.80-3.37) and 1.25 (0.58-2.71) respectively. Conclusions: Membrane EGFR overexpression was associated with lymph node status and cytoplasmic EFGR overexpression with margin positivity. There was no association of EFGR expression and clinical outcomes. No significant financial relationships to disclose.

Bio-engineered cell membrane nanovesicles as precision theranostics for perihilar cholangiocarcinoma

2020 ◽  
Vol 8 (6) ◽  
pp. 1575-1579 ◽  
Author(s):  
Xiaojie Zhang ◽  
Yang Zhang ◽  
Yunming Zhang ◽  
Peng Lv ◽  
Pengfei Zhang ◽  
...  
Keyword(s):  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Membrane ◽  
Indocyanine Green ◽  
Growth Factor Receptor ◽  
Perihilar Cholangiocarcinoma ◽  
Human Epidermal Growth Factor ◽  
Epidermal Growth

We engineered a human epidermal growth factor receptor 2 (HER2) affibody to the surface of cell membrane nanovesicles (A-NVs) in a ligand-oriented manner and loaded them with indocyanine green (ICG) as precision theranostics for PHCC treatment.

scholarly journals Triggering of Suicidal Erythrocyte Death by Gefitinib

2017 ◽  
Vol 41 (4) ◽  
pp. 1697-1708 ◽  
Author(s):  
Abdulla Al Mamun Bhuyan ◽  
Teresa Wagner ◽  
Hang Cao ◽  
Florian Lang
Keyword(s):  
Oxidative Stress ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Cell Membrane ◽  
Kinase Inhibitor ◽  
Growth Factor Receptor ◽  
Annexin V ◽  
Forward Scatter ◽  
Epidermal Growth

Background/Aims: The epidermal growth factor receptor-tyrosine kinase inhibitor gefitinib is effective against several malignancies and is mainly utilized in the treatment of epidermal growth factor receptor mutation positive non-small cell lung cancer. The anti-cancer effect of the drug involves stimulation of apoptosis. Side effects of gefitinib include anemia. At least in theory, the development of anemia during gefitinib treatment could result from triggering of eryptosis, the suicidal erythrocyte death characterized by cell shrinkage and by cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signaling potentially stimulating eryptosis include increase of cytosolic Ca2+ activity ([Ca2+]i) and generation of oxidative stress. The present study explored, whether gefitinib stimulates eryptosis and, if so, whether its effect involves Ca2+ entry and/or oxidative stress. Methods: Flow cytometry was employed to quantify cell volume from forward scatter, phosphatidylserine exposure at the cell surface from annexin-V-binding, [Ca2+]i from Fluo3-fluorescence, and reactive oxygen species (ROS) abundance from 2’,7’-dichlorodihydrofluorescein diacetate (DCFDA) dependent fluorescence. Results: A 48 hours exposure of human erythrocytes to gefitinib (≥ 2 µg/ml) significantly decreased forward scatter and significantly increased the percentage of annexin-V-binding cells. Gefitinib did not significantly increase Fluo3-fluorescence but the effect of gefitinib on annexin-V-binding was significantly blunted by removal of extracellular Ca2+. Gefitinib further significantly increased DCFDA fluorescence. Conclusions: Gefitinib triggers erythrocyte shrinkage and phospholipid scrambling of the erythrocyte cell membrane, an effect at least in part dependent on extracellular Ca2+ and paralleled by oxidative stress.

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