Egfr Mutated Cells
Egfr Mutated Cells - Related Videos
15:05
Deciphering the Structural Effects of Activating EGFR Somatic Mutations with Molecular Dynamics Simulation
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Cited by 7 •
2020
The objective of this protocol is to use molecular dynamics simulations to examine the dynamic structural changes that occur due to activating mutations of the EGFR kinase protein.
07:53
Quantification of Colonic Stem Cell Mutations
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Cited by 1 •
2015
We report significant improvements for the reproducible measurement of somatic colonic stem cell mutations after exposure of mice to potential DNA damaging agents.
09:38
Establishing Dual Resistance to EGFR-TKI and MET-TKI in Lung Adenocarcinoma Cells In Vitro with a 2-step Dose-escalation Procedure
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Cited by 4 •
2017
An in vitro method for establishing dual resistance to an EGFR-TKI and a MET-TKI in cancer cells is described. This method is useful for developing treatments for patients with EGFR-mutations, who exhibit disease progression despite EGFR-TKI treatment with MET-amplification. It can also be modified for inhibitors targeting other molecules.
00:36
Viral Mutations
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2019
A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material for adaptive...
13:34
A Combined 3D Tissue Engineered In Vitro/In Silico Lung Tumor Model for Predicting Drug Effectiveness in Specific Mutational Backgrounds
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Cited by 29 •
2016
We present a three-dimensional (3D) lung cancer model based on a biological collagen scaffold to study sensitivity towards non-small-cell-lung-cancer-(NSCLC)-targeted therapies. We demonstrate different read-out techniques to determine the proliferation index, apoptosis and epithelial-mesenchymal transition (EMT) status. Collected data are integrated into an in silico model for prediction of drug sensitivity.
FAQs
Mutations can shift EGFR signaling from ligand-regulated activation toward persistent tyrosine-kinase activity. This change can continuously engage the RAS-RAF-MEK-ERK and PI3K-AKT pathways, linking the altered receptor to signals that influence proliferation and survival. Tracking these downstream pathways helps bioengineers connect a specific receptor alteration with measurable cellular responses during model development and inhibitor testing.
Normal ligand control provides a reference for judging whether receptor signaling remains dependent on its usual activating context. Comparing that baseline with cells carrying EGFR alterations can reveal whether downstream RAS-RAF-MEK-ERK or PI3K-AKT activity is associated with altered receptor regulation. This comparison supports clearer interpretation of growth, survival, and inhibitor-response measurements in engineered models.
Growth and survival outcomes provide practical readouts of altered EGFR signaling in engineered cells. By observing these outcomes alongside activity in downstream RAS-RAF-MEK-ERK and PI3K-AKT pathways, researchers can examine how receptor alterations affect cellular behavior. Such measurements help connect molecular signaling events to phenotypes relevant to cancer models and bioengineering experiments.
An engineered cell model provides a system in which receptor alterations and their consequences can be examined together. Researchers can use these cells to connect EGFR status with signaling, growth, survival, and responses to mutation-specific inhibitors. This role makes the models useful for studying abnormal receptor activity while supporting bioengineering efforts focused on disease modeling and drug evaluation.
Testing mutation-specific inhibitors can show whether an altered EGFR state is associated with a measurable treatment response. In the same experimental framework, researchers can examine how that response changes as resistance develops. These results help distinguish initial drug sensitivity from reduced effectiveness and can guide the design of more precise therapeutic strategies for cancers driven by abnormal EGFR activity.
Beyond inhibitor testing, engineered EGFR-mutated cells support drug screening and disease modeling. They can also help investigate treatment resistance and inform more precise diagnostic and therapeutic strategies for cancers driven by abnormal EGFR activity. In bioengineering, these applications connect molecular signaling changes with practical research goals, including evaluating candidate treatments and modeling disease-associated cellular behavior.