Egfr Mutant Lung
Egfr Mutant Lung - Related Videos
08:52
Profiling Sensitivity to Targeted Therapies in EGFR-Mutant NSCLC Patient-Derived Organoids
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Cited by 7 •
2021
This protocol describes a standardized evaluation of drug sensitivities to targeted signaling inhibitors in NSCLC patient-derived organoid models.
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 5 •
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.
05:17
Detection of Targetable Alterations in Non-small Cell Lung Cancer using Next-generation Sequencing
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2025
This protocol describes an automated, ISO15189-accredited next-generation sequencing workflow for detecting targetable genomic alterations in non-small cell lung cancer (NSCLC) formalin-fixed paraffin-embedded tissues.
08:12
Identification of EGFR and RAS Inhibitors using Caenorhabditis elegans
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Cited by 4 •
2020
The genetically tractable nematode Caenorhabditis elegans can be used as a simple and inexpensive model for drug discovery. Described here is a protocol to identify anticancer therapeutics that inhibit the downstream signaling of RAS and EGFR proteins.
07:06
A Simple Method of Mouse Lung Intubation
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Cited by 50 •
2013
This paper describes a striaghforward and efficient method of intubating mice for pulmonary function measurements or pulmonary instillation, that allows the mice to recover and be studied at later times. The procedure involves an inexpensive fiberoptic light source that directly illuminates the trachea.
FAQs
Activating EGFR changes can keep the receptor tyrosine kinase signaling system switched on. Persistent signaling sends growth- and survival-supporting messages to tumor cells, helping explain why the altered receptor is biologically important in this cancer. This mechanism gives researchers a basis for studying tumor behavior and identifying treatments designed to counter its effects.
Molecular testing links a patient's tumor biology to treatment selection by determining whether an actionable EGFR variant is present. Testing may use tumor tissue or other clinical samples, allowing clinicians and investigators to obtain the molecular information needed to consider targeted therapy. Its value lies in matching a specific finding with a potentially relevant treatment approach.
An initial treatment response does not end the scientific question. Studying acquired resistance examines why a cancer that previously responded may no longer remain sensitive to a targeted approach. This work connects observed treatment outcomes with changing disease biology and can inform development of new therapies and strategies for advanced disease.
Tumor tissue and other clinical samples can provide material for molecular testing. The purpose is to identify EGFR variants that may be actionable, rather than relying only on the cancer's clinical description. Results contribute to diagnosis and treatment selection by supplying molecular evidence about whether a targeted therapy should be considered.
It is especially relevant when molecular testing identifies an actionable EGFR variant. In that setting, the result can help match the patient with a targeted therapy rather than treating the molecular finding as descriptive information only. This approach shows how laboratory characterization can directly inform clinical decisions in medicine.
Research combines molecular testing, treatment-response observations, and analysis of acquired resistance to improve understanding of advanced disease. These investigations can reveal whether current targeted approaches remain effective and guide the search for new therapies. The broader medical value is an evidence base for adapting treatment strategies as disease behavior and therapeutic needs change.