Egfr-tki Resistance
Egfr-tki Resistance - Related Videos
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.
04:17
Dose Escalation: A Method for Developing Drug Resistance in Cancer Cells
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2023
The video describes the development of drug resistance in cancer cells by exposing cells to escalating doses of a drug after calculating IC50 values of the drug previously with MTT assay. The sample protocol describes the step-by-step process of developing drug-resistant cells.
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.
01:22
Resistivity
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2023
When a voltage is applied to a conductor, an electrical field is generated, and charges in the conductor feel the force due to the electrical field. The current density that results depends on the electrical field and the properties of the material. In some materials, including metals at a given temperature, the current density is approximately proportional to the electrical field. In these cases, the current density can be modeled as: where σ is the electrical conductivity and is represented...
01:19
Resistance
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2023
When a current moves through any conductor, the conductor causes some level of difficulty for the current to flow. The measure of that difficulty is known as the resistance of the material and is represented by R. Every material has its own resistance. In the case of conductors, heat is emitted whenever a current passes through them. Resistance depends on the resistivity of the material. Resistivity is a characteristic of the material used to fabricate electrical components, whereas the...
FAQs
Secondary alterations in EGFR can change the receptor in ways that prevent an inhibitor from binding effectively. As a result, cancer cells may continue receiving growth-related signals even while treatment is present. Detecting these changes helps explain why sensitivity has declined and can support selection of a next-generation inhibitor designed to address the altered target.
Activation of bypass pathways, including MET or AXL signaling, can provide cancer cells with alternative routes for maintaining growth when EGFR is blocked. This mechanism differs from a change in the drug-binding site because resistance arises through reliance on another signaling input. Recognizing bypass activation supports investigation of combination strategies that target more than one pathway.
Resistance may develop through changes below EGFR in the signaling network, allowing growth-related signals to persist despite receptor inhibition. In this situation, the inhibitor can still affect EGFR without fully suppressing the processes that support tumor progression. Studying downstream alterations therefore broadens resistance analysis beyond the receptor itself and may reveal additional therapeutic targets.
Histologic transformation changes the biological characteristics of the tumor so that continued growth becomes possible despite EGFR-TKI treatment. This mechanism is distinct from a secondary receptor alteration or bypass signaling because it involves a change in tumor form and behavior. Identifying transformation helps interpret disease progression and prevents resistance analysis from focusing only on molecular alterations.
Investigation can combine molecular profiling with repeat analysis of tumor tissue or a liquid-biopsy sample. These approaches can be used to look for secondary EGFR alterations, bypass-pathway activation, downstream signaling changes, or evidence consistent with histologic transformation. The resulting profile helps connect progression with a specific resistance mechanism and informs decisions about subsequent treatment.
Resistance findings can guide treatment toward next-generation inhibitors or combination strategies, depending on the mechanism identified. This makes molecular information clinically relevant rather than merely descriptive: it helps refine treatment selection, clarify why progression occurred, and support development of approaches intended to delay or overcome resistance. The same analyses also reveal recurring patterns of progression across cancer research studies.