| Quick Inquiry |
|
EML4-ALK Fusion Expression Plasmid Vectors
RGBiotech offers EML4-ALK fusion expression plasmid vectors to assist researchers to study the resistance mechanisms to tyrosine kinase inhibitors (TKIs), and to develop new treatment strategies to improve outcomes for patients with non-small cell lung cancer (NSCLC).
Product List for EML4-ALK Fusion Expression Plasmid Vectors
EML4
Echinoderm microtubule-associated protein (EMAP) like 4, is a protein that in humans is encoded by the EML4 gene (Gene ID: 27436). Alternative splicing of EML4 gene results in three isoforms with different sizes, which are isoform a/b/c. EML4 protein is involved in cancers when fused with the anaplastic lymphoma kinase (ALK), and may be involved in microtubule formation. Abnormal fusion of parts of EML4 gene with portions of the ALK gene, generating EML4-ALK fusion transcripts, which is associated with non-small cell lung cancer (NSCLC).
ALK
ALK receptor tyrosine kinase, also known as anaplastic lymphoma kinase (ALK), ALK tyrosine kinase receptor, or CD246 (cluster of differentiation 246), is an enzyme that in humans is encoded by the ALK gene (Gene ID: 238). Alternative splicing of ALK gene results in two isoforms with different sizes, which are long isoform 1 and short isoform 2. ALK is a single transmembrane protein which has an extracellular ligand-binding domain, a transmembrane domain and an intracellular tyrosine kinase domain (TKD). ALK protein plays an important role in the development of the brain and exerts its effects on specific neurons in the nervous system. ALK is associated with many cancers, such as anaplastic large cell lymphomas, neuroblastoma, and non-small cell lung cancer (NSCLC), through rearrangements, mutations and amplification. ALK fusion genes involved in tumourigenesis include ALK/EML4, ALK/RANBP2, ALK/ATIC, ALK/TFG, ALK/NPM1, ALK/SQSTM1, ALK/KIF5B, ALK/CLTC, ALK/TPM4, ALK/MSN.
EML4-ALK
The EML4-ALK fusion gene was first discovered in patients suffering non-small cell lung cancer (NSCLC) in recent years. It is a fusion between the EML4 (echinoderm microtubule-associated protein-like) on chromosome 2 and the ALK (anaplastic lymphoma kinase) gene on chromosome 2 as well. This fusion results in the production of a hybrid EML4-ALK protein that has oncogenic properties by acting as a constitutively active tyrosine kinase, leading to the activation of downstream signaling pathways, uncontrolled cell proliferation, and promote cancer development. There are different EML4‐ALK variants with different sizes and properties resulted from different breakpoints of EML4 and ALK. The breakpoint in the ALK gene lies most frequently at exon 20, with rare examples at exon 19, while the breakpoint in the EML4 gene is variable including different exons (e.g., 2, 6, 13, 14, 15, 18, and 20). The formation of the EML4-ALK fusion oncogene, is primarily associated with non-small cell lung cancer (NSCLC).
TKIs
Treatment of cancer patients carrying EML4-ALK fusion gene involves using ALK inhibitors which are a class of targeted drugs. Some ALK inhibitors include Crizotinib, Ceritinib, Alectinib, Brigatinib, Lorlatinib, Entrectinib. ALK inhibitors can be effective in most cases, but there are also some patients don’t respond well and can develop resistance via point‐mutations within the kinase domain of the ALK region over time, for example G1202R, reducing inhibitor effectiveness.
|
