肺癌qBiomarker体细胞突变PCR芯片 Lung Ca

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Lung Cancer qBiomarker Mutation PCR Array

肺癌qBiomarker体细胞突变PCR芯片

Product	Species	Technology	Cat. No.
Lung Cancer qBiomarker Mutation PCR Array	Human	Somatic Mutation	SMH-023A

The Human Lung Cancer qBiomarker Somatic Mutation PCR Array is a translational research tool that allows rapid, accurate, and comprehensive profiling of the top somatic mutations in human lung cancer samples in the following genes: AKT1, BRAF, CTNNB1/beta-catenin, EGFR, ERBB2, HRAS, KRAS, NRAS, PIK3CA, LKB1/STK11, and P53. These mutations warrant extensive investigation to enhance the understanding of carcinogenesis and identify potential drug targets. Numerous research studies have demonstrated the utility of individual and multiple somatic mutation status information in identifying key signaling transduction disruptions. For example, the mutation status of the EGFR and KRAS genes can predict the physiological response to certain drugs targeting these molecules. The Human Lung Cancer qBiomarker Somatic Mutation PCR Array, with its comprehensive content coverage, is designed for the study of mutations in the context of lung cancer and has the potential for discovery and verification of drug target biomarkers for this cancer type and other cancer types in which these mutations have been identified. This array includes 83 DNA sequence mutation assays designed to detect the most frequent, functionally verified, and biologically significant mutations in human lung cancer. These mutations were chosen from curated, comprehensive somatic mutation databases and peer-reviewed scientific literature, and represent the most frequently recurring somatic mutations compiled from over 13000 lung cancer samples. The simplicity of the product format and operating procedure allows routine somatic mutation profiling in any research laboratory with access to real-time PCR instruments.

肺癌qBiomarker体细胞突变PCR芯片是一个翻译研究工具,用于快速,准确,全面剖析人类肺癌体细胞突变相关基因: AKT1, BRAF, CTNNB1/beta-catenin, EGFR, ERBB2, HRAS, KRAS, NRAS, PIK3CA, LKB1/STK11, and P53.这些突变保证广泛的研究,以提高致癌作用的理解和鉴定潜在的药物靶点。已有许多研究通过单个和多个体细胞突变状态信息鉴定关键信号转导中断。例如,EGFR和KRAS基因的突变状态可以预测某些药物针对这些分子的生理反应。人类肺癌qBiomarker体细胞突变PCR芯片以其全面的内容覆盖范围，用于研究肺癌的环境突变且有潜力用于发现靶向药物的生物标记和验证这些癌症和其他这些突变已确定的癌症。这个芯片包含83个DNA突变序列用于检测最频繁的，功能性验证，在人类肺癌具有生物学意义的突变。这些突变的选择根据全面的体细胞突变数据库和科学文献，来自1300多个肺癌样本发生最频繁重复编译的体细胞突变。简单的产品模式和操作程序让任何一个具备实时定量PCR仪的实验室都可进行常规的体细胞突变分析。AKT1: 1 Assay
The mutation assay detects the best known AKT1 mutation, c.49G>A, p.E17K. This is a PH domain mutation that results in constitutive targeting of AKT1 to plasma membrane.
BRAF: 4 Assays
There are two major classes of BRAF mutations. One class leads to increased BRAF kinase activity, such as the p. V600E mutation. The other class leads to impaired kinase activity, such as the p.G469A mutation.
CTNNB1: 2 Assays
The most frequently detected CTNNB1/beta-catenin mutations result in abnormal signaling in the WNT signaling pathway. The mutated codons are mainly several serine/threonine residues targeted for phosphorylation by GSK-3beta.
EGFR: 22 Assays
The most frequently identified EGFR mutations include P-loop and activation loop point mutations, kinase domain deletions, and insertion mutations.
ERBB2: 2 Assays
The most frequently identified ERBB2 activating mutations cluster in the ERBB2 kinase domain region.
HRAS: 1 Assay
The most important HRAS mutation in lung cancer occurs at codon 61.
KRAS: 13 Assays
The mutation assays include the most frequently occurring mutations in KRAS codons 12, 13, and 61. Mutations at these positions result in reduced intrinsic GTPase activity and/or cause KRAS to become unresponsive to RasGAP.
NRAS: 1 Assay
The most important NRAS mutation in lung cancer occurs at codon 61.
PIK3CA: 2 Assays
The most frequently occurring PIK3CA mutations mainly belong to two classes: gain-of-function kinase domain activating mutations and helical domain mutations that mimic activation by growth factors.
STK11: 2 Assays
The most commonly detected STK11/LKB1 inactivation mutations are mainly due to truncation or point mutations.
TP53: 33 Assays
The most frequently detected somatic mutations in TP53 are largely composed of DNA-binding domain mutations which disrupt either DNA binding or protein structure.