The Lung Cancer RTK Antibody Sampler Kit provides an economical means of detecting receptor tyrosine kinases (RTKs) associated with lung cancer. The kit includes enough antibodies to perform two western blot experiments with each primary antibody.
Specificity / Sensitivity
Each antibody in the Lung Cancer RTK Antibody Sampler Kit detects endogenous levels of its target protein. FGF Receptor 1 (D8E4) XP® Rabbit mAb may slightly cross-react with overexpressed FGF receptor family members. IHC staining for ROS1 (D4D6®) Rabbit mAb may be observed in ROS1 rearranged lung carcinomas, macrophages/giant cells, reactive type II pneumocyte hyperplasia, and the epithelium in areas of bronchiolar metaplasia. Staining of unknown specificity has been observed in cholangiocarcinoma, hepatocellular carcinoma, and kidney tissues. HER2/ErbB2 (D8F12) XP® Rabbit mAb may cross-react slightly with other overexpressed RTKs. EGF Receptor (D38B1) XP® Rabbit mAb does not cross-react with other proteins of the ErbB family. Species cross-reactivity for IHC-P, IHC-BOND, and IF-IC is human only. EGFR (L858R Mutant Specific) (43B2) Rabbit mAb may cross-react with wild-type EGFR and other HER family members when highly overexpressed. Careful titration of this antibody may be required to obtain optimal specificity.
Source / Purification
Monoclonal antibodies are produced by immunizing animals with synthetic peptides corresponding to residues surrounding E746-A750del and L865 mutant sequences of human EGFR, Pro320 of human Ret protein, and residues near the carboxy terminus of human Met protein, or recombinant proteins specific to the carboxy terminus of human FGF receptor 1, human ALK, human ROS1, the amino terminus of human HER2/ErbB2, and the cytoplasmic domain of human EGF receptor.
Lung cancer is the leading cause of cancer-related mortality worldwide (1). It is generally divided into two broad histological classifications: small cell lung cancer (SCLC) and non-small cell lung cancer (NSCLC). NSCLC comprises about 80-85% of all lung cancers. Receptor tyrosine kinases (RTKs) are essential components to cellular signaling pathways and are often overexpressed or otherwise dysregulated by genetic mutations, fusion, or gene amplification (2,3). RTKs are generally activated by receptor specific ligands, leading to autophosphorylation and the subsequent recruitment of downstream signaling proteins. The most common RTK amplification in NSCLC is that for epidermal growth factor receptor (EGFR). Also, two of the most common mutations in EGFR include an exon 19 deletion, E746-A750, and a point mutation L858R (4,5). In addition to EGFR, several other RTKs may become aberrantly activated in NSCLC, including ALK, ROS1, HER2/ErbB2, Met, Ret, FGF Receptor 1, and NTRK (6). Specific tyrosine kinase inhibitors (TKIs) have been part of the arsenal of treating the disease and so analyzing the expression and mutational status of these receptors plays an important role in personalized treatment.
For Research Use Only. Not For Use In Diagnostic Procedures.
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D4D6 is a registered trademark of Cell Signaling Technology, Inc.
XP is a registered trademark of Cell Signaling Technology, Inc.
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