|EGF Receptor (D38B1) XP® Rabbit mAb 4267||20 µl||
||H M Mk||175||Rabbit IgG|
|EGF Receptor (L858R Mutant Specific) (43B2) Rabbit mAb 3197||20 µl||
|EGF Receptor (E746-A750del Specific) (D6B6) XP® Rabbit mAb 2085||20 µl||
|ALK (D5F3®) XP® Rabbit mAb 3633||20 µl||
||H||220 (ALK), 80 (NPM-ALK), 117 (EML4-ALK v1), 86 (EML4-ALK v3)||Rabbit IgG|
|HER2/ErbB2 (D8F12) XP® Rabbit mAb 4290||20 µl||
||H M||185||Rabbit IgG|
|FGF Receptor 1 (D8E4) XP® Rabbit mAb 9740||20 µl||
||H M R Mk||92 , 120, 145||Rabbit IgG|
|ROS1 (D4D6®) Rabbit mAb 3287||20 µl||
||H||258, 110, 50-80||Rabbit IgG|
|Ret (E1N8X) XP® Rabbit mAb 14556||20 µl||
||H M||150, 175||Rabbit IgG|
|Met (D1C2) XP® Rabbit mAb 8198||20 µl||
||H||140, 170||Rabbit IgG|
|Anti-rabbit IgG, HRP-linked Antibody 7074||100 µl||
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.
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