Somatic mutations of epidermal growth factor receptor signaling pathway in lung cancers

By H. Shigematsu, Adi F. Gazdar. International Journal of Cancer, 2006

661 citations recorded by the source corpus.

Subfields: Molecular Biology, Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/106565b4bd2c35110ba329ad0e86c27a6c023c52

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Molecular Biology

In Oncology

In Pulmonary and Respiratory Medicine

Citations in the corpus

ErbB receptors and signaling pathways in cancer. (2009, background): “Genetic changes that have been detected in human tumors include gene amplification leading to receptor overexpression, activating kinase domain mutations mainly in EGFR, but also in ErbB2 [6–8], in-frame deletions in the extracellular domain of EGFR (EGFR vIII) [9], and coexpression of ErbB ligands ”
Lung cancer in never smokers — a different disease (2007, background): “EGFR mutations, and hence TKI response, occur in specific lung cancer subtypes: adenocarcinoma histology, never smoking status, East Asian ethnicity and female gende”
An allosteric mechanism for activation of the kinase domain of epidermal growth factor receptor. (2006, background): “…in an alternative numbering of the human EGFR sequence), has been found frequently in lung cancer patients (accounting for 41% of EGFR mutations in these cancers) (Jiang et al., 2005; Lynch et al., 2004; Paez et al., 2004; Pao et al., 2004; Shigematsu and Gazdar, 2006; Sordella et al., 2004).”
Activating and resistance mutations of EGFR in non-small-cell lung cancer: role in clinical response to EGFR tyrosine kinase inhibitors (2009, neutral): “The activating mutations of the EGFR gene are found in the first four exons (18 through 21) of the TK domain (Figure 1b) (Shigematsu and Gazdar, 2006; Kumar et al., 2008).”
Structures of lung cancer-derived EGFR mutants and inhibitor complexes: mechanism of activation and insights into differential inhibitor sensitivity. (2007, background): “The two most frequent mutations are the exon 19 deletion that removes residues 746–750 of the expressed protein and the exon 19 point substitution that replaces leucine 858 with arginine (L858R) (Chan et al., 2006; Shigematsu and Gazdar, 2006).”
The epidermal growth factor receptor family: Biology driving targeted therapeutics (2008, background): “Such a phenomenon is seen in approximately 14 % of lung adenocarcinomas [155,180].”