Brian W. Brannigan

TL;DR: A subgroup of patients with non-small-cell lung cancer have specific mutations in the EGFR gene which correlate with clinical responsiveness to the tyrosine kinase inhibitor gefitinib, and these mutations lead to increased growth factor signaling and confer susceptibility to the inhibitor.

TL;DR: Using mouse models with tagged mammary tumors, it is demonstrated that CTC clusters arise from oligoclonal tumor cell groupings and not from intravascular aggregation events, and though rare in the circulation, they greatly contribute to the metastatic spread of cancer.

TL;DR: Molecular analysis of circulating tumor cells from the blood of patients with lung cancer offers the possibility of monitoring changes in epithelial tumor genotypes during the course of treatment, and shows that a reduction in the number of captured cells was associated with a radiographic tumor response; an increase in theNumber of cells wasassociated with tumor progression, with the emergence of additional EGFR mutations in some cases.

TL;DR: These findings suggest that one of these, HKI-272, may prove highly effective in the treatment of EGFR-mutant NSCLCs, including tumors that have become resistant to gefitinib or erlotinib.

TL;DR: EGFR mutations and, to a lesser extent, amplification appear to identify distinct subsets of NSCLC with an increased response to gefitinib, and the combination of gefithinib with chemotherapy does not improve survival in patients with these molecular markers.