EML4-ALK mutations in lung cancer that confer resistance to ALK inhibitors.

By Y. L. Choi, M. Soda, Y. Yamashita, Toshihide Ueno, Junpei Takashima, T. Nakajima, Yasushi Yatabe, K. Takeuchi, T. Hamada, H. Haruta and 5 more. New England Journal of Medicine, 2010

1,200 citations recorded by the source corpus.

Subfields: Hematology, Pathology and Forensic Medicine, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/c974f562919545a85bf9e7ab2dfa9e74c659b325

How researchers see this paper

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

In Hematology

1. Nathanael S. Gray
2. P. Jänne

In Pathology and Forensic Medicine

1. J. Engelman
2. R. Roskoski

In Pulmonary and Respiratory Medicine

1. J. Engelman
2. L. Sequist
3. P. Jänne
4. Carlos L. Arteaga
5. Jin-Yuan Shih

Citations in the corpus

• A novel ALK secondary mutation and EGFR signaling cause resistance to ALK kinase inhibitors (2011, background): “11 (C1156Y, L1196M and F1174L) were stably expressed in H3122 cells and the cells were examined for crizotinib resistance (14, 15).”
• Mechanisms of Resistance to Crizotinib in Patients with ALK Gene Rearranged Non-Small Cell Lung Cancer (2012, neutral): “However, unlike EGFR-TKI resistance in NSCLC, there seems to be a greater diversity of resistance mutations as 4 different mutations have now been identified in patients with ALKþ NSCLC (12, 13).”
• Mechanisms of Acquired Crizotinib Resistance in ALK-Rearranged Lung Cancers (2012, background): “One patient’s tumor harbored two nonoverlapping mutations within the ALK tyrosine kinase (TK) domain, the gatekeeper L1196M substitution [which is analogous to T790M in epidermal growth factor receptor (EGFR) and T315I in ABL] and C1156Y (15), whereas the second patient’s tumor harbored a single L11”