Resistance to EGFR TKIs

Boehringer Ingelheim

Resistance to Epidermal Growth Factor Receptor (EGFR) Tyrosine Kinase Inhibitors (TKIs) due to EGFR-activating mutations can lead to signal transduction cascades promoting cell growth, proliferation, migration, survival, and angiogenesis.1

In non-small cell lung cancer (NSCLC), the presence of an EGFR activating mutation is predictive for response to an EGFR TKI.2,3

Most patients with NSCLC receiving first-generation TKIs will ultimately develop resistance. Fifty percent of these patients develop T790M-positive disease.1,4 To date, only T790M has been consistently demonstrated to be clinically associated with resistance in patients with NSCLC, although other secondary mutations that confer resistance may eventually be identified.3,4

References

1. Herbst RS, Heymach JV, Lippman SM. N Engl J Med. 2008;359(13):1367-1380.

2. Mok TS, Wu YL, Thongprasert S, et al. N Engl J Med. 2009;361(9):947-957.

3. National Comprehensive Cancer Network. NCCN Clinical Practice Guidelines in Oncology:

Non-Small Cell Lung Cancer —v2.2010. Fort Washington, PA: National Comprehensive

Cancer Network; 2009.

4. Gazdar AF. Cancer Metastasis Rev. 2010;29(1):37-48.

Source for healthcare professionals: www.inoncology.com
* Nintedanib (BIBF 1120), afatinib (BIBW 2992) and volasertib (BI 6727) are investigational compounds. Their safety and efficacy have not yet been fully established.

† Not an official event of the 2012 ASCO Annual Meeting. Not sponsored or endorsed by ASCO or the Conquer Cancer Foundation.

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