Paper - Review

DOI: 10.1038/nrc.2017.84

Abstract

The expanding spectrum
← of 1⃣ established 2⃣ candidate oncogenic driver mutations
→ identified ← in NSCLC
← coupled ← with the increasing number of (clinically available signal transduction pathway inhibitors) → targeting these driver mutations
→ offers → the tremendous opportunity → to enhance patient outcomes

❓: Advanced-stage NSCLC
→ remains largely incurable
∵ therapeutic resistance

❗: discuss → alterations
← 1⃣ in the targeted oncogene 2⃣ in other downstream & parallel pathways
→ leading to resistance → to targeted therapies in NSCLC
❗: provide → an overview of (the current understanding) ← of (the bidirectional interactions)
← with the tumor micro-environment ← that promote therapeutic resistance

❗: highlight common mechanistic themes
← underpinning resistance → to targeted therapies
← that are shared by NSCLC subtypes
→ e.g. 1⃣ EGRF 2⃣ ALK 3⃣ ROS1 4⃣ BRAF

❗: How understanding these themes
→ can inform therapeutic strategies ← including combination therapy approaches
→ can overcome the challenge of tumor heterogeneity

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