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TRK Inhibition: A New Tumor-Agnostic Treatment Strategy

Shivaani Kummar1, Ulrik N Lassen2

  • 1Division of Medical Oncology, Stanford University School of Medicine, 780 Welch Road, Rm CJ250L, Palo Alto, CA, 94305, USA. skummar@stanford.edu.

Targeted Oncology
|October 3, 2018
PubMed

Insights

NTRK gene fusions are found in various solid tumors, driving cancer growth. TRK inhibitors like larotrectinib show durable responses, validating these fusions as key therapeutic targets.

Area of Science:

  • Oncology
  • Genetics
  • Pharmacology

Background:

  • NTRK gene fusions, present in up to 1% of solid tumors, lead to constitutively active TRK tyrosine kinases.
  • These activated kinases represent promising therapeutic targets for anticancer drug development.

Purpose of the Study:

  • To review clinical data on TRK inhibitors in tumors with NTRK gene fusions.
  • To discuss screening methods, resistance mechanisms, and regulatory aspects of TRK inhibitor development.

Main Methods:

  • Review of clinical trial data for TRK inhibitors (larotrectinib, entrectinib).
  • Analysis of diagnostic approaches for NTRK gene fusions.
  • Exploration of acquired resistance and regulatory considerations.

Main Results:

  • Larotrectinib demonstrates good tolerability and high, durable response rates across tumor types.
  • NTRK gene fusions are validated as actionable genomic alterations.
  • TRK inhibition shows significant clinical effectiveness.

Conclusions:

  • TRK inhibitors are effective in treating tumors with NTRK gene fusions.
  • Routine screening and understanding resistance are crucial for optimizing TRK inhibitor therapy.
  • Tumor-agnostic drug development for TRK inhibitors is supported by clinical data.

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