Real-world outcomes associated with afatinib use in patients with solid tumors harboring NRG1 gene fusions

Stephen V Liu1, Claas Frohn2, Lori Minasi3

  • 1Georgetown University, Washington, DC 20007, USA.

PubMed
Abstract

Insights

Neuregulin-1 (NRG1) fusions can drive cancer by activating ErbB signaling. Afatinib, an ErbB inhibitor, showed activity in patients with NRG1 fusion-positive solid tumors, though outcomes varied between treatment groups in this real-world study.

Area of Science:

  • Oncology
  • Molecular Biology
  • Pharmacology

Background:

  • Neuregulin-1 (NRG1) fusions are implicated in oncogenesis through constitutive ErbB signaling.
  • NRG1 fusion-driven tumors may respond to ErbB-targeted therapies like afatinib.
  • Afatinib, an irreversible pan-ErbB inhibitor, has shown promise in individual cases.

Purpose of the Study:

  • To collect and analyze real-world data on patients with NRG1 fusion-positive solid tumors.
  • To describe the demographics, clinical characteristics, and outcomes of patients treated with afatinib versus other systemic therapies.
  • To evaluate the efficacy of afatinib in this patient population.

Main Methods:

  • Retrospective, multicenter, non-comparative cohort study.
  • Data collected from medical records of patients with NRG1 fusion-positive solid tumors.
  • Outcomes assessed included overall response rate (ORR), progression-free survival (PFS), and overall survival (OS).

Main Results:

  • 110 patients included: 72 received afatinib, 38 received other therapies.
  • Afatinib cohort: ORR 37.5%, median PFS 5.5 months, median OS 7.2 months.
  • Non-afatinib cohort: ORR 76.3%, median PFS 12.9 months, median OS 22.6 months.

Conclusions:

  • Real-world data show durable responses in patients with NRG1 fusion-positive solid tumors treated with afatinib or other therapies.
  • Significant imbalances between treatment cohorts limit direct outcome comparisons.
  • Further prospective and retrospective trials are necessary to confirm these findings.