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New Test May Help Risk Stratify Patients With NSCLC for Treatment

By: Cordi Craig
Posted: Monday, September 24, 2018

A retrospective analysis of the prognostic role of a serum proteomic test (VeriStrat) suggests that it may help identify EGFR mutation–positive patients with non–small cell lung cancer (NSCLC) who are likely to show a poor response to EGFR tyrosine kinase inhibitors. Although these individuals are a small proportion of the population (1%–3%), this subgroup should be monitored closely when treated with TKI monotherapy and may benefit from additional therapeutic agents.

“The ability to risk stratify patients using [the test] supports further work on the use of [it] among first-line patients as candidates for third-generation [tyrosine kinase inhibitor] therapy,” Consuelo Buttigliero, MD, of the University of Torino, Turin, Italy, and colleagues concluded in The Oncologist.

The study authors investigated the test’s performance among patients from the phase III MARQUEE trial in which previously treated patients with advanced NSCLC received tivantinib plus erlotinib or placebo plus erlotinib. Pretreatment plasma samples from 996 patients with NSCLC were analyzed using mass spectrometry to generate a “good” or “poor” prognostic label.

Regardless of treatment group, patients classified as having a good prognosis achieved significantly longer progression-free (3.8 months with tivantinib; 2.0 months without) and overall survival (11.6 months with tivantinib; 10.2 months without) compared with those classified as having a poor prognosis (1.9 months for both arms). Interestingly, patients who had EGFR-positive disease with a good status had a median overall survival more than double that of any other group (31.6 with tivantinib; 22.8 without). However, in patients with EGFR–wild-type disease, the authors observed similar survival rates among patients who had a poor or good prognosis (13.7 months with tivantinib; 6.5 months without). These findings indicate that the test can identify those who will not respond well to TKI monotherapy, despite the presence of EGFR-activating mutations, according to the authors.



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