Abstract 366P
Background
TRK fusions are oncogenic drivers of a variety of tumors, many of which can involve the central nervous system (CNS). Larotrectinib is an FDA-approved selective TRK inhibitor for the treatment of TRK fusion cancer (Drilon et al., NEJM 2018). Here we report on the clinical activity of larotrectinib in an expanded set of TRK fusion-positive primary CNS tumors.
Methods
Patients with primary CNS tumors harboring an NTRK gene fusion detected by local molecular testing who were treated with larotrectinib in two clinical trials (NCT02637687 and NCT02576431) were identified. Larotrectinib was administered until disease progression, withdrawal, or unacceptable toxicity. Disease status was investigator assessed (RANO). Data cutoff: February 19, 2019.
Results
18 patients with various histological types of glial tumors (11 high grade, 4 low grade, 3 unknown) were identified. The patients had gene fusions involving NTRK2 (n = 13), NTRK1 (n = 3) and NTRK3 (n = 2). Median age was 10.5 years (range 1.3–79.0); 14 patients were pediatric (< 18). In 14 evaluable patients, the objective response rate was 36% (2 CR [pending confirmation], 3 PR), with responses seen in high- and low-grade disease and across histologies. Nine patients had SD. The 24-week disease control rate was 71%. The duration of treatment ranged from 0.03+ to 16.6+ months.
Conclusions
Larotrectinib is active in patients with TRK fusion cancer with intracranial disease. Objective responses and durable disease control were seen in primary CNS tumors of various grades and histologies. These results further support expanded testing for NTRK gene fusions in patients with primary CNS tumors.
Clinical trial identification
NCT02637687 and NCT02576431.
Editorial acknowledgement
Legal entity responsible for the study
Bayer.
Funding
Bayer.
Disclosure
All authors have declared no conflicts of interest.
Resources from the same session
41P - Clinical verification on the relationship between serum lipid metabolism and the immune microenvironment in breast cancer patients
Presenter: Wataru Goto
Session: Poster display session
Resources:
Abstract
42P - Genome wide copy number analysis of circulating tumour cells in breast cancer liver metastasis
Presenter: Saber Imani
Session: Poster display session
Resources:
Abstract
43P - A hotspot variants p.H1047R and p.H1047L in p110α/ΔNp63α complex affects structure, function and contributes to susceptibility metastatic breast cancer
Presenter: Zou Linglin
Session: Poster display session
Resources:
Abstract
44P - Correlation of circulating tumour cells with PET-CT in metastatic breast cancer
Presenter: Venkata Pradeep Babu Koyyala
Session: Poster display session
Resources:
Abstract
45P - The challenge of evaluating new targeted therapies: Opportunities in stratifying the therapeutic response per tumour location
Presenter: Hubert Beaumont
Session: Poster display session
Resources:
Abstract
46P - Plasma soluble CD36 of breast cancer based on pathological and clinical characteristics
Presenter: Aditia Romadhoni
Session: Poster display session
Resources:
Abstract
47P - Investigation of the use of a novel S-1 administration method for treating metastatic and recurrent breast cancer
Presenter: MAYUKO MIKI
Session: Poster display session
Resources:
Abstract
48P - Development of MDA-MB-231-3D-Spheroid as a reliable model for studying Nav1.5 and nNav1.5-mediated breast cancer metastasis
Presenter: Ahmad Murtadha
Session: Poster display session
Resources:
Abstract
49P - Biochemical study on modifying role of variants of leptin gene and its receptor on serum leptin levels in breast cancer
Presenter: Alshimaa Alhanafy
Session: Poster display session
Resources:
Abstract
50P - Prognostic factors of recurrence or distant metastasis in elderly breast cancer patients
Presenter: Seungju Lee
Session: Poster display session
Resources:
Abstract