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
258P - Assessment of sexual health in patients treated for ovarian cancer
Presenter: Renu Madan
Session: Poster display session
Resources:
Abstract
259P - The BOT patients fail to benefit from surgical staging procedures in prognosis and fertility outcomes: A retrospective analysis
Presenter: Li Na
Session: Poster display session
Resources:
Abstract
260P - Malignant ovarian germ cell tumours (MOGCT): Treatment results of 149 pts
Presenter: Dzhennet Chekini
Session: Poster display session
Resources:
Abstract
261P - Ovarian germ cell tumours - challenges and outcomes from a tertiary care centre in South India
Presenter: Vishnu Sreedath
Session: Poster display session
Resources:
Abstract
262P - Gestational trophoblastic tumours: Experience of the medical oncology department Hassan II University Hospital-Morocco about 29 cases
Presenter: Karima Oualla
Session: Poster display session
Resources:
Abstract
263TiP - ATHENA (GOG-3020/ENGOT-ov45): A randomised, double-blind, placebo-controlled phase III study of the poly (ADP-ribose) polymerase (PARP) inhibitor rucaparib + the PD-1 inhibitor nivolumab following frontline platinum-based chemotherapy in ovarian cancer
Presenter: Keiichi Fujiwara
Session: Poster display session
Resources:
Abstract
264TiP - ENGOT-ov43/KEYLYNK-001: A phase III trial of pembrolizumab plus chemotherapy with olaparib maintenance for first-line treatment of BRCA¬-nonmutated advanced epithelial ovarian cancer
Presenter: Keiichi Fujiwara
Session: Poster display session
Resources:
Abstract
265TiP - KEYNOTE-826: A phase III randomized study of chemotherapy with or without pembrolizumab for first-line treatment of persistent, recurrent, or metastatic cervical cancer
Presenter: Keiichi Fujiwara
Session: Poster display session
Resources:
Abstract
271P - Comparison between CHOP like regimens and DAEPOCH with or without Rituximab in adult high grade B cell lymphoma NOS; A retrospective study from a tertiary cancer hospital in South India
Presenter: LALATENDU MOHARANA
Session: Poster display session
Resources:
Abstract
272P - Melatonin increases the chemosensitivity of diffuse large Bell lymphoma cells to Epirubicin by inhibiting P-glycoprotein expression via the NF-κB pathway
Presenter: Xiuhua Sun
Session: Poster display session
Resources:
Abstract