CNSC-16 - Molecular profiling and actionable mutations in adult patients with IDH wild type gliomas and glioneuronal and neuronal tumors

Friday, November 17, 2023

7:30 PM – 9:30 PM PT

Location: Exhibit Hall A/B

Poster Presenter(s)

Alessia Pellerino

Division of Neuro-Oncology, Department of Neuroscience "Rita Levi Montalcini", University and City of Health and Science Hospital, Turin, Italy
Torino, Italy

Author(s)

EM

Elena Maria Marchesani

Division of Neuro-Oncology, Department of Neuroscience “Rita Levi Montalcini”, University and City of Health and Science Hospital
Torino, Italy
LB

Luca Bertero

Pathology Unit, Department of Medical Sciences, University of Turin, Italy
Torino, Piemonte, Italy
AR

Alessia Andrea Ricci

Pathology Unit, Department of Medical Sciences, University of Turin
Torino, Italy
LM

Luca Mangherini

Pathology Unit, Department of Medical Sciences, University of Turin
Torino, Italy
Francesco Bruno

Division of Neuro-Oncology, Department of Neuroscience "Rita Levi Montalcini", University and City of Health and Science Hospital, Turin, Italy
Turin, Italy
Riccardo Soffietti

University of Turin
Torino, Piemonte, Italy
Roberta Rudà

Division of Neuro-Oncology, Department of Neuroscience, University of Turin
Turin, Piemonte, Italy

Background. Next generation sequencing (NGS) assays enable the identification of genetic alterations that may guide a personalized treatment in glioma patients. Material and Methods. From July 2021 to May 2023 a NGS analysis (Myriapod® NGS Cancer DNA and RNA panels) was performed in a cohort of 211 adults IDH wild type (wt) gliomas or circumscribed astrocytoma or glioneuronal/neuronal tumors. The aim was to identify actionable molecular alterations and provide targeted therapy at recurrence accordingly.Results. NGS analysis was available in 211 patients (95.5%), while NGS was not feasible in 10 patients (4.5%). 188/211 (89.1%) had an IDH wt glioblastoma (GBM) (median age 61 years), 6 (2.8%) had IDH wt lower grade gliomas (LGG) (median age 63 years), and 17 (8.1%) had circumscribed astrocytoma or glioneuronal/neuronal tumor (median age 37 years). Overall, actionable molecular alterations were found in 13/211 patients (6.2%). 7/211 patients (3.3%) had BRAF V600E mutation (3 IDH wt GBM, 1 IDH wt LGG, and 3 circumscribed/glioneuronal and neuronal tumor), 4/211 patients (1.9%) had FGFR3-TACC3 fusion (all GBM), 1/211 patients (0.5%) had PIK3CA mutation (GBM), and 1/211 patients (0.5%) had NTRK1 fusion (glioneuronal tumor). Other molecular mutations, including ALK, ERBB2, MET, KIT, KRAS, PDGFRA, and RET have not been detected. Three patients recurred after first-line therapy: 1 with BRAF mutated GBM, 1 with GBM harboring FGFR3-TACC3 fusion, and 1 with NTRK1 fusion positive glioneuronal tumor received specific BRAF/MEK inhibitor (dabrafenib/trametinib), FGFR inhibitor (pemigatinib), and NTRK inhibitor (larotrectinib), respectively. A remarkable activity of BRAF/MEK and NTRK inhibitors was observed (9 and 6 months, respectively *), while FGFR inhibitor did not display an activity to control disease (9 weeks). * ongoingConclusion. The incidence of actionable molecular alterations in IDH wt gliomas and glioneuronal/neuronal tumors was low. However, the use of targeted therapies may lead to significant impact on the outcome.