Academic Journal
LGG-50. POOR RESPONSE TO MEKI RE-INITIATION IN PEDIATRIC LOW-GRADE GLIOMA AFTER TREATMENT DISCONTINUATION. A PLGG TASKFORCE STUDY
| العنوان: | LGG-50. POOR RESPONSE TO MEKI RE-INITIATION IN PEDIATRIC LOW-GRADE GLIOMA AFTER TREATMENT DISCONTINUATION. A PLGG TASKFORCE STUDY |
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| المؤلفون: | Bajin, Inci Yaman, Siddaway, Robert, Levine, Adrian, McKeown, Tara, Nobre, Liana, Das, Anirban, Bennett, Julie, Ramaswamy, Vijay, Huang, Annie, Bouffet, Eric, Lafay-Cousin, Lucie, Quang, Dong Anh Khuong, Hansford, Jordan, Rajagopal, Revathi, Gottardo, Nicholas G, Rowe, Rachel, Dutton, Jordann, Li, Amanda, McThenia, Sheila, Fangusaro, Jason, Perreault, Sébastien, Hawkins, Cynthia, Tabori, Uri |
| المصدر: | Neuro-Oncology ; volume 26, issue Supplement_4, page 0-0 ; ISSN 1522-8517 1523-5866 |
| بيانات النشر: | Oxford University Press (OUP) |
| سنة النشر: | 2024 |
| الوصف: | BACKGROUND Pediatric low-grade gliomas (pLGG) exhibit dramatic objective response to treatment with MEKi (Mitogen-Activated Protein Kinase inhibitors). Although the initial response to MEKi is promising, it is unknown whether it is safe to stop MEKi therapy and if the response to re-initiating MEKi would have the same impact. The study objective was to compare the first and second response to MEKi in patients with pLGG who stopped therapy and had further tumor progression. METHODS PLGG identified at neurooncology centers in Canada, Australia, and US, which were treated twice with MEKi were included. Second therapy was defined as MEKi upon progression for tumors where treatment was stopped. Response to MEKi between 2 treatments (MEKi1, MEKi2) were analyzed by using RANO criteria. RESULTS Mature data on 19 patients reveals a median patient age of 13 years (range 7–24), and the most common tumor location is hypothalamic/chiasmatic (89%). PLGG alterations include KIAA1549:BRAF fusion in 69%, NF1 in 21%, and other alterations in 10%. The overall response (minor and partial) to MEKi1 was 63% compared to 26% in MEKi2 (p=0.04). Furthermore, upon restarting MEKi2, 11% had further growth on therapy in contrast to none at MEKi1. MEKi1 resulted in average of 37% size decrease (range, 3%-98%), including 6 PLGG with over 50% response. In contrast, the average decrease to MEKi2 was 10% (range, 6%-40%, p=0.005), and none had >50% size reduction. Comparing each patient MEKi1 to MEKi2 revealed that initial response was superior to the second one in all PLGG. CONCLUSION These data suggest that the second response to MEKi is inferior when compared to initial therapy. Expansion of this cohort and biomarker correlates are ongoing. Biological insights are required for this observation, and careful consideration should be made for stopping MEKi, especially in strategic locations such as the optic pathway. |
| نوع الوثيقة: | article in journal/newspaper |
| اللغة: | English |
| DOI: | 10.1093/neuonc/noae064.441 |
| الاتاحة: | http://dx.doi.org/10.1093/neuonc/noae064.441 https://academic.oup.com/neuro-oncology/article-pdf/26/Supplement_4/0/58252314/noae064.441.pdf |
| Rights: | https://creativecommons.org/licenses/by-nc/4.0/ |
| رقم الانضمام: | edsbas.E5939766 |
| قاعدة البيانات: | BASE |
| DOI: | 10.1093/neuonc/noae064.441 |
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