"FOXR2 activation is not exclusive of CNS neuroblastoma" by Alexa N. Siskar, Emily Hanzlik et al.
 

FOXR2 activation is not exclusive of CNS neuroblastoma

Authors

Alexa N. Siskar, Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Emily Hanzlik, Department of Pediatric Medicine, St. Jude Children's Research Hospital, Memphis, TN, USA.
Maria F. Cardenas, Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Mohammad K. Eldomery, Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Soniya Pinto, Department of Radiology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Christopher L. Tinkle, Department of Radiation Oncology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Qunyu Zhang, Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Xiaoyu Li, Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Tong Lin, Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, TN, USA.
Sandeep K. Dhanda, Department of Oncology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Gerald Reis, Memorial Healthcare System, Hollywood, FL, USA.
Daphne Li, Advocate Health - MidwestFollow
Ravi Raghavan, Department of Pathology, Loma Linda University Medical Center, Loma Linda, CA, USA.
Alexander Vortmeyer, Department of Pathology, University of Mississippi Medical Center, Jackson, MS, USA.
Matthias A. Karajannis, Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, NY, USA.
Giles W. Robinson, Department of Oncology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Arzu Onar-Thomas, Department of Biostatistics, St. Jude Children's Research Hospital, Memphis, TN, USA.
Patrick R. Blackburn, Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.
David A. Wheeler, Department of Computational Biology, St. Jude Children's Research Hospital, Memphis, TN, USA.
Jason Chiang, Department of Pathology, St. Jude Children's Research Hospital, Memphis, TN, USA.

Affiliations

Advocate Children's Hospital, Park Ridge

Abstract

Background:FOXR2 activation is regarded as pathognomonic for CNS neuroblastoma (NB). However, a comprehensive understanding of the landscape for CNS tumors exhibiting FOXR2 activation is lacking.

Methods:Histopathologic, molecular, imaging, and clinical data of 42 CNS tumors with FOXR2 overexpression identified through screening institutional datasets and published institutional cases were analyzed.

Results:Among the 42 tumors, 21 (50.0%) were high-grade gliomas (HGGs), and 18 (42.9%) were embryonal tumors. The HGGs included ten H3 K27M-mutant diffuse midline gliomas (DMGs) and eight radiation-associated tumors. The embryonal tumors included 11 CNS NBs and six pineoblastomas (PBs). FOXR2 expression was similar between CNS NB and other tumor types (P = 0.82). HGGs with FOXR2 overexpression, unlike NBs and PBs, displayed diverse concomitant genetic alterations. The most common mechanisms of FOXR2 activation involved structural alterations causing promoter donation and enhancer hijacking from active genes essential for brain development, followed by alternative promoter activation or truncated LINE-1 retrotransposition. The preferential activation mechanism varied by tumor type. All but two aberrant FOXR2 transcripts incorporated non-canonical, non-coding exons. Gene set enrichment analysis demonstrated shared downstream effects of FOXR2 activation at the epigenome and transcriptome levels across tumor types. DMGs and PBs with FOXR2 overexpression were aggressive, with 0% 2-year overall survival, whereas CNS NBs responded well to combined chemotherapy and radiation.

Conclusions:CNS tumors with FOXR2 overexpression manifest significant histological, molecular, imaging, and clinical diversity. While HGGs and PBs with FOXR2 overexpression demonstrated inferior prognosis, CNS NBs showed favorable outcomes. Integrating histologic and molecular diagnostic approaches is imperative for accurate prognostication and optimal therapeutic decision-making.

Document Type

Article

PubMed ID

40237561


 

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