Abnormal spindle-like microcephaly-associated (ASPM) gene expression in posterior fossa brain tumors of childhood and adolescence

Author(s)

Cabral de Carvalho Correa, Debora ^{[1, 2]} ; Dias Oliveira, Indhira ^[1] ; Mascaro Cordeiro, Bruna ^[1] ; Silva, Frederico Adolfo ^{[1, 3]} ; de Seixas Alves, Maria Teresa ^{[4, 1]} ; Saba-Silva, Nasjla ^[1] ; Capellano, Andrea Maria ^[1] ; Dastoli, Patricia ^[1] ; Cavalheiro, Sergio ^{[5, 1]} ; Caminada de Toledo, Silvia Regina ^{[1, 2]}

Affiliation

^[1] Univ Fed Sao Paulo, Pediat Oncol Inst GRAACC, Dept Pediat, Sao Paulo, SP - Brazil

^[2] Univ Fed Sao Paulo, Dept Morphol & Genet, Div Genet, Sao Paulo, SP - Brazil

^[3] Univ Fed Sao Paulo, Dept Imaging Diag, Sao Paulo, SP - Brazil

^[4] Univ Fed Sao Paulo, Dept Pathol, Sao Paulo, SP - Brazil

^[5] Univ Fed Sao Paulo, Dept Neurol, Sao Paulo, SP - Brazil

• Document type: Journal article
• Source: CHILD'S NERVOUS SYSTEM; v. 37, n. 1 JUN 2020.
• Web of Science Citations: 0

Abstract

Purpose In neurogenesis,ASPM(abnormal spindle-like microcephaly-associated) gene is expressed mainly in the ventricular zone of posterior fossa and is the major determinant in the cerebral cortex. Besides its role in embryonic development,ASPMoverexpression promotes tumor growth, including central nervous system (CNS) tumors. This study aims to investigateASPMexpression levels in most frequent posterior fossa brain tumors of childhood and adolescence: medulloblastoma (MB), ependymoma (EPN), and astrocytoma (AS), correlating them with clinicopathological characteristics and tumor solid portion size. Methods Quantitative reverse transcription (qRT-PCR) is used to quantifyASPMmRNA levels in 80 pre-treatment tumor samples: 28 MB, 22 EPN, and 30 AS. The tumor solid portion size was determined by IOP-GRAACC Diagnostic Imaging Center. We correlated these findings with clinicopathological characteristics and tumor solid portion size. Results Our results demonstrated thatASPMgene was overexpressed in MB (p = 0.007) and EPN (p = 0.0260) samples.ASPMhigh expression was significantly associated to MB samples from patients with worse overall survival (p = 0.0123) and death due to disease progression (p = 0.0039). Interestingly, two patients with AS progressed toward higher grade showedASPMoverexpression (p = 0.0046). No correlation was found between the tumor solid portion size andASPMexpression levels in MB (p = 0.1154 andr = - 0.4825) and EPN (p = 0.1108 andr = - 0.3495) samples. Conclusion Taking in account thatASPMgene has several functions to support cell proliferation, as mitotic defects and premature differentiation, we suggest that its overexpression, presumably, plays a critical role in disease progression of posterior fossa brain tumors of childhood and adolescence. (AU)

• FAPESP's process: 17/26902-1 - The cerebral cortex size controlling gene, ASPM, gene expression in childhood and adolescence brain tumors
• Grantee: Débora Cabral de Carvalho Corrêa
• Support Opportunities: Scholarships in Brazil - Scientific Initiation