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A glioneuronal tumor with CLIP2-MET fusion.

ABSTRACT: We report a case of glioneuronal tumor (GNT) with a discovery of novel gene fusion of CLIP2-MET resulting from aberrant chromosome 7 abnormalities. We executed an elaborate genomic study on this case including whole-exome sequencing and RNA sequencing. Genomic analysis of the tumor revealed aberrations in chromosomes 1 and 7 and a CLIP2-MET fusion. Further analysis of the upregulated genes revealed substantial connections with MAPK pathway activation. We concluded that the chromosome 7 abnormalities prompted CLIP2-MET gene fusion which successively leads to MAPK pathway activation. We deliberated that MAPK pathway activation is one of the driver pathways responsible for the oncogenesis of GNT.

SUBMITTER: Chowdhury T

PROVIDER: S-EPMC7270112 | biostudies-literature | 2020

REPOSITORIES: biostudies-literature

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A glioneuronal tumor with CLIP2-MET fusion.

Chowdhury Tamrin T Lee Yeajina Y Kim Sojin S Yu Hyeon Jong HJ Ji So Young SY Bae Jeong Mo JM Won Jae Kyung JK Shin Joo Heon JH Weinberger Daniel R DR Choi Seung Hong SH Park Chul-Kee CK Kim Jong-Il JI Park Sung-Hye SH

NPJ genomic medicine 20200603

We report a case of glioneuronal tumor (GNT) with a discovery of novel gene fusion of CLIP2-MET resulting from aberrant chromosome 7 abnormalities. We executed an elaborate genomic study on this case including whole-exome sequencing and RNA sequencing. Genomic analysis of the tumor revealed aberrations in chromosomes 1 and 7 and a CLIP2-MET fusion. Further analysis of the upregulated genes revealed substantial connections with MAPK pathway activation. We concluded that the chromoso ...[more]

PMID: 32550005

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Glioneuronal tumor with CLIP2-MET fusion: A case report

Project description:Glioneuronal tumor (GN) is one type of biphasic central nervous system (CNS) tumor that exhibits both glial and neuronal immunohistological characteristics. We report a case of glioneuronal tumor (GN) with a discovery of novel gene fusion of CLIP2-MET resulting from aberrant chromosome 7 abnormalities. The tumor exhibited typical characteristics on histological examinations. We executed an elaborate genomic study on this case including whole-exome sequencing and RNA sequencing. Genomic analysis of the tumor revealed aberrations in chromosomes 1 and 7 and a CLIP2-MET fusion. Further analysis of the upregulated genes revealed substantial connections with MAPK pathway activation. We concluded that the chromosome 7 abnormalities prompted CLIP2-MET gene fusion which successively leads to MAPK pathway activation. We deliberated that MAPK pathway activation is responsible for the oncogenesis of GN based on our case and other previously reported ones.

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