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Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion

ABSTRACT: Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion

PROVIDER: PRJNA1066350 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27630210_1.fastq.gz	Fastqsanger.gz
	SRR27630210_2.fastq.gz	Fastqsanger.gz

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Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion [RNA-seq]

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Glioneuronal tumor with ATRX alteration, kinase fusion and anaplastic features (GTAKA) with leptomeningeal dissemination and ZMIZ1::RET fusion

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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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Project description:Myeloproliferative neoplasms are frequently associated with aberrant constitutive tyrosine kinase (TK) activity resulting from point mutations or chimaeric fusion genes, such as BCR ABL1 or JAK2 V617F. We report here for the first time in hematological malignancies, two novel fusion genes involving the TK RET, BCR-RET and FGFR1OP-RET, in chronic myelo monocytic leukemia (CMML) cases. The two RET fusion genes lead to the aberrant activation of RET, are able to transform hematopoietic cells and skew the hematopoietic differentiation program towards the monocytic/macrophage lineage. We also report that the BCR-RET fusion protein is insensitive to Imatinib but sensitive to Sorafenib in vivo. CMML is an hematopoietic malignancy associated with the frequent activation of the RAS pathway. The RET fusion genes seems to constitutively mimic the same signaling pathway than RAS mutations. Overall, the RET fusion genes behaviors in the monocytic lineage underlie the role of the normal RET TK activity during the physiological monocytic differentiation. We analysed BAF/3 cells infected by BCR-RET, FGFR1OP-RET or BCR-ABL1P210 fusion genes retroviruses and sorted out using EGFP fluorescence, with Affymetrix GeneChip MouseGene 1.0 ST platform.

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Glioneuronal tumor with CLIP2-MET fusion: A case report

Project description:Glioneuronal tumor with CLIP2-MET fusion: A case report

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