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Transcriptome analysis of human glioblastoma tumor cells driven by PIK3CA mutation variants

ABSTRACT: Transcriptome analysis of human glioblastoma tumor cells driven by PIK3CA mutation variants

PROVIDER: PRJNA549965 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR9333380_1.fastq.gz	Fastqsanger.gz
	SRR9333380_2.fastq.gz	Fastqsanger.gz
	SRR9333390_1.fastq.gz	Fastqsanger.gz
	SRR9333390_2.fastq.gz	Fastqsanger.gz
	SRR9333400_1.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of mouse tumors driven by PIK3CA mutation variants

Project description:Transcriptome analysis of mouse tumors driven by PIK3CA mutation variants

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Transcriptome analysis of mouse tumors driven by PIK3CA mutation variants

Project description:The RTK/RAS/PI3K pathway is a key driver of tumorigenesis across all cancers, with 90% of Glioblastoma (GBM) tumors exhibiting alterations in this pathway. Among the specific genes in this pathway mutations in PI3K’s catalytic subunit, PIK3CA, are found in 11% of GBM tumors. Sequencing of GBM samples has revealed several known hotspot mutations that drive tumorigenesis in several cancers (E545K, H1047R), as well as a series of 63 in frame mutations (as indexed in COSMIC) that remain largely unclassified. To decode which of these PIK3CA variants function as drivers of GBM, we established an in vivo complementation screening platform for GBM. Our mouse GBM model relies on in utero electroporation (IUE) and CRISPR-Cas9 mediated knockout of NF1, p53, and PTEN (termed 3xCR). Because PTEN catalyzes the reverse reaction of PIK3CA, phosphorylation of PIP2 to PIP3, we complemented loss of PTEN with overexpression of E545K or H1047R, two bona fide hot spot driver mutations of PIK3CA. Both these variants accelerated tumor associated death, demonstrating that known PIK3CA drivers can complement PTEN loss in our system.

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Patogenic Mutation in 5 Genes

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Loss of HDAC-mediated repression and gain of NF-kB activation underlies cytokine induction in ARID1A and PIK3CA mutation-driven ovarian cancer

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RNA sequencing of PIK3CA-WT/WT and PIK3CA-WT/H1047R primary mouse embryonic fibroblasts

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