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Defining function of wild-type and three patient specific TP53 mutations in a zebrafish model of embryonal rhabdomyosarcoma

ABSTRACT: Defining function of wild-type and three patient specific TP53 mutations in a zebrafish model of embryonal rhabdomyosarcoma

PROVIDER: PRJNA882818 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21659014.fastq.gz	Fastqsanger.gz
	SRR21659015.fastq.gz	Fastqsanger.gz
	SRR21659016.fastq.gz	Fastqsanger.gz
	SRR21659017.fastq.gz	Fastqsanger.gz
	SRR21659018.fastq.gz	Fastqsanger.gz

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Defining function of wild-type and three patient specific TP53 mutations in a zebrafish model of embryonal rhabdomyosarcoma

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Defining function of wild-type and three patient-specific <i>TP53</i> mutations in a zebrafish model of embryonal rhabdomyosarcoma.

Project description:In embryonal rhabdomyosarcoma (ERMS) and generally in sarcomas, the role of wild-type and loss- or gain-of-function TP53 mutations remains largely undefined. Eliminating mutant or restoring wild-type p53 is challenging; nevertheless, understanding p53 variant effects on tumorigenesis remains central to realizing better treatment outcomes. In ERMS, >70% of patients retain wild-type TP53, yet mutations when present are associated with worse prognosis. Employing a kRASG12D-driven ERMS tumor model and tp53 null (tp53-/-) zebrafish, we define wild-type and patient-specific TP53 mutant effects on tumorigenesis. We demonstrate that tp53 is a major suppressor of tumorigenesis, where tp53 loss expands tumor initiation from <35% to >97% of animals. Characterizing three patient-specific alleles reveals that TP53C176F partially retains wild-type p53 apoptotic activity that can be exploited, whereas TP53P153Δ and TP53Y220C encode two structurally related proteins with gain-of-function effects that predispose to head musculature ERMS. TP53P153Δ unexpectedly also predisposes to hedgehog-expressing medulloblastomas in the kRASG12D-driven ERMS-model.

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Expression profile of zebrafish embryonal rhabdomyosarcoma

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