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Integrative and comparative genomics identifies the tyrosine kinase FES as a key melanoma tumor supppressor: WGS part 2

ABSTRACT: Integrative and comparative genomics identifies the tyrosine kinase FES as a key melanoma tumor supppressor: WGS part 2

PROVIDER: PRJEB20010 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR1884250.fastq.gz	Fastqsanger.gz
	ERR1884260.fastq.gz	Fastqsanger.gz
	ERR1884251.fastq.gz	Fastqsanger.gz
	ERR1884261.fastq.gz	Fastqsanger.gz
	ERR1884252.fastq.gz	Fastqsanger.gz

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Integrative and comparative genomics identifies the tyrosine kinase FES as a key melanoma tumor supppressor: WGS part 2

Project description:An incomplete view of the (epi)genetic events that drive melanoma initiation and progression has been a major barrier to rational development of effective therapeutics and prognostic diagnostics for melanoma patients. Recent approaches that integrate human melanoma genomic and transcriptomic data provide unprecedented opportunities to discover oncogenic melanoma drivers. One limitation, however, is that human melanoma genome exhibits a radically altered cytogenetic profile. Hence there is a need for biologically-meaningful approaches to identify and validate lesions that drive melanomagenesis. We combined comparative oncogenomic approaches with mouse modeling to identify new cancer genes/pathways that drive melanoma progression. Spontaneously acquired genetic alterations such as copy-number alterations and specific mutations in mouse tumors of defined genetic origin were identified and used to prioritize relevant lesions from the complex human melanoma genomes. This integrated effort confirmed the importance of several genes and pathways previously implicated in melanoma and identified new putative melanoma tumor suppressor genes. Genetic ablation of one such gene, Fes, cooperated with BRafv600E to accelerate melanomagenesis in mice. This comparative oncogenomic approach has therefore helped discover a series of novel melanoma tumor suppressor genes, including FES, with prognostic and therapeutic relevance in human melanoma.

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Integrative and comparative genomics identifies the tyrosine kinase FES as a key melanoma tumor supppressor: WGS

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Integrative and comparative genomics identifies the tyrosine kinase FES as a key melanoma tumor supppressor: WES

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Integrative and comparative genomics identifies the tyrosine kinase FES as a key melanoma tumor supppressor: WGS

Project description:Integrative and comparative genomics identifies the tyrosine kinase FES as a key melanoma tumor supppressor: WGS

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Integrative and comparative genomics identifies the tyrosine kinase FES as a key melanoma tumor supppressor: WES

Project description:Integrative and comparative genomics identifies the tyrosine kinase FES as a key melanoma tumor supppressor: WES

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Tyrosine Kinase Inhibitor Cardiotoxicity

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Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

Project description:Fms-like tyrosine kinase 3 (Flt3) is a regulator of hematopoietic progenitor cells. It is a target of tyrosine kinase inhibitors (TKIs) used for acute myeloid leukemia treatment. Flt3 and its ligand (Flt3L) are expressed in the heart and cardiac side effects occur under Flt3-targeting TKIs. Whether Flt3/Flt3L also regulate cardiac progenitor cells (CPCs), however, is not known. The cardiac side population (SP) is a pool of heterogenous CPCs that can give rise to all cardiac lineages, hence contributing to cardiovascular homeostasis. Here we show that SP-CPCs produce and are responsive to Flt3L. Compared to wild-type, SP-CPCs from flt3L-/- mice are less abundant, with less contribution of CD45-CD34+ cells, and lower expression of gene sets related to epithelial-to-mesenchymal transition, cardiovascular development and stem cell differentiation. Upon culturing and compared to wild-type, flt3L-/- Sca1+CD31- SP-CPCs show increased proliferation and less vasculogenic commitment, but differentiation can be induced in the presence of receptor tyrosine kinase-activating growth factors. The observed differences are associated with decreased microvascularisation and global systolic function of flt3L-/- hearts. Thus, Flt3 contributes to a receptor tyrosine kinase signature necessary for the maintenance and functionality of SP-CPCs. These findings have potential implications regarding cardiovascular side effects observed under TKI therapy.

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Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

Project description:Fms-like tyrosine kinase 3 (Flt3) contributes to a receptor tyrosine kinase signature regulating the cardiac side population

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