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Characterization of a novelÃ‚Â MEF2D-BCL9Ã‚Â fusion positive acute lymphoblastic leukemia cell line WXS

ABSTRACT: The lack of a well-characterized model system for many subtypes ofÃ‚Â leukemiaÃ‚Â hinders the development of targeted therapy and immunotherapy.Ã‚Â A novel in-house-made pediatricÃ‚Â MEF2D-BCL9Ã‚Â fusion positive acute lymphoblastic leukemia cell line was characterized. This cell line is highly presentative for the major clone of the original material and thus a valuable resource to examine novel therapeutic forÃ‚Â MEF2DÃ‚Â fused patients.

PROVIDER: EGAS00001006800 | EGA |

REPOSITORIES: EGA

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Characterization of a novelÃ‚Â MEF2D-BCL9Ã‚Â fusion positive acute lymphoblastic leukemia cell line RNA-Seq

Project description:The lack of a well-characterized model system for many subtypes ofÃ‚Â leukemiaÃ‚Â hinders the development of targeted therapy and immunotherapy.Ã‚Â A novel in-house-made pediatricÃ‚Â MEF2D-BCL9Ã‚Â fusion positive acute lymphoblastic leukemia cell line was characterized. This cell line is highly presentative for the major clone of the original material and thus a valuable resource to examine novel therapeutic forÃ‚Â MEF2DÃ‚Â fused patients.

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Glycation modulates glutamatergic signaling and exacerbates ParkinsonÃ¢â‚¬â„¢s disease-like phenotypes

Project description:Alpha-synuclein (aSyn) is a central player in the pathogenesis of synucleinopathies due to its accumulation in typical protein aggregates in the brain. However, it is still unclear how it contributes to neurodegeneration. Type-2 diabetes mellitus is a risk factor for ParkinsonÃ¢â‚¬â„¢s disease (PD) and, interestingly, a common molecular alteration among these disorders is the age-associated increase in protein glycation. We hypothesized that glycation-induced neuronal dysfunction might be a contributing factor in synucleinopathies. Here, we dissected the specific impact of methylglyoxal (MGO, a glycating agent) in mice overexpressing aSyn in the brain. We found that MGO-glycation potentiates motor, cognitive, olfactory, and colonic dysfunction in aSyn transgenic (Thy1-aSyn) mice that received a single dose of MGO via intracerebroventricular (ICV) injection. aSyn accumulates in the midbrain, striatum, and prefrontal cortex, and protein glycation is increased in the cerebellum and midbrain. SWATH mass spectrometry analysis, used to quantify changes in the brain proteome, revealed that MGO mainly increase glutamatergic-associated proteins in the midbrain (NMDA, AMPA, glutaminase, VGLUT and EAAT1), but not in the prefrontal cortex, where it mainly affects the electron transport chain. Notably, the glycated proteins in the midbrain of Thy1-aSyn mice that received MGO strongly correlate with PD and dopaminergic pathways. Overall, we demonstrated that MGO-induced glycation accelerates PD-like sensorimotor and cognitive alterations and suggest that the increase of glutamatergic signaling may underly these events. Our study sheds new light into the enhanced vulnerability of the midbrain in PD-related synaptic dysfunction and suggests that glycation suppressors and anti-glutamatergic drugs may hold promise as disease-modifying therapies for synucleinopathies.

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Project description:A novel alternative splicing isoform of LOXL2 â³e13 was expressed ubiquitously in all cell lines and ESCC tissues. In contrast to the impaired deamination enzymatic activity compared with full length LOXL2, LOXL2 â³e13 showed an enhanced ability to promote cell mobility and invasiveness in ESCC cells than full length LOXL2 through a different mechanism. We used cDNA microarrays to identify genes that were differentially expressed upon LOXL2 â³ e13 overexpressed. For this purpose, we selected LOXL2 â³ e13, WT and empty vector control transfeced ESCC KYSE150 cell lines. Total RNA was extracted,compare the gene expression patterns between LOXL2 â³e13, LOXL2 WT and empty vector control transfected cells through the Genechip Primeview Human Gene Expression Array.

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MetabolicÃ‚Â profilingÃ‚Â ofÃ‚Â patient-derivedÃ‚Â organoidsÃ‚Â revealsÃ‚Â nucleotide synthesisÃ‚Â asÃ‚Â aÃ‚Â metabolicÃ‚Â vulnerabilityÃ‚Â inÃ‚Â malignantÃ‚Â rhabdoidÃ‚Â tumors

Project description:MalignantÃ‚Â rhabdoidÃ‚Â tumor (MRT) is oneÃ‚Â ofÃ‚Â the mostÃ‚Â aggressive childhood cancers for which no effective treatment optionsÃ‚Â areÃ‚Â available. ReprogrammingÃ‚Â ofÃ‚Â cellular metabolism isÃ‚Â an important hallmarkÃ‚Â ofÃ‚Â cancer, with various metabolism-based drugs beingÃ‚Â approved cancer treatment.Ã‚Â InÃ‚Â this study,Ã‚Â we use patient derived tumorÃ‚Â organoidsÃ‚Â (tumoroids) to map theÃ‚Â metabolicÃ‚Â landscapeÃ‚Â ofÃ‚Â several pediatric cancers. Combining gene expressionÃ‚Â analysesÃ‚Â and metaboliteÃ‚Â profilingÃ‚Â using mass spectrometry, we findÃ‚Â nucleotideÃ‚Â biosynthesisÃ‚Â to beÃ‚Â aÃ‚Â particularÃ‚Â vulnerabilityÃ‚Â ofÃ‚Â MRT. TreatmentÃ‚Â ofÃ‚Â MRT tumoroids withÃ‚Â de novoÃ‚Â nucleotideÃ‚Â synthesisÃ‚Â inhibitors lowersÃ‚Â nucleotideÃ‚Â levelsÃ‚Â inÃ‚Â MRT tumoroidsÃ‚Â andÃ‚Â inducesÃ‚Â apoptosis. Lastly, we demonstrateÃ‚Â invivoÃ‚Â efficacyÃ‚Â ofÃ‚Â methotrexateÃ‚Â inÃ‚Â an MRT PDX mouse model. Our studyÃ‚Â revealsnucleotideÃ‚Â biosynthesisÃ‚Â asÃ‚Â an MRT-specificÃ‚Â metabolicÃ‚Â vulnerability, which can ultimately lead to better treatment options for children suffering from this lethal pediatric malignancy.

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