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• The effects of inhaled corticosteroids on healthy airways

  Study EGAS00001007538

• A critical spotlight on the paradigms of FFPE-DNA sequencing

  Study EGAS00001005757

• DNA methylation profiles of samples included in the EORTC 26091 TAVAREC trial

  Study EGAS00001006015

• Measuring the Efficiency of Purging by Nonrandom Mating in Human Populations

  Study EGAS00001007831

• CeD_meta_analysis

  Results of the celiac diease meta-analysis

  Dataset EGAD00010001770

• CeD_Argentina_1

  Association results from the Agentinian cohort one

  Dataset EGAD00010001768

• EGAD00000000060

  Samples from the UK Glomerulonephritis DNA bank

  Dataset EGAD00000000060

• Single-Cell Profiling of Premature Neonate Airways Reveals a Continuum of Myeloid Differentiation

  We set out to develop a reference single-cell transcriptomic profile of airway aspirate samples from extremely premature neonates (collected within an hour of birth). In this study, we profiled samples from 10 subjects. We identified cells in the airways of premature neonates representing a continuum of myeloid differentiation, including fetal monocytes, differentiating myeloid cells, and macrophages. Trajectory analysis identified two trajectories consistent with interstitial and alveolar macrophages, and a bridging trajectory providing an alternative route between these terminal states. We defined 259 alveolar-specific genes, 666 interstitial-specific genes, and 285 bridging-specific genes providing the first single-cell transcriptional map of differentiating airway macrophages in humans.

  Study phs003427

• Case Report: Precision medicine target revealed by in-vitro modelling of relapsed, refractory ALL from a child with neurofibromatosis

  Children with neurofibromatosis have a higher risk of developing juvenile myelomonocytic leukaemia and acute myeloid leukaemia, but rarely develop B-cell acute lymphoblastic leukaemia (B-ALL). Through in-vitro modelling, a novel NF1 p.L2467 frameshift (fs) mutation identified in a relapsed/refractory Ph-like B-ALL patient with neurofibromatosis demonstrated cytokine independence and increased RAS signalling, indicative of leukaemic transformation. Furthermore, these cells were sensitive to the MEK inhibitors trametinib and mirdametinib. Bi-allelic NF1 loss of function may be a contributing factor to relapse and with sensitivity to MEK inhibitors, suggests a novel precision medicine target in the setting of neurofibromatosis patients with B-ALL.

  Study EGAS00001006187

• Data Access Policy of the HCEMM - Semmelweis University, Molecular Oncohematology Research Group

  Dac EGAC00001003240