Publications by authors named "M Dede"

Decoding cellular state transitions is crucial for understanding complex biological processes in development and disease. While recent advancements in single-cell RNA sequencing (scRNA-seq) offer insights into cellular trajectories, existing tools primarily study expressional rather than regulatory state shifts. We present CellTran, a statistical approach utilizing paired-gene expression correlations to detect transition cells from scRNA-seq data without explicitly resolving gene regulatory networks.

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During crime scene investigations, numerous traces are secured and may be used as evidence for the evaluation of source and/or activity level propositions. The rapid chemical analysis of a biological trace enables the identification of body fluids and can provide significant donor profiling information, including age, sex, drug abuse, and lifestyle. Such information can be used to provide new leads, exclude from, or restrict the list of possible suspects during the investigative phase.

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Article Synopsis
  • Oncogenic mutations in and are key drivers of intraductal papillary mucinous neoplasms (IPMNs), which can lead to pancreatic cancer, and prior research showed that these mutations lead to cystic lesions in a specific mouse model.
  • The study investigated how these mutations affect cell characteristics and gene expression using advanced transcriptional profiling techniques and CRISPR screens to find potential weaknesses in cells with these mutations.
  • The findings revealed that co-expression of and led to a distinct gene signature and increased reliance on glycolysis, suggesting that targeting metabolic changes could be a promising strategy for treating or preventing IPMNs.
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Myelodysplastic syndrome and acute myeloid leukemia (AML) belong to a continuous disease spectrum of myeloid malignancies with poor prognosis in the relapsed/refractory setting necessitating novel therapies. Natural killer (NK) cells from patients with myeloid malignancies display global dysfunction with impaired killing capacity, altered metabolism, and an exhausted phenotype at the single-cell transcriptomic and proteomic levels. In this study, we identified that this dysfunction was mediated through a cross-talk between NK cells and myeloid blasts necessitating cell-cell contact.

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