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Multiple cellular origins may have profoundly different genomic landscapes and key signaling pathways, driving phenotypic variation and thereby posing significant challenges to personalized medicine in terms of achieving the optimal drug response and patient outcome.
Recent evidence suggests that ICC has multiple cellular origins, including differentiated hepatocytes; intrahepatic biliary epithelial cells (IBECs)/cholangiocytes; pluripotent stem cells, such as hepatic stem/progenitor cells (HPCs) and biliary tree stem/progenitor cells (BTSCs); and peribiliary gland (PBG).
Plasma AChE is likely to have multiple cellular origins, including cells from the brain.
In order to systematically evaluate potential diversities among CGIs and ultimately to illuminate the link between diversity of CGIs and their epigenetic variation, we analyzed the nucleotide-resolution DNA methylation maps (methylomes) of multiple cellular origins.
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We utilized recently generated nucleotide-resolution whole genome DNA methylation maps to study variation of DNA methylation across multiple methylomes with distinct cellular origins.
Since human AML LSC are very likely to also retain multiple cellular and molecular traits of their cells of origin, it is to be expected that HSC- and GMP-derived patient LSC might react differently to treatment and thus show different clinical responses to standard chemotherapy.
Profiling of a set of novel NP markers (CD24, CA12, PAX1, PTN, FOXF1 and KRT19 mRNA) in a representative set of subclones substantiated successful immortalization of multiple cellular subpopulations from primary isolates and confirmed their NP origin and/or phenotype.
Consistent with their origin from neural crest-derived multipotent precursors, NBs are often composed of multiple cellular phenotypes.
First, we identified significant global changes across multiple cellular pathways.
Here we review recent developments in deciphering the cellular origins of solid cancers.
They play major roles in multiple cellular processes, including energy production, calcium homoeostasis, cellular signaling, and apoptosis (Chan, 2006).
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