Reprogramming somatic cells into pluripotent stem cells (iPSCs) enables the study of systems in vitro. To increase the throughput of reprogramming, we present induction of pluripotency from pooled cells (iPPC)-an efficient, scalable, and reliable reprogramming procedure. Using our deconvolution algorithm that employs pooled sequencing of single-nucleotide polymorphisms (SNPs), we accurately estimated individual donor proportions of the pooled iPSCs. With iPPC, we concurrently reprogrammed over one hundred donor lymphoblastoid cell lines (LCLs) into iPSCs and found strong correlations of individual donors' reprogramming ability across multiple experiments. Individual donors' reprogramming ability remains consistent across both same-day replicates and multiple experimental runs, and the expression of certain immunoglobulin precursor genes may impact reprogramming ability. The pooled iPSCs were also able to differentiate into cerebral organoids. Our procedure enables a multiplex framework of using pooled libraries of donor iPSCs for downstream research and investigation of in vitro phenotypes.
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http://dx.doi.org/10.1016/j.crmeth.2023.100570 | DOI Listing |
Cancer Sci
January 2025
Hepatobiliary Surgery Center, Department of General Surgery, Huashan Hospital, Fudan University, Shanghai, China.
Immunotherapy has revolutionized cancer treatment, making it a challenge to noninvasively monitor immune infiltration. Metabolic reprogramming in cancers, including hepatocellular carcinoma (HCC), is closely linked to immune status. In this study, we aimed to evaluate the ability of carbon-11 acetate (C-acetate) and fluorine-18 fluorodeoxyglucose (F-FDG) PET/CT findings in predicting overall survival (OS) and immune infiltration in HCC patients.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Department of Biosciences, Biotechnologies and Environment, University of Bari, 70125 Bari, Italy.
Neurodegenerative diseases are characterized by progressive loss of neurons and persistent inflammation. Neurons are terminally differentiated cells, and lost neurons cannot be replaced since neurogenesis is restricted to only two neurogenic niches in the adult brain, whose neurogenic potential decreases with age. In this regard, the astrocytes reprogramming into neurons may represent a promising strategy for restoring the lost neurons and rebuilding neural circuits.
View Article and Find Full Text PDFTrends Cancer
January 2025
Center for Systems Biology, Massachusetts General Hospital, 185 Cambridge St, CPZN 5206, Boston, MA 02114, USA; Department of Pathology, Massachusetts General Hospital, 55 Fruit St, Boston, MA 02114, USA. Electronic address:
Myeloid cells play a crucial dual role in cancer progression and response to therapy, promoting tumor growth, enabling immune suppression, and contributing to metastatic spread. The ability of these cells to modulate the immune system has made them attractive targets for therapeutic strategies aimed at shifting their function from tumor promotion to fostering antitumor immunity. Therapeutic approaches targeting myeloid cells focus on modifying their numbers, genetics, metabolism, and interactions within the tumor microenvironment.
View Article and Find Full Text PDFBiotechnol Adv
January 2025
Frontier Science Center for Synthetic Biology (Ministry of Education), Key Laboratory of Systems Bioengineering, and School of Chemical Engineering and Technology, Tianjin University, Tianjin 300350, China; College of Life and Health Sciences, Northeastern University, Shenyang 110169, China. Electronic address:
Ralstonia eutropha H16, a facultative chemolithoautotrophic Gram-negative bacterium, demonstrates remarkable metabolic flexibility by utilizing either diverse organic substrates or CO as the sole carbon source, with H serving as the electron donor under aerobic conditions. The capacity of carbon and energy metabolism of R. eutropha H16 enabled development of synthetic biology technologies and strategies to engineer its metabolism for biosynthesis of value-added chemicals.
View Article and Find Full Text PDFGut
January 2025
Nuffield Department of Surgical Sciences, University of Oxford, Oxford, UK
Background: The immune suppression mechanisms in pancreatic ductal adenocarcinoma (PDAC) remain unknown, but preclinical studies have implicated macrophage-mediated immune tolerance. Hence, pathways that regulate macrophage phenotype are of strategic interest, with reprogramming strategies focusing on inhibitors of phosphoinositide 3-kinase-gamma (PI3Kγ) due to restricted immune cell expression. Inhibition of PI3Kγ alone is ineffective in PDAC, despite increased infiltration of CD8+ T cells.
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