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accession-icon GSE12505
Plasmacytoid dendritic cells (pDCs) from E2-2 heterozygous mice
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
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Description

Analysis of expression profiles of pDCs from wild type and heterozygous E2-2 mice. Results show the control by E2-2 of the expression of pDC-enriched genes.

Publication Title

Transcription factor E2-2 is an essential and specific regulator of plasmacytoid dendritic cell development.

Sample Metadata Fields

No sample metadata fields

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accession-icon GSE51250
Combined targeting of JAK2 and Bcl-xL/Bcl-2 as a novel curative treatment for malignancies expressing mutant JAK2 and overcoming acquired resistance to single agent JAK2 inhibitors
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

Combined targeting of JAK2 and Bcl-2/Bcl-xL to cure mutant JAK2-driven malignancies and overcome acquired resistance to JAK2 inhibitors.

Sample Metadata Fields

Specimen part, Disease, Disease stage

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accession-icon GSE32277
Kras is required for pancreatic tumor maintenance through regulation of hexosamine biosynthesis and the non-oxidative pentose phosphate pathway
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon

Description

The maintenance of advanced malignancies relies on continued activity of driver oncogenes, although their rate-limiting role is highly context-dependent with respect to tumor types and associated genetic alterations. Oncogenic Kras mutation is the signature event in human pancreatic ductal adenocarcinoma (PDAC), serving a critical role in tumor initiation. Here, an inducible KrasG12D-driven p53 mutant PDAC mouse model establishes that advanced PDAC remains strictly dependent on continued KrasG12D expression and that KrasG12D serves a vital role in the control of tumor metabolism, through stimulation of glucose uptake and channeling of glucose intermediates through the hexosamine biosynthesis pathway (HBP) and the pentose phosphate pathway (PPP). Notably, these studies reveal that oncogenic Kras regulates ribose biogenesis. Unlike canonical models of PPP-mediated ribose biogenesis, we demonstrate that oncogenic Kras drives intermediates from enhanced glycolytic flux into the non-oxidative arm of the PPP, thereby decoupling ribose biogenesis from NADPNADPH-mediated redox control. Together, this work provides in vivo mechanistic insights into how oncogenic Kras promotes metabolic reprogramming in native tumors and illuminates potential metabolic targets that can be exploited for therapeutic benefit in Kras-driven PDAC.

Publication Title

Oncogenic Kras maintains pancreatic tumors through regulation of anabolic glucose metabolism.

Sample Metadata Fields

Specimen part, Treatment

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