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accession-icon GSE54589
Role of Notch signaling pathway in urothelial cancer
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

The Notch signaling pathway controls cell fates through interactions between neighboring cells by positively or negatively affecting, in a context-dependent manner, processes of proliferation, differentiation, and apoptosis1. It has been implicated in human cancer both as an oncogene and a tumor suppressor2. Here we report, for the first time, novel inactivating mutations in the Notch pathway components in over forty percent of the human bladder cancers examined. Bladder cancer is the fourth most commonly diagnosed malignancy in the US male population3. Thus far, driver mutations in the FGFR3 and less commonly RAS proteins have been identified4,5. We show that Notch activation in bladder cancer cells suppresses proliferation both in vitro and in vivo by directly upregulating dual specificity phosphatases (DUSPs), thus reducing ERK1/2 phosphorylation. In mouse models, genetic inactivation of Notch signaling leads to ERK1/2 phosphorylation resulting in tumorigenesis in the urinary tract. In recent years, the tumor suppressor role of Notch has been recognized by loss-of-function mutations identified in myeloid cancers6 as well as squamous cell carcinomas of the skin, lung7, and the head and neck8,9. Of the 4 Notch receptors (N1-4), only N1 and 2 have been implicated in human cancer.

Publication Title

A new tumor suppressor role for the Notch pathway in bladder cancer.

Sample Metadata Fields

Specimen part

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accession-icon GSE43022
ZFX controls the propagation and cell-of-origin characteristics of acute leukemia
  • organism-icon Mus musculus, Homo sapiens
  • sample-icon 28 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

ZFX controls propagation and prevents differentiation of acute T-lymphoblastic and myeloid leukemia.

Sample Metadata Fields

Specimen part, Cell line, Treatment

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accession-icon GSE36921
Effect of genetic Zfx deletion on gene expression in c-Kit + MLL-AF9 AML cells
  • organism-icon Mus musculus
  • sample-icon 10 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Acute myeloid leukemia (AML) propagates as a cellular hierarchy which is maintained by a rare subpopulation of self-renewing leukemia-initiating cells (LICs). These LICs phenotypically resemble HSCs and early myeloid progenitors, and they are functionally defined by their ability to reconstitute AML in xenografted mice.

Publication Title

ZFX controls propagation and prevents differentiation of acute T-lymphoblastic and myeloid leukemia.

Sample Metadata Fields

Cell line, Treatment

View Samples
accession-icon GSE43020
Effect of genetic Zfx deletion on gene expression in Notch induced T-ALL
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Acute myeloid leukemia (AML) and acute T-lymphoblastic leukemia (T-ALL) maintain the undifferentiated phenotype and proliferative capacity of their respective cells of origin, hematopoietic stem/progenitor cells and immature thymocytes. The mechanisms that maintain these progenitor-like characteristics are poorly understood. We report that the transcription factor Zfx is required for the development and propagation of experimental AML caused by MLL-AF9 fusion, and of T-ALL caused by Notch1 activation. In both leukemia types, Zfx activated progenitor-associated gene expression programs and prevented differentiation. Key Zfx target genes included mitochondrial enzymes Ptpmt1 and Idh2, whose overexpression partially rescued the propagation of Zfx-deficient AML. These studies identify a common mechanism that controls the cell-of-origin characteristics of acute leukemias derived from disparate lineages and transformation mechanisms.

Publication Title

ZFX controls propagation and prevents differentiation of acute T-lymphoblastic and myeloid leukemia.

Sample Metadata Fields

Specimen part, Cell line

View Samples
accession-icon GSE31551
Notch2 receptor signaling controls functional differentiation of dendritic cells in the spleen and intestine
  • organism-icon Mus musculus
  • sample-icon 3 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Dendritic cells (DCs) in tissues and lymphoid organs comprise distinct functional subsets that differentiate in situ from circulating progenitors. Tissue-specific signals that regulate DC subset differentiation are poorly understood. We report that DC-specific deletion of the Notch2 receptor caused a reduction of DC populations in the spleen. Within the splenic CD11b+ DCs, Notch signaling blockade ablated a distinct population marked by high expression of adhesion molecule Esam. The Notch-dependent Esamhi DC subset also required lymphotoxin beta receptor signaling, proliferated in situ and facilitated efficient CD4+ T cell priming. The Notch-independent Esamlo DCs expressed monocyte-related genes and showed superior cytokine responses. In addition, Notch2 deletion led to the loss of CD11b+ CD103+ DCs in the intestinal lamina propria and to the corresponding decrease of IL-17-producing CD4+ T cells in the intestine. Thus,Notch2 is a common differentiation signal for T cell-priming CD11b+ DC subsets in the spleen and intestine.

Publication Title

Notch2 receptor signaling controls functional differentiation of dendritic cells in the spleen and intestine.

Sample Metadata Fields

Specimen part

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accession-icon GSE27833
Notch signaling in HSC
  • organism-icon Mus musculus
  • sample-icon 19 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia.

Sample Metadata Fields

Sex, Age

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accession-icon GSE27811
Expression data from LSK WT, GMP WT and GMP NcstnKO
  • organism-icon Mus musculus
  • sample-icon 9 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2

Publication Title

A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia.

Sample Metadata Fields

Sex, Age

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accession-icon GSE27799
Expression data from LSK WT and LSK N1-C+
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2

Publication Title

A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE27794
Expression data from LSK WT and LSK NcstnKO
  • organism-icon Mus musculus
  • sample-icon 4 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

Description

Notch signaling is one of the central regulators of differentiation in a variety of organisms and tissue types. Within the hematopoietic system, Notch is essential for the emergence of definitive HSC during fetal life and controls adult HSC differentiation to the T-cell lineage. Notch activation is controlled by the gamma-secretase complex complex, composed of presenilin, nicastrin (Ncstn), anterior pharynx-1 (Aph1), and presenilin enhancer-2

Publication Title

A novel tumour-suppressor function for the Notch pathway in myeloid leukaemia.

Sample Metadata Fields

Sex, Age

View Samples
accession-icon GSE13535
Rat lung gene expression during acute pulmonary embolism
  • organism-icon Rattus norvegicus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Rat Genome 230 2.0 Array (rat2302)

Description

Rats were given pulmonary embolism by i.v. injection of 25 micron polystyrene microspheres or 0.01% Tween20 solution as vehicle control

Publication Title

Differential effect of mild and severe pulmonary embolism on the rat lung transcriptome.

Sample Metadata Fields

No sample metadata fields

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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