Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling. - Wikidata - wikimedia - TriplyDB

Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.

Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.

http://www.wikidata.org/entity/Q33902576

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Bladder cancer stem cells: clonal origin and therapeutic perspectives.Interferon-beta represses cancer stem cell properties in triple-negative breast cancer.Integrated miRNA-mRNA spatial signature for oral squamous cell carcinoma: a prospective profiling study of Narrow Band Imaging guided resection.Targeting Pancreatic Cancer Cell Plasticity: The Latest in Therapeutics.Smad3-STAT3 crosstalk in pathophysiological contexts.IL-6 family cytokines: Key inflammatory mediators as biomarkers and potential therapeutic targets.OSM potentiates preintravasation events, increases CTC counts, and promotes breast cancer metastasis to the lung.Using Supervised Learning Methods for Gene Selection in RNA-Seq Case-Control Studies

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Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.

http://www.wikidata.org/entity/Q33902576

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2017 թուականի Մարտին հրատարակուած գիտական յօդուած

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2017 թվականի մարտին հրատարակված գիտական հոդված

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2017年の論文

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2017年論文

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2017年論文

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2017年論文

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2017年论文

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name

Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.

@ast

Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.

@en

type

label

Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.

@ast

Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.

@en

prefLabel

Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.

@ast

Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.

@en

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Oncostatin M promotes cancer cell plasticity through cooperative STAT3-SMAD3 signaling.

@en

P2093

C A Bartel

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D J Junk

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J M Smigiel

http://www.w3.org/2001/XMLSchema#string

M W Jackson

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N Parameswaran

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P2860

Smad7 is inactivated through a direct physical interaction with the LIM protein Hic-5/ARA55

The epithelial-mesenchymal transition generates cells with properties of stem cells

Prospective identification of tumorigenic breast cancer cells

Cancer Stem Cell Plasticity Drives Therapeutic Resistance

Cancer stem cells: targeting the roots of cancer, seeds of metastasis, and sources of therapy resistance

Cell-of-Origin of Cancer versus Cancer Stem Cells: Assays and Interpretations

From Darwin's Origin of Species toward a theory of natural history

Non-redundant signal transduction of interleukin-6-type cytokines. The adapter protein Shc is specifically recruited to rhe oncostatin M receptor

Hematopoiesis controlled by distinct TIF1gamma and Smad4 branches of the TGFbeta pathway

ONCOMINE: a cancer microarray database and integrated data-mining platform

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4001-4013

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scholarly article

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10.1038/ONC.2017.33

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28

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36

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Benjamin L. Bryson

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2017-03-13T00:00:00Z

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1084129925

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28288136

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5509502

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