The STATs of cancer--new molecular targets come of age (Q29614601)

Europe PubMed Central

title

The STATs of cancer--new molecular targets come of age (English)

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30 April 2017

author name string

Yu H

series ordinal

1

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Jove R

series ordinal

2

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https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&retmode=json&id=14964307

30 April 2017

language of work or name

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30 April 2017

publication date

February 2004

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published in

Nature Reviews Cancer

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volume

4

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page(s)

97-105

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issue

2

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The molecular genetics of cancer

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cites work

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The multistep nature of cancer

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Rules for making human tumor cells

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The phosphoinositide 3-kinase pathway

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Transcription factors as targets for cancer therapy

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The pathway to signal achievement

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The phosphatidylinositol 3-Kinase AKT pathway in human cancer

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The Hallmarks of Cancer

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Jak-STAT pathways and transcriptional activation in response to IFNs and other extracellular signaling proteins

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STATs and gene regulation

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The role of STATs in transcriptional control and their impact on cellular function

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Studies of IFN-induced transcriptional activation uncover the Jak-Stat pathway.

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How cells respond to interferons

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Protein tyrosine kinase inhibitors as novel therapeutic agents

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Mechanism-based target identification and drug discovery in cancer research

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Gp130 and the interleukin-6 family of cytokines

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The Stat family in cytokine signaling

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IL-3 signaling and the role of Src kinases, JAKs and STATs: a covert liaison unveiled

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Stats: transcriptional control and biological impact

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Roles of STAT3 in mediating the cell growth, differentiation and survival signals relayed through the IL-6 family of cytokine receptors

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Principles of interleukin (IL)-6-type cytokine signalling and its regulation

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Ras-independent growth factor signaling by transcription factor tyrosine phosphorylation

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Stat3: a STAT family member activated by tyrosine phosphorylation in response to epidermal growth factor and interleukin-6

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Oncogenic kinase signalling

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Src family protein tyrosine kinases: cooperating with growth factor and adhesion signaling pathways

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Role of Src expression and activation in human cancer

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JAK-STAT signaling activated by Abl oncogenes

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STAT signaling in the pathogenesis and treatment of leukemias

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Enhanced DNA-binding activity of a Stat3-related protein in cells transformed by the Src oncoprotein

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Stat3 activation is required for cellular transformation by v-src

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Stat3 activation by Src induces specific gene regulation and is required for cell transformation

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Requirement of Stat3 but not Stat1 activation for epidermal growth factor receptor- mediated cell growth In vitro

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Constitutive activation of Stat3 signaling confers resistance to apoptosis in human U266 myeloma cells

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Interleukin-6 induces prostate cancer cell growth accompanied by activation of stat3 signaling pathway .

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STAT signaling in head and neck cancer

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Co-operative effect of c-Src tyrosine kinase and Stat3 in activation of hepatocyte growth factor expression in mammary carcinoma cells

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Requirement of Stat3 signaling for HGF/SF-Met mediated tumorigenesis

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Constitutive activation of Stat3 by the Src and JAK tyrosine kinases participates in growth regulation of human breast carcinoma cells

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Roles of activated Src and Stat3 signaling in melanoma tumor cell growth

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Activation of Stat3 by receptor tyrosine kinases and cytokines regulates survival in human non-small cell carcinoma cells

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Src kinases mediate STAT growth pathways in squamous cell carcinoma of the head and neck

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StAT signaling in cancer: insights into pathogenesis and treatment strategies.

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Stat5 is essential for the myelo- and lymphoproliferative disease induced by TEL/JAK2

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Inhibition of Bcr-Abl kinase activity by PD180970 blocks constitutive activation of Stat5 and growth of CML cells

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A FLT3-targeted tyrosine kinase inhibitor is cytotoxic to leukemia cells in vitro and in vivo

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Identification and characterization of a constitutively active STAT5 mutant that promotes cell proliferation

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Transcriptionally active Stat1 is required for the antiproliferative effects of both interferon alpha and interferon gamma

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IFNgamma and lymphocytes prevent primary tumour development and shape tumour immunogenicity

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STAT proteins as novel targets for cancer therapy. Signal transducer an activator of transcription

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STAT proteins: novel molecular targets for cancer drug discovery

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Constitutive activation of Stat3 signaling abrogates apoptosis in squamous cell carcinogenesis in vivo

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Blockade of the Bcr-Abl kinase activity induces apoptosis of chronic myelogenous leukemia cells by suppressing signal transducer and activator of transcription 5-dependent expression of Bcl-xL

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Anaplastic lymphoma kinase (ALK) activates Stat3 and protects hematopoietic cells from cell death

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Inhibition of STAT3 signaling leads to apoptosis of leukemic large granular lymphocytes and decreased Mcl-1 expression

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Inhibition of STAT3 signaling induces apoptosis and decreases survivin expression in primary effusion lymphoma

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c-Myc target genes involved in cell growth, apoptosis, and metabolism

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Mechanisms of apoptosis by c-Myc

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Stat3-mediated Myc expression is required for Src transformation and PDGF-induced mitogenesis

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Regulation of c-myc expression by IFN-gamma through Stat1-dependent and -independent pathways.

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Stat5 and Sp1 regulate transcription of the cyclin D2 gene in response to IL-2.

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Induction of p21WAF1/CIP1 and cyclin D1 expression by the Src oncoprotein in mouse fibroblasts: role of activated STAT3 signaling

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Surfing the p53 network

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Compromised HOXA5 function can limit p53 expression in human breast tumours

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What Is the Evidence That Tumors Are Angiogenesis Dependent?

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Patterns and emerging mechanisms of the angiogenic switch during tumorigenesis

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Oncogenes and angiogenesis: signaling three-dimensional tumor growth

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Glioblastoma growth inhibited in vivo by a dominant-negative Flk-1 mutant

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Vascular endothelial growth factor is a potential tumour angiogenesis factor in human gliomas in vivo.

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VEGFs, receptors and angiogenesis

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Constitutive Stat3 activity up-regulates VEGF expression and tumor angiogenesis

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Stat3 activation regulates the expression of vascular endothelial growth factor and human pancreatic cancer angiogenesis and metastasis

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Interleukin-6 promotes cervical tumor growth by VEGF-dependent angiogenesis via a STAT3 pathway

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Targeting HIF-1 for cancer therapy

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VEGF differentially activates STAT3 in microvascular endothelial cells

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Nuclear translocation of phosphorylated STAT3 is essential for vascular endothelial growth factor-induced human dermal microvascular endothelial cell migration and tube formation.

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Phosphorylation of STAT-3 in response to basic fibroblast growth factor occurs through a mechanism involving platelet-activating factor, JAK-2, and Src in human umbilical vein endothelial cells. Evidence for a dual kinase mechanism

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Spinning molecular immunology into successful immunotherapy

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Does the immune system see tumors as foreign or self?

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Enhanced Th1 activity and development of chronic enterocolitis in mice devoid of Stat3 in macrophages and neutrophils.

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STAT3 is a negative regulator of granulopoiesis but is not required for G-CSF-dependent differentiation

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STAT3 deletion during hematopoiesis causes Crohn's disease-like pathogenesis and lethality: a critical role of STAT3 in innate immunity

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Regulation of the innate and adaptive immune responses by Stat-3 signaling in tumor cells

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Production of vascular endothelial growth factor by human tumors inhibits the functional maturation of dendritic cells

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Dendritic cells are functionally defective in multiple myeloma: the role of interleukin-6.

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Prostanoids play a major role in the primary tumor-induced inhibition of dendritic cell differentiation

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Hyperactivation of STAT3 is involved in abnormal differentiation of dendritic cells in cancer.

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A critical role for Stat3 signaling in immune tolerance

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Targeted disruption of the mouse Stat3 gene leads to early embryonic lethality

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Roles of STAT3 defined by tissue-specific gene targeting

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Stat5a is mandatory for adult mammary gland development and lactogenesis.

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Fetal anemia and apoptosis of red cell progenitors in Stat5a-/-5b-/- mice: a direct role for Stat5 in Bcl-X(L) induction

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Stat5a and Stat5b proteins have essential and nonessential, or redundant, roles in cytokine responses

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The role of STATs in apoptosis

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Phosphotyrosyl peptides block Stat3-mediated DNA binding activity, gene regulation, and cell transformation

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Knockdown of STAT3 expression by RNAi induces apoptosis in astrocytoma cells

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Targeted inhibition of Stat3 with a decoy oligonucleotide abrogates head and neck cancer cell growth

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Negative regulation of the JAK/STAT pathway

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Negative regulation of cytokine signaling: STAT-induced STAT inhibitor

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Modulation of STAT signaling by STAT-interacting proteins

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SOCS-1, a negative regulator of cytokine signaling, is frequently silenced by methylation in multiple myeloma

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SOCS1 methylation in patients with newly diagnosed acute myeloid leukemia

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Multilevel dysregulation of STAT3 activation in anaplastic lymphoma kinase-positive T/null-cell lymphoma

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Small-molecule antagonists of Myc/Max dimerization inhibit Myc-induced transformation of chicken embryo fibroblasts

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Identifiers

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30 April 2017

Consolidated OpenCitations Corpus – April 2017

Dimensions Publication ID

321642

1031068002

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321642

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Consolidated OpenCitations Corpus – April 2017

https://eutils.ncbi.nlm.nih.gov/entrez/eutils/esummary.fcgi?db=pubmed&retmode=json&id=14964307

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30 April 2017

Consolidated OpenCitations Corpus – April 2017