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Activin A does not drive post-traumatic heterotopic ossification

Bone (New York, N.Y.), 2020-09, Vol.138, p.115473-115473, Article 115473

2020

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Anti-ACVR1 antibodies exacerbate heterotopic ossification in fibrodysplasia ossificans progressiva (FOP) by activating FOP-mutant ACVR1

The Journal of clinical investigation, 2022-06, Vol.132 (12), p.1-13

2022

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Targeting CXCR2 enhances chemotherapeutic response, inhibits mammary tumor growth, angiogenesis, and lung metastasis

Molecular cancer therapeutics, 2013-05, Vol.12 (5), p.799-808

2013

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CXCR2: A Novel Mediator of Mammary Tumor Bone Metastasis

International journal of molecular sciences, 2019-03, Vol.20 (5), p.1237

2019

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Small-Molecule Antagonists for CXCR2 and CXCR1 Inhibit Human Melanoma Growth by Decreasing Tumor Cell Proliferation, Survival, and Angiogenesis

Clinical cancer research, 2009-04, Vol.15 (7), p.2380-2386

2009

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Host Cxcr2-dependent regulation of mammary tumor growth and metastasis

Clinical & experimental metastasis, 2015-01, Vol.32 (1), p.65-72

2015

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Cathepsin G-mediated enhanced TGF-β signaling promotes angiogenesis via upregulation of VEGF and MCP-1

Cancer letters, 2010-02, Vol.288 (2), p.162-169

2010

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Matrix Metalloproteinase (MMP)-13 Regulates Mammary Tumor-Induced Osteolysis by Activating MMP9 and Transforming Growth Factor-β Signaling at the Tumor-Bone Interface

Cancer research (Chicago, Ill.), 2010-05, Vol.70 (9), p.3494-3504

2010

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Cathepsin G–Mediated Activation of Pro–Matrix Metalloproteinase 9 at the Tumor-Bone Interface Promotes Transforming Growth Factor-β Signaling and Bone Destruction

Molecular cancer research, 2009-08, Vol.7 (8), p.1224-1233

2009

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The Expansion of Heterotopic Bone in Fibrodysplasia Ossificans Progressiva Is Activin A‐Dependent

Journal of bone and mineral research, 2017-12, Vol.32 (12), p.2489-2499

2017

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Small interfering RNA‐mediated CXCR1 or CXCR2 knock‐down inhibits melanoma tumor growth and invasion

International journal of cancer, 2010-01, Vol.126 (2), p.328-336

2010

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Transforming growth factor‐β signaling at the tumor–bone interface promotes mammary tumor growth and osteoclast activation

Cancer science, 2009-01, Vol.100 (1), p.71-81

2009

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Cathepsin G Recruits Osteoclast Precursors via Proteolytic Activation of Protease-Activated Receptor-1

Cancer research (Chicago, Ill.), 2009-04, Vol.69 (7), p.3188-3195

2009

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In Vivo Quantitative Microcomputed Tomographic Analysis of Vasculature and Organs in a Normal and Diseased Mouse Model

PloS one, 2016-02, Vol.11 (2), p.e0150085-e0150085

2016

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Skeletal phenotype amelioration in mucopolysaccharidosis VI requires intervention at the earliest stages of postnatal development

JCI insight, 2023-11, Vol.8 (21)

2023

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Tumor-Stromal Interactions in Bone Metastasis

Current osteoporosis reports, 2010-06, Vol.8 (2), p.105-113

2010

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ACVR1R206H receptor mutation causes fibrodysplasia ossificans progressiva by imparting responsiveness to activin A

Science translational medicine, 2015-09, Vol.7 (303), p.303ra137

2015

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Enhanced expression and shedding of receptor activator of NF-κB ligand during tumor-bone interaction potentiates mammary tumor-induced osteolysis

Clinical & experimental metastasis, 2009-10, Vol.26 (7), p.797-808

2009

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Cathepsin G Enhances Mammary Tumor–Induced Osteolysis by Generating Soluble Receptor Activator of Nuclear Factor-κB Ligand

Cancer research (Chicago, Ill.), 2008-07, Vol.68 (14), p.5803-5811

2008

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Anti-ACVRI antibodies exacerbate heterotopic ossification in fibrodysplasia ossificans progressive

The Journal of clinical investigation, 2022-06, Vol.132 (12)

2022

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Anti-ACVRI antibodies exacerbate heterotopic ossification in fibrodysplasia ossificans progressive by activating FOP-mutant ACVR1

The Journal of clinical investigation, 2022-06, Vol.132 (12)

2022

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Defining phenotype reversibility in lysosomal disease: Leveraging a COIN model in mucopolysaccharidosis type VI (MPS VI)

Molecular genetics and metabolism, 2022-02, Vol.135 (2), p.S60-S60

2022

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Functional biology of the Steel syndrome founder allele and evidence for clan genomics derivation of COL27A1 pathogenic alleles worldwide

European journal of human genetics : EJHG, 2020-09, Vol.28 (9), p.1243-1264

2020

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Abstract 2281: Host CXCR2 expression regulates mammary tumor growth, angiogenesis and progression

Cancer research (Chicago, Ill.), 2010-04, Vol.70 (8_Supplement), p.2281-2281

2010

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Activin A does not drive post-traumatic heterotopic ossification

Anti-ACVR1 antibodies exacerbate heterotopic ossification in fibrodysplasia ossificans progressiva (FOP) by activating FOP-mutant ACVR1

Targeting CXCR2 enhances chemotherapeutic response, inhibits mammary tumor growth, angiogenesis, and lung metastasis

Activin A forms a non-signaling complex with ACVR1 and type II Activin/BMP receptors via its finger 2 tip loop

CXCR2: A Novel Mediator of Mammary Tumor Bone Metastasis

Small-Molecule Antagonists for CXCR2 and CXCR1 Inhibit Human Melanoma Growth by Decreasing Tumor Cell Proliferation, Survival, and Angiogenesis

Host Cxcr2-dependent regulation of mammary tumor growth and metastasis

Cathepsin G-mediated enhanced TGF-β signaling promotes angiogenesis via upregulation of VEGF and MCP-1

Matrix Metalloproteinase (MMP)-13 Regulates Mammary Tumor-Induced Osteolysis by Activating MMP9 and Transforming Growth Factor-β Signaling at the Tumor-Bone Interface

Cathepsin G–Mediated Activation of Pro–Matrix Metalloproteinase 9 at the Tumor-Bone Interface Promotes Transforming Growth Factor-β Signaling and Bone Destruction

The Expansion of Heterotopic Bone in Fibrodysplasia Ossificans Progressiva Is Activin A‐Dependent

Small interfering RNA‐mediated CXCR1 or CXCR2 knock‐down inhibits melanoma tumor growth and invasion

Transforming growth factor‐β signaling at the tumor–bone interface promotes mammary tumor growth and osteoclast activation

Cathepsin G Recruits Osteoclast Precursors via Proteolytic Activation of Protease-Activated Receptor-1

In Vivo Quantitative Microcomputed Tomographic Analysis of Vasculature and Organs in a Normal and Diseased Mouse Model

Skeletal phenotype amelioration in mucopolysaccharidosis VI requires intervention at the earliest stages of postnatal development

Tumor-Stromal Interactions in Bone Metastasis

ACVR1R206H receptor mutation causes fibrodysplasia ossificans progressiva by imparting responsiveness to activin A

Enhanced expression and shedding of receptor activator of NF-κB ligand during tumor-bone interaction potentiates mammary tumor-induced osteolysis

Cathepsin G Enhances Mammary Tumor–Induced Osteolysis by Generating Soluble Receptor Activator of Nuclear Factor-κB Ligand

Anti-ACVRI antibodies exacerbate heterotopic ossification in fibrodysplasia ossificans progressive

Anti-ACVRI antibodies exacerbate heterotopic ossification in fibrodysplasia ossificans progressive by activating FOP-mutant ACVR1

Defining phenotype reversibility in lysosomal disease: Leveraging a COIN model in mucopolysaccharidosis type VI (MPS VI)

Functional biology of the Steel syndrome founder allele and evidence for clan genomics derivation of COL27A1 pathogenic alleles worldwide

Abstract 2281: Host CXCR2 expression regulates mammary tumor growth, angiogenesis and progression

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