CXCR2 Inhibition Profoundly Suppresses Metastases and Augments Immunotherapy in Pancreatic Ductal Adenocarcinoma

CXCR2 has been suggested to have both tumor-promoting and tumor-suppressive properties. Here we show that CXCR2 signaling is upregulated in human pancreatic cancer, predominantly in neutrophil/myeloid-derived suppressor cells, but rarely in tumor cells. Genetic ablation or inhibition of CXCR2 abroga...

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Veröffentlicht in:Cancer cell Jg. 29; H. 6; S. 832
Hauptverfasser: Steele, Colin W, Karim, Saadia A, Leach, Joshua D G, Bailey, Peter, Upstill-Goddard, Rosanna, Rishi, Loveena, Foth, Mona, Bryson, Sheila, McDaid, Karen, Wilson, Zena, Eberlein, Catherine, Candido, Juliana B, Clarke, Mairi, Nixon, Colin, Connelly, John, Jamieson, Nigel, Carter, C Ross, Balkwill, Frances, Chang, David K, Evans, T R Jeffry, Strathdee, Douglas, Biankin, Andrew V, Nibbs, Robert J B, Barry, Simon T, Sansom, Owen J, Morton, Jennifer P
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 13.06.2016
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ISSN:1878-3686, 1878-3686
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Abstract CXCR2 has been suggested to have both tumor-promoting and tumor-suppressive properties. Here we show that CXCR2 signaling is upregulated in human pancreatic cancer, predominantly in neutrophil/myeloid-derived suppressor cells, but rarely in tumor cells. Genetic ablation or inhibition of CXCR2 abrogated metastasis, but only inhibition slowed tumorigenesis. Depletion of neutrophils/myeloid-derived suppressor cells also suppressed metastasis suggesting a key role for CXCR2 in establishing and maintaining the metastatic niche. Importantly, loss or inhibition of CXCR2 improved T cell entry, and combined inhibition of CXCR2 and PD1 in mice with established disease significantly extended survival. We show that CXCR2 signaling in the myeloid compartment can promote pancreatic tumorigenesis and is required for pancreatic cancer metastasis, making it an excellent therapeutic target.
AbstractList CXCR2 has been suggested to have both tumor-promoting and tumor-suppressive properties. Here we show that CXCR2 signaling is upregulated in human pancreatic cancer, predominantly in neutrophil/myeloid-derived suppressor cells, but rarely in tumor cells. Genetic ablation or inhibition of CXCR2 abrogated metastasis, but only inhibition slowed tumorigenesis. Depletion of neutrophils/myeloid-derived suppressor cells also suppressed metastasis suggesting a key role for CXCR2 in establishing and maintaining the metastatic niche. Importantly, loss or inhibition of CXCR2 improved T cell entry, and combined inhibition of CXCR2 and PD1 in mice with established disease significantly extended survival. We show that CXCR2 signaling in the myeloid compartment can promote pancreatic tumorigenesis and is required for pancreatic cancer metastasis, making it an excellent therapeutic target.
CXCR2 has been suggested to have both tumor-promoting and tumor-suppressive properties. Here we show that CXCR2 signaling is upregulated in human pancreatic cancer, predominantly in neutrophil/myeloid-derived suppressor cells, but rarely in tumor cells. Genetic ablation or inhibition of CXCR2 abrogated metastasis, but only inhibition slowed tumorigenesis. Depletion of neutrophils/myeloid-derived suppressor cells also suppressed metastasis suggesting a key role for CXCR2 in establishing and maintaining the metastatic niche. Importantly, loss or inhibition of CXCR2 improved T cell entry, and combined inhibition of CXCR2 and PD1 in mice with established disease significantly extended survival. We show that CXCR2 signaling in the myeloid compartment can promote pancreatic tumorigenesis and is required for pancreatic cancer metastasis, making it an excellent therapeutic target.CXCR2 has been suggested to have both tumor-promoting and tumor-suppressive properties. Here we show that CXCR2 signaling is upregulated in human pancreatic cancer, predominantly in neutrophil/myeloid-derived suppressor cells, but rarely in tumor cells. Genetic ablation or inhibition of CXCR2 abrogated metastasis, but only inhibition slowed tumorigenesis. Depletion of neutrophils/myeloid-derived suppressor cells also suppressed metastasis suggesting a key role for CXCR2 in establishing and maintaining the metastatic niche. Importantly, loss or inhibition of CXCR2 improved T cell entry, and combined inhibition of CXCR2 and PD1 in mice with established disease significantly extended survival. We show that CXCR2 signaling in the myeloid compartment can promote pancreatic tumorigenesis and is required for pancreatic cancer metastasis, making it an excellent therapeutic target.
Author Sansom, Owen J
Carter, C Ross
Clarke, Mairi
Connelly, John
Foth, Mona
Eberlein, Catherine
Leach, Joshua D G
Rishi, Loveena
Morton, Jennifer P
Bailey, Peter
Karim, Saadia A
Chang, David K
Upstill-Goddard, Rosanna
Evans, T R Jeffry
Biankin, Andrew V
Strathdee, Douglas
Bryson, Sheila
Nixon, Colin
McDaid, Karen
Nibbs, Robert J B
Wilson, Zena
Jamieson, Nigel
Balkwill, Frances
Barry, Simon T
Steele, Colin W
Candido, Juliana B
Author_xml – sequence: 1
  givenname: Colin W
  surname: Steele
  fullname: Steele, Colin W
  organization: Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK
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  givenname: Saadia A
  surname: Karim
  fullname: Karim, Saadia A
  organization: Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK
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  givenname: Joshua D G
  surname: Leach
  fullname: Leach, Joshua D G
  organization: Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK
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  surname: Bailey
  fullname: Bailey, Peter
  organization: Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK
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  organization: Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK
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  organization: Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK
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  organization: Oncology iMED, AstraZeneca, Alderley Park, Macclesfield SK10 4TG, UK
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  fullname: Wilson, Zena
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  givenname: Juliana B
  surname: Candido
  fullname: Candido, Juliana B
  organization: Centre for Cancer and Inflammation, Barts Cancer Institute, London EC1M 6BQ, UK
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  organization: Institute of Infection, Immunity and Inflammation, University of Glasgow, Glasgow G12 8QQ UK
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  organization: Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK
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  organization: Department of Surgery, Glasgow Royal Infirmary, Glasgow G4 0SF, UK
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  organization: Department of Surgery, Glasgow Royal Infirmary, Glasgow G4 0SF, UK
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  organization: Centre for Cancer and Inflammation, Barts Cancer Institute, London EC1M 6BQ, UK
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  surname: Chang
  fullname: Chang, David K
  organization: Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK
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  givenname: T R Jeffry
  surname: Evans
  fullname: Evans, T R Jeffry
  organization: Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK; Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK
– sequence: 21
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  organization: Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK
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  email: o.sansom@beatson.gla.ac.uk
  organization: Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK; Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK. Electronic address: o.sansom@beatson.gla.ac.uk
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  surname: Morton
  fullname: Morton, Jennifer P
  organization: Cancer Research UK Beatson Institute, Garscube Estate, Switchback Road, Glasgow G61 1BD, UK; Institute of Cancer Sciences, University of Glasgow, Glasgow G61 1BD, UK
BackLink https://www.ncbi.nlm.nih.gov/pubmed/27265504$$D View this record in MEDLINE/PubMed
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PublicationTitle Cancer cell
PublicationTitleAlternate Cancer Cell
PublicationYear 2016
References 27300430 - Cancer Cell. 2016 Jun 13;29(6):774-776. doi: 10.1016/j.ccell.2016.05.013.
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Snippet CXCR2 has been suggested to have both tumor-promoting and tumor-suppressive properties. Here we show that CXCR2 signaling is upregulated in human pancreatic...
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SubjectTerms Animals
Antibodies, Monoclonal - administration & dosage
Antibodies, Monoclonal - pharmacology
Antibodies, Monoclonal, Humanized
Carcinoma, Pancreatic Ductal - drug therapy
Carcinoma, Pancreatic Ductal - genetics
Carcinoma, Pancreatic Ductal - pathology
Cell Line, Tumor
Deoxycytidine - administration & dosage
Deoxycytidine - analogs & derivatives
Deoxycytidine - pharmacology
Gemcitabine
Gene Expression Regulation, Neoplastic - drug effects
Humans
Immunotherapy
Mice
Neoplasm Metastasis
Pancreatic Neoplasms - drug therapy
Pancreatic Neoplasms - genetics
Pancreatic Neoplasms - pathology
Prognosis
Receptors, Interleukin-8B - antagonists & inhibitors
Receptors, Interleukin-8B - genetics
Signal Transduction
Small Molecule Libraries - administration & dosage
Small Molecule Libraries - pharmacology
Survival Analysis
Up-Regulation
Xenograft Model Antitumor Assays
Title CXCR2 Inhibition Profoundly Suppresses Metastases and Augments Immunotherapy in Pancreatic Ductal Adenocarcinoma
URI https://www.ncbi.nlm.nih.gov/pubmed/27265504
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