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Daniel D. Von Hoff - One of the best experts on this subject based on the ideXlab platform.

  • Abstract 393: The Chemokine Receptor, CXCR2/IL8RB, contributes to the survival of pancreatic adenocarcinoma, and may play a role in stroma-tumor communication
    Tumor Biology, 2011
    Co-Authors: Carolyn V. Ustach, Aprill Watanabe, Meraj Aziz, Caroline H. Diep, Galen Hostetter, Demeure Michael, Haiyong Han, Daniel D. Von Hoff
    Abstract:

    The failure of most chemotherapeutic agents to treat pancreatic cancer could be related to poor delivery of drug due to the physical barrier of dense fibrosis surrounding the tumor. Targeting and attenuating the fibrotic stroma may result in better access of drug to tumor. Our current studies show that CXCR2/IL8RB is over-expressed in the surrounding stroma of pancreatic ductal adenocarcinoma tumors. CXCR2/IL8RB and its ligands are well known to be involved in fibrosis, and recently published papers suggest a role for CXCR2 in tumor proliferation, as well. Therefore, CXCR2 is a good target for pancreatic cancer therapy, because it has the potential to target both the stroma surrounding the tumor, as well as the tumor itself. When comparing matched samples of patient tumor and adjacent normal tissue, the mean IHC score of stroma surrounding normal pancreatic ducts is 0.61 (95% CI 0.38-0.84), while the mean IHC score of stroma surrounding ductal adenocarcinoma is 1.6 (95% CI: 1.3-1.9; Mann-Whitney test p This work was supported by NIH P01 Grant CA109552. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 393. doi:10.1158/1538-7445.AM2011-393

  • abstract 393 the Chemokine Receptor CXCR2 il8rb contributes to the survival of pancreatic adenocarcinoma and may play a role in stroma tumor communication
    Cancer Research, 2011
    Co-Authors: Carolyn V. Ustach, Aprill Watanabe, Meraj Aziz, Caroline H. Diep, Galen Hostetter, Demeure Michael, Haiyong Han, Daniel D. Von Hoff
    Abstract:

    The failure of most chemotherapeutic agents to treat pancreatic cancer could be related to poor delivery of drug due to the physical barrier of dense fibrosis surrounding the tumor. Targeting and attenuating the fibrotic stroma may result in better access of drug to tumor. Our current studies show that CXCR2/IL8RB is over-expressed in the surrounding stroma of pancreatic ductal adenocarcinoma tumors. CXCR2/IL8RB and its ligands are well known to be involved in fibrosis, and recently published papers suggest a role for CXCR2 in tumor proliferation, as well. Therefore, CXCR2 is a good target for pancreatic cancer therapy, because it has the potential to target both the stroma surrounding the tumor, as well as the tumor itself. When comparing matched samples of patient tumor and adjacent normal tissue, the mean IHC score of stroma surrounding normal pancreatic ducts is 0.61 (95% CI 0.38-0.84), while the mean IHC score of stroma surrounding ductal adenocarcinoma is 1.6 (95% CI: 1.3-1.9; Mann-Whitney test p This work was supported by NIH P01 Grant CA109552. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 393. doi:10.1158/1538-7445.AM2011-393

Carolyn V. Ustach - One of the best experts on this subject based on the ideXlab platform.

  • Abstract 393: The Chemokine Receptor, CXCR2/IL8RB, contributes to the survival of pancreatic adenocarcinoma, and may play a role in stroma-tumor communication
    Tumor Biology, 2011
    Co-Authors: Carolyn V. Ustach, Aprill Watanabe, Meraj Aziz, Caroline H. Diep, Galen Hostetter, Demeure Michael, Haiyong Han, Daniel D. Von Hoff
    Abstract:

    The failure of most chemotherapeutic agents to treat pancreatic cancer could be related to poor delivery of drug due to the physical barrier of dense fibrosis surrounding the tumor. Targeting and attenuating the fibrotic stroma may result in better access of drug to tumor. Our current studies show that CXCR2/IL8RB is over-expressed in the surrounding stroma of pancreatic ductal adenocarcinoma tumors. CXCR2/IL8RB and its ligands are well known to be involved in fibrosis, and recently published papers suggest a role for CXCR2 in tumor proliferation, as well. Therefore, CXCR2 is a good target for pancreatic cancer therapy, because it has the potential to target both the stroma surrounding the tumor, as well as the tumor itself. When comparing matched samples of patient tumor and adjacent normal tissue, the mean IHC score of stroma surrounding normal pancreatic ducts is 0.61 (95% CI 0.38-0.84), while the mean IHC score of stroma surrounding ductal adenocarcinoma is 1.6 (95% CI: 1.3-1.9; Mann-Whitney test p This work was supported by NIH P01 Grant CA109552. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 393. doi:10.1158/1538-7445.AM2011-393

  • abstract 393 the Chemokine Receptor CXCR2 il8rb contributes to the survival of pancreatic adenocarcinoma and may play a role in stroma tumor communication
    Cancer Research, 2011
    Co-Authors: Carolyn V. Ustach, Aprill Watanabe, Meraj Aziz, Caroline H. Diep, Galen Hostetter, Demeure Michael, Haiyong Han, Daniel D. Von Hoff
    Abstract:

    The failure of most chemotherapeutic agents to treat pancreatic cancer could be related to poor delivery of drug due to the physical barrier of dense fibrosis surrounding the tumor. Targeting and attenuating the fibrotic stroma may result in better access of drug to tumor. Our current studies show that CXCR2/IL8RB is over-expressed in the surrounding stroma of pancreatic ductal adenocarcinoma tumors. CXCR2/IL8RB and its ligands are well known to be involved in fibrosis, and recently published papers suggest a role for CXCR2 in tumor proliferation, as well. Therefore, CXCR2 is a good target for pancreatic cancer therapy, because it has the potential to target both the stroma surrounding the tumor, as well as the tumor itself. When comparing matched samples of patient tumor and adjacent normal tissue, the mean IHC score of stroma surrounding normal pancreatic ducts is 0.61 (95% CI 0.38-0.84), while the mean IHC score of stroma surrounding ductal adenocarcinoma is 1.6 (95% CI: 1.3-1.9; Mann-Whitney test p This work was supported by NIH P01 Grant CA109552. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 393. doi:10.1158/1538-7445.AM2011-393

Ariela Benigni - One of the best experts on this subject based on the ideXlab platform.

  • inhibition of the Chemokine Receptor CXCR2 prevents kidney graft function deterioration due to ischemia reperfusion
    Kidney International, 2005
    Co-Authors: Daniela Cugini, Marina Noris, Nadia Azzollini, Paola Cassis, Francesco Colotta, Elena Gagliardini, Riccardo Bertini, Giuseppe Remuzzi, Ariela Benigni
    Abstract:

    Inhibition of the Chemokine Receptor CXCR2 prevents kidney graft function deterioration due to ischemia/reperfusion. Background Ischemia/reperfusion (I/R) injury after organ transplantation is a major cause of delayed graft function. Following I/R, locally produced CXC Chemokines attract and activate granulocytes, which in turn promote graft damage. Methods We examined the involvement of granulocyte recruitment via the CXCR2 pathway in a rat model of 4 hours cold ischemia followed by kidney transplantation. Serum creatinine and intragraft granulocyte infiltration were monitored in the early phase posttransplant. A CXCR2 inhibitor, repertaxin, was given to recipients before transplantation (at -24 hours or -8 hours or -2 hours), immediately before reperfusion and 2 hours later. Results An increase of granulocyte chemoattractant CINC-1/interleukin-8 (IL-8) mRNA expression after I/R both in syngeneic and allogeneic transplantation was associated with a marked infiltration of granulocytes in renal tissue. In syngeneic transplantation, Lewis rats given 15 mg/kg repertaxin 24 hours before surgery had granulocyte graft infiltration and serum creatinine levels significantly reduced in respect to vehicle-treated animals. Intermediate effects were observed with 5 mg/kg, whereas the dose of 30 mg/kg had toxic effects. We found that reducing the pretreatment time to 8 hours before surgery was still effective. Prevention of granulocyte infiltration and serum creatinine increase was also obtained in allogeneic transplantation, when Brown Norway recipients of Lewis kidneys were given 15 mg/kg repertaxin starting 8 hours before surgery. Conclusion Repertaxin treatment of the recipient animal was effective in preventing granulocyte infiltration and renal function impairment both in syngeneic and in allogeneic settings. The possibility to modulate I/R injury in this rat model opens new perspectives for preventing posttransplant delayed graft function in humans.

  • Inhibition of the Chemokine Receptor CXCR2 prevents kidney graft function deterioration due to ischemia/reperfusion.
    Kidney international, 2005
    Co-Authors: Daniela Cugini, Marina Noris, Nadia Azzollini, Paola Cassis, Francesco Colotta, Elena Gagliardini, Riccardo Bertini, Giuseppe Remuzzi, Ariela Benigni
    Abstract:

    Inhibition of the Chemokine Receptor CXCR2 prevents kidney graft function deterioration due to ischemia/reperfusion. Background Ischemia/reperfusion (I/R) injury after organ transplantation is a major cause of delayed graft function. Following I/R, locally produced CXC Chemokines attract and activate granulocytes, which in turn promote graft damage. Methods We examined the involvement of granulocyte recruitment via the CXCR2 pathway in a rat model of 4 hours cold ischemia followed by kidney transplantation. Serum creatinine and intragraft granulocyte infiltration were monitored in the early phase posttransplant. A CXCR2 inhibitor, repertaxin, was given to recipients before transplantation (at -24 hours or -8 hours or -2 hours), immediately before reperfusion and 2 hours later. Results An increase of granulocyte chemoattractant CINC-1/interleukin-8 (IL-8) mRNA expression after I/R both in syngeneic and allogeneic transplantation was associated with a marked infiltration of granulocytes in renal tissue. In syngeneic transplantation, Lewis rats given 15 mg/kg repertaxin 24 hours before surgery had granulocyte graft infiltration and serum creatinine levels significantly reduced in respect to vehicle-treated animals. Intermediate effects were observed with 5 mg/kg, whereas the dose of 30 mg/kg had toxic effects. We found that reducing the pretreatment time to 8 hours before surgery was still effective. Prevention of granulocyte infiltration and serum creatinine increase was also obtained in allogeneic transplantation, when Brown Norway recipients of Lewis kidneys were given 15 mg/kg repertaxin starting 8 hours before surgery. Conclusion Repertaxin treatment of the recipient animal was effective in preventing granulocyte infiltration and renal function impairment both in syngeneic and in allogeneic settings. The possibility to modulate I/R injury in this rat model opens new perspectives for preventing posttransplant delayed graft function in humans.

Thomas E. Lane - One of the best experts on this subject based on the ideXlab platform.

  • CXCR2 Signaling and Remyelination in Preclinical Models of Demyelination.
    DNA and cell biology, 2019
    Co-Authors: Dominic D. Skinner, Thomas E. Lane
    Abstract:

    The Chemokine Receptor CXCR2 is a Receptor for CXC Chemokines, including CXCL1 and CXCL2. CXCR2 is expressed by resident cells of the central nervous system, including neurons, microglia, oligodendrocyte progenitor cells (OPCs), and oligodendrocytes. CXCR2 signaling is important in regulating OPC biology with regard to positional migration and myelination during development. More recently, studies have argued that CXCR2 is involved in controlling events related to remyelination after experimentally induced demyelination. This review examines the concept that targeting CXCR2 may offer a novel therapeutic target for promoting remyelination.

  • ELR(+) Chemokine signaling in host defense and disease in a viral model of central nervous system disease.
    Frontiers in cellular neuroscience, 2014
    Co-Authors: Martin P. Hosking, Thomas E. Lane
    Abstract:

    Intracranial infection of the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the central nervous system (CNS) of susceptible strains of mice results in an acute encephalomyelitis, accompanied by viral replication in glial cells and robust infiltration of virus-specific T cells that contribute to host defense through cytokine secretion and cytolytic activity. Mice surviving the acute stage of disease develop an immune-mediated demyelinating disease, characterized by viral persistence in white matter tracts and a chronic neuroinflammatory response dominated by T cells and macrophages. Chemokines and their corresponding Chemokine Receptors are dynamically expressed throughout viral infection of the CNS, influencing neuroinflammation by regulating immune cell infltration and glial biology. This review is focused upon the pleiotropic Chemokine Receptor CXCR2 and its effects upon neutrophils and oligodendrocytes during JHMV infection and a number of other models of CNS inflammation.

  • The Chemokine Receptor CXCR2 and coronavirus-induced neurologic disease
    Virology, 2013
    Co-Authors: Jason G. Weinger, Brett S. Marro, Martin P. Hosking, Thomas E. Lane
    Abstract:

    Inoculation with the neurotropic JHM strain of mouse hepatitis virus (MHV) into the central nervous system (CNS) of susceptible strains of mice results in an acute encephalomyelitis in which virus preferentially replicates within glial cells while excluding neurons. Control of viral replication during acute disease is mediated by infiltrating virus-specific T cells via cytokine secretion and cytolytic activity, however sterile immunity is not achieved and virus persists resulting in chronic neuroinflammation associated with demyelination. CXCR2 is a Chemokine Receptor that upon binding to specific ligands promotes host defense through recruitment of myeloid cells to the CNS as well as protecting oligodendroglia from cytokine-mediated death in response to MHV infection. These findings highlight growing evidence of the diverse and important role of CXCR2 in regulating neuroinflammatory diseases.

  • CXCR2-positive neutrophils are essential for cuprizone-induced demyelination: relevance to multiple sclerosis
    Nature neuroscience, 2010
    Co-Authors: Liping Liu, Dolly Ann Padovani-claudio, Abdelmadjid Belkadi, Lindsey Darnall, Caitlin Drescher, Anne C. Cotleur, Karen Choi, Thomas E. Lane
    Abstract:

    Cuprizone causes demyelination and oligodendrocyte death in mice. Cuprizone lesions resemble a particular form of white-matter lesions that is seen in multiple sclerosis. This study reports that infiltrating neutrophils expressing the Chemokine Receptor CXCR2 contribute to oligodendrocyte death in the cuprizone model of demyelination.

Demeure Michael - One of the best experts on this subject based on the ideXlab platform.

  • Abstract 393: The Chemokine Receptor, CXCR2/IL8RB, contributes to the survival of pancreatic adenocarcinoma, and may play a role in stroma-tumor communication
    Tumor Biology, 2011
    Co-Authors: Carolyn V. Ustach, Aprill Watanabe, Meraj Aziz, Caroline H. Diep, Galen Hostetter, Demeure Michael, Haiyong Han, Daniel D. Von Hoff
    Abstract:

    The failure of most chemotherapeutic agents to treat pancreatic cancer could be related to poor delivery of drug due to the physical barrier of dense fibrosis surrounding the tumor. Targeting and attenuating the fibrotic stroma may result in better access of drug to tumor. Our current studies show that CXCR2/IL8RB is over-expressed in the surrounding stroma of pancreatic ductal adenocarcinoma tumors. CXCR2/IL8RB and its ligands are well known to be involved in fibrosis, and recently published papers suggest a role for CXCR2 in tumor proliferation, as well. Therefore, CXCR2 is a good target for pancreatic cancer therapy, because it has the potential to target both the stroma surrounding the tumor, as well as the tumor itself. When comparing matched samples of patient tumor and adjacent normal tissue, the mean IHC score of stroma surrounding normal pancreatic ducts is 0.61 (95% CI 0.38-0.84), while the mean IHC score of stroma surrounding ductal adenocarcinoma is 1.6 (95% CI: 1.3-1.9; Mann-Whitney test p This work was supported by NIH P01 Grant CA109552. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 393. doi:10.1158/1538-7445.AM2011-393

  • abstract 393 the Chemokine Receptor CXCR2 il8rb contributes to the survival of pancreatic adenocarcinoma and may play a role in stroma tumor communication
    Cancer Research, 2011
    Co-Authors: Carolyn V. Ustach, Aprill Watanabe, Meraj Aziz, Caroline H. Diep, Galen Hostetter, Demeure Michael, Haiyong Han, Daniel D. Von Hoff
    Abstract:

    The failure of most chemotherapeutic agents to treat pancreatic cancer could be related to poor delivery of drug due to the physical barrier of dense fibrosis surrounding the tumor. Targeting and attenuating the fibrotic stroma may result in better access of drug to tumor. Our current studies show that CXCR2/IL8RB is over-expressed in the surrounding stroma of pancreatic ductal adenocarcinoma tumors. CXCR2/IL8RB and its ligands are well known to be involved in fibrosis, and recently published papers suggest a role for CXCR2 in tumor proliferation, as well. Therefore, CXCR2 is a good target for pancreatic cancer therapy, because it has the potential to target both the stroma surrounding the tumor, as well as the tumor itself. When comparing matched samples of patient tumor and adjacent normal tissue, the mean IHC score of stroma surrounding normal pancreatic ducts is 0.61 (95% CI 0.38-0.84), while the mean IHC score of stroma surrounding ductal adenocarcinoma is 1.6 (95% CI: 1.3-1.9; Mann-Whitney test p This work was supported by NIH P01 Grant CA109552. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 393. doi:10.1158/1538-7445.AM2011-393