Tissue micro array analysis of ganglioside N-glycolyl GM3 expression and signal transducer and activator of transcription (STAT)-3 activation in relation to dendritic cell infiltration and microvessel density in non-small cell lung cancer

Background Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of transcription (STAT)-3 are implicated in these processes. As both are considered as novel therapeutic targets, we assessed the possible association o...

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Published in:	BMC cancer Vol. 9; no. 1; p. 180
Main Authors:	van Cruijsen, Hester, Ruiz, Mariëlle Gallegos, van der Valk, Paul, de Gruijl, Tanja D, Giaccone, Giuseppe
Format:	Journal Article
Language:	English
Published:	London BioMed Central 11.06.2009 BioMed Central Ltd BMC
Subjects:	Biomedical and Life Sciences Biomedicine Cancer Research Carcinoma, Non-Small-Cell Lung - blood supply Carcinoma, Non-Small-Cell Lung - immunology Dendritic cells Dendritic Cells - immunology Dendritic Cells - pathology Female G(M3) Ganglioside - biosynthesis G(M3) Ganglioside - immunology Genetic aspects Genetic transcription Health Promotion and Disease Prevention Humans Immunohistochemistry Lung cancer, Non-small cell Lung Neoplasms - blood supply Lung Neoplasms - immunology Male Medicine/Public Health Microvessels - immunology Microvessels - pathology Middle Aged Neovascularization, Pathologic - immunology Neovascularization, Pathologic - pathology Oncology Physiological aspects Research Article Risk factors STAT3 Transcription Factor - biosynthesis STAT3 Transcription Factor - immunology Surgical Oncology Tissue Array Analysis Tissue microarrays United States Netherlands Vascular Endothelial Growth Factor pSTAT3 Expression NSCLC Patient NSCLC Tissue NSCLC Sample
ISSN:	1471-2407, 1471-2407
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Abstract	Background Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of transcription (STAT)-3 are implicated in these processes. As both are considered as novel therapeutic targets, we assessed the possible association of ganglioside GM3 expression and STAT3 activation with suppression of dendritic cell (DC) activation and angiogenesis in non-small cell lung cancer (NSCLC). Methods Immunohistochemistry was performed on a tissue array to determine N -glycolyl GM3 (GM3) and phosphorylated STAT3 (pSTAT3) expression in 176 primary NSCLC resections. Median values of GM3 and pSTAT3 expression were used as cut off. Microvessel density (MVD) was determined by CD34 staining and morphology. CD1a and CD83 were used to determine infiltrating immature and mature dendritic cells, respectively. Results 94% and 71% of the NSCLC samples expressed GM3 and nuclear pSTAT3, respectively. Median overall survival was 40.0 months. Both low GM3 expression and high pSTAT3 expression were associated with a worse survival, which reached near significance for GM3 ( P = 0.08). Microvessel density (MVD), determined by CD34 staining and morphology, was lower in NSCLC samples with high GM3 expression. CD1a + cells (immature DCs) were more frequent in NSCLC tissues as compared to peritumoral lung tissue, while CD83 + cells (mature DCs) were more frequent in peritumoral lung tissue. CD83 + DCs were less frequent in NSCLC tissues with high GM3 expression. Conclusion GM3 and pSTAT3 are widely expressed in NSCLC. Based on CD83 expression, GM3, but not pSTAT3, appeared to be involved in tumor-induced DC suppression. pSTAT3 expression was not associated with MVD, while GM3 might play an anti-angiogenic role.
AbstractList	Background Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of transcription (STAT)-3 are implicated in these processes. As both are considered as novel therapeutic targets, we assessed the possible association of ganglioside GM3 expression and STAT3 activation with suppression of dendritic cell (DC) activation and angiogenesis in non-small cell lung cancer (NSCLC). Methods Immunohistochemistry was performed on a tissue array to determine N-glycolyl GM3 (GM3) and phosphorylated STAT3 (pSTAT3) expression in 176 primary NSCLC resections. Median values of GM3 and pSTAT3 expression were used as cut off. Microvessel density (MVD) was determined by CD34 staining and morphology. CD1a and CD83 were used to determine infiltrating immature and mature dendritic cells, respectively. Results 94% and 71% of the NSCLC samples expressed GM3 and nuclear pSTAT3, respectively. Median overall survival was 40.0 months. Both low GM3 expression and high pSTAT3 expression were associated with a worse survival, which reached near significance for GM3 (P = 0.08). Microvessel density (MVD), determined by CD34 staining and morphology, was lower in NSCLC samples with high GM3 expression. CD1a.sup.+ .sup.cells (immature DCs) were more frequent in NSCLC tissues as compared to peritumoral lung tissue, while CD83.sup.+ .sup.cells (mature DCs) were more frequent in peritumoral lung tissue. CD83.sup.+ .sup.DCs were less frequent in NSCLC tissues with high GM3 expression. Conclusion GM3 and pSTAT3 are widely expressed in NSCLC. Based on CD83 expression, GM3, but not pSTAT3, appeared to be involved in tumor-induced DC suppression. pSTAT3 expression was not associated with MVD, while GM3 might play an anti-angiogenic role. Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of transcription (STAT)-3 are implicated in these processes. As both are considered as novel therapeutic targets, we assessed the possible association of ganglioside GM3 expression and STAT3 activation with suppression of dendritic cell (DC) activation and angiogenesis in non-small cell lung cancer (NSCLC). Immunohistochemistry was performed on a tissue array to determine N-glycolyl GM3 (GM3) and phosphorylated STAT3 (pSTAT3) expression in 176 primary NSCLC resections. Median values of GM3 and pSTAT3 expression were used as cut off. Microvessel density (MVD) was determined by CD34 staining and morphology. CD1a and CD83 were used to determine infiltrating immature and mature dendritic cells, respectively. 94% and 71% of the NSCLC samples expressed GM3 and nuclear pSTAT3, respectively. Median overall survival was 40.0 months. Both low GM3 expression and high pSTAT3 expression were associated with a worse survival, which reached near significance for GM3 (P = 0.08). Microvessel density (MVD), determined by CD34 staining and morphology, was lower in NSCLC samples with high GM3 expression. CD1a.sup.+ .sup.cells (immature DCs) were more frequent in NSCLC tissues as compared to peritumoral lung tissue, while CD83.sup.+ .sup.cells (mature DCs) were more frequent in peritumoral lung tissue. CD83.sup.+ .sup.DCs were less frequent in NSCLC tissues with high GM3 expression. GM3 and pSTAT3 are widely expressed in NSCLC. Based on CD83 expression, GM3, but not pSTAT3, appeared to be involved in tumor-induced DC suppression. pSTAT3 expression was not associated with MVD, while GM3 might play an anti-angiogenic role. Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of transcription (STAT)-3 are implicated in these processes. As both are considered as novel therapeutic targets, we assessed the possible association of ganglioside GM3 expression and STAT3 activation with suppression of dendritic cell (DC) activation and angiogenesis in non-small cell lung cancer (NSCLC).BACKGROUNDTumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of transcription (STAT)-3 are implicated in these processes. As both are considered as novel therapeutic targets, we assessed the possible association of ganglioside GM3 expression and STAT3 activation with suppression of dendritic cell (DC) activation and angiogenesis in non-small cell lung cancer (NSCLC).Immunohistochemistry was performed on a tissue array to determine N-glycolyl GM3 (GM3) and phosphorylated STAT3 (pSTAT3) expression in 176 primary NSCLC resections. Median values of GM3 and pSTAT3 expression were used as cut off. Microvessel density (MVD) was determined by CD34 staining and morphology. CD1a and CD83 were used to determine infiltrating immature and mature dendritic cells, respectively.METHODSImmunohistochemistry was performed on a tissue array to determine N-glycolyl GM3 (GM3) and phosphorylated STAT3 (pSTAT3) expression in 176 primary NSCLC resections. Median values of GM3 and pSTAT3 expression were used as cut off. Microvessel density (MVD) was determined by CD34 staining and morphology. CD1a and CD83 were used to determine infiltrating immature and mature dendritic cells, respectively.94% and 71% of the NSCLC samples expressed GM3 and nuclear pSTAT3, respectively. Median overall survival was 40.0 months. Both low GM3 expression and high pSTAT3 expression were associated with a worse survival, which reached near significance for GM3 (P = 0.08). Microvessel density (MVD), determined by CD34 staining and morphology, was lower in NSCLC samples with high GM3 expression. CD1a+ cells (immature DCs) were more frequent in NSCLC tissues as compared to peritumoral lung tissue, while CD83+ cells (mature DCs) were more frequent in peritumoral lung tissue. CD83+ DCs were less frequent in NSCLC tissues with high GM3 expression.RESULTS94% and 71% of the NSCLC samples expressed GM3 and nuclear pSTAT3, respectively. Median overall survival was 40.0 months. Both low GM3 expression and high pSTAT3 expression were associated with a worse survival, which reached near significance for GM3 (P = 0.08). Microvessel density (MVD), determined by CD34 staining and morphology, was lower in NSCLC samples with high GM3 expression. CD1a+ cells (immature DCs) were more frequent in NSCLC tissues as compared to peritumoral lung tissue, while CD83+ cells (mature DCs) were more frequent in peritumoral lung tissue. CD83+ DCs were less frequent in NSCLC tissues with high GM3 expression.GM3 and pSTAT3 are widely expressed in NSCLC. Based on CD83 expression, GM3, but not pSTAT3, appeared to be involved in tumor-induced DC suppression. pSTAT3 expression was not associated with MVD, while GM3 might play an anti-angiogenic role.CONCLUSIONGM3 and pSTAT3 are widely expressed in NSCLC. Based on CD83 expression, GM3, but not pSTAT3, appeared to be involved in tumor-induced DC suppression. pSTAT3 expression was not associated with MVD, while GM3 might play an anti-angiogenic role. Abstract Background Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of transcription (STAT)-3 are implicated in these processes. As both are considered as novel therapeutic targets, we assessed the possible association of ganglioside GM3 expression and STAT3 activation with suppression of dendritic cell (DC) activation and angiogenesis in non-small cell lung cancer (NSCLC). Methods Immunohistochemistry was performed on a tissue array to determine N-glycolyl GM3 (GM3) and phosphorylated STAT3 (pSTAT3) expression in 176 primary NSCLC resections. Median values of GM3 and pSTAT3 expression were used as cut off. Microvessel density (MVD) was determined by CD34 staining and morphology. CD1a and CD83 were used to determine infiltrating immature and mature dendritic cells, respectively. Results 94% and 71% of the NSCLC samples expressed GM3 and nuclear pSTAT3, respectively. Median overall survival was 40.0 months. Both low GM3 expression and high pSTAT3 expression were associated with a worse survival, which reached near significance for GM3 (P = 0.08). Microvessel density (MVD), determined by CD34 staining and morphology, was lower in NSCLC samples with high GM3 expression. CD1a+ cells (immature DCs) were more frequent in NSCLC tissues as compared to peritumoral lung tissue, while CD83+ cells (mature DCs) were more frequent in peritumoral lung tissue. CD83+ DCs were less frequent in NSCLC tissues with high GM3 expression. Conclusion GM3 and pSTAT3 are widely expressed in NSCLC. Based on CD83 expression, GM3, but not pSTAT3, appeared to be involved in tumor-induced DC suppression. pSTAT3 expression was not associated with MVD, while GM3 might play an anti-angiogenic role. Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of transcription (STAT)-3 are implicated in these processes. As both are considered as novel therapeutic targets, we assessed the possible association of ganglioside GM3 expression and STAT3 activation with suppression of dendritic cell (DC) activation and angiogenesis in non-small cell lung cancer (NSCLC). Immunohistochemistry was performed on a tissue array to determine N-glycolyl GM3 (GM3) and phosphorylated STAT3 (pSTAT3) expression in 176 primary NSCLC resections. Median values of GM3 and pSTAT3 expression were used as cut off. Microvessel density (MVD) was determined by CD34 staining and morphology. CD1a and CD83 were used to determine infiltrating immature and mature dendritic cells, respectively. 94% and 71% of the NSCLC samples expressed GM3 and nuclear pSTAT3, respectively. Median overall survival was 40.0 months. Both low GM3 expression and high pSTAT3 expression were associated with a worse survival, which reached near significance for GM3 (P = 0.08). Microvessel density (MVD), determined by CD34 staining and morphology, was lower in NSCLC samples with high GM3 expression. CD1a+ cells (immature DCs) were more frequent in NSCLC tissues as compared to peritumoral lung tissue, while CD83+ cells (mature DCs) were more frequent in peritumoral lung tissue. CD83+ DCs were less frequent in NSCLC tissues with high GM3 expression. GM3 and pSTAT3 are widely expressed in NSCLC. Based on CD83 expression, GM3, but not pSTAT3, appeared to be involved in tumor-induced DC suppression. pSTAT3 expression was not associated with MVD, while GM3 might play an anti-angiogenic role. Background Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of transcription (STAT)-3 are implicated in these processes. As both are considered as novel therapeutic targets, we assessed the possible association of ganglioside GM3 expression and STAT3 activation with suppression of dendritic cell (DC) activation and angiogenesis in non-small cell lung cancer (NSCLC). Methods Immunohistochemistry was performed on a tissue array to determine N -glycolyl GM3 (GM3) and phosphorylated STAT3 (pSTAT3) expression in 176 primary NSCLC resections. Median values of GM3 and pSTAT3 expression were used as cut off. Microvessel density (MVD) was determined by CD34 staining and morphology. CD1a and CD83 were used to determine infiltrating immature and mature dendritic cells, respectively. Results 94% and 71% of the NSCLC samples expressed GM3 and nuclear pSTAT3, respectively. Median overall survival was 40.0 months. Both low GM3 expression and high pSTAT3 expression were associated with a worse survival, which reached near significance for GM3 ( P = 0.08). Microvessel density (MVD), determined by CD34 staining and morphology, was lower in NSCLC samples with high GM3 expression. CD1a + cells (immature DCs) were more frequent in NSCLC tissues as compared to peritumoral lung tissue, while CD83 + cells (mature DCs) were more frequent in peritumoral lung tissue. CD83 + DCs were less frequent in NSCLC tissues with high GM3 expression. Conclusion GM3 and pSTAT3 are widely expressed in NSCLC. Based on CD83 expression, GM3, but not pSTAT3, appeared to be involved in tumor-induced DC suppression. pSTAT3 expression was not associated with MVD, while GM3 might play an anti-angiogenic role.
ArticleNumber	180
Audience	Academic
Author	van Cruijsen, Hester de Gruijl, Tanja D Giaccone, Giuseppe van der Valk, Paul Ruiz, Mariëlle Gallegos
AuthorAffiliation	2 Department of Pathology, VU University Medical Center, Boelelaan 1117, 1081 HV Amsterdam, The Netherlands 3 Medical Oncology Branch, CCR, National Cancer Institute, NIH, Bethesda, MD 20892-1906, USA 1 Department of Medical Oncology, VU University Medical Center, Boelelaan 1117, 1081 HV Amsterdam, The Netherlands
AuthorAffiliation_xml	– name: 1 Department of Medical Oncology, VU University Medical Center, Boelelaan 1117, 1081 HV Amsterdam, The Netherlands – name: 2 Department of Pathology, VU University Medical Center, Boelelaan 1117, 1081 HV Amsterdam, The Netherlands – name: 3 Medical Oncology Branch, CCR, National Cancer Institute, NIH, Bethesda, MD 20892-1906, USA
Author_xml	– sequence: 1 givenname: Hester surname: van Cruijsen fullname: van Cruijsen, Hester organization: Department of Medical Oncology, VU University Medical Center – sequence: 2 givenname: Mariëlle Gallegos surname: Ruiz fullname: Ruiz, Mariëlle Gallegos organization: Department of Medical Oncology, VU University Medical Center – sequence: 3 givenname: Paul surname: van der Valk fullname: van der Valk, Paul organization: Department of Pathology, VU University Medical Center – sequence: 4 givenname: Tanja D surname: de Gruijl fullname: de Gruijl, Tanja D organization: Department of Medical Oncology, VU University Medical Center – sequence: 5 givenname: Giuseppe surname: Giaccone fullname: Giaccone, Giuseppe email: giacconeg@mail.nih.gov organization: Department of Medical Oncology, VU University Medical Center, Medical Oncology Branch, CCR, National Cancer Institute, NIH
BackLink	https://www.ncbi.nlm.nih.gov/pubmed/19519895$$D View this record in MEDLINE/PubMed
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Keywords	Vascular Endothelial Growth Factor pSTAT3 Expression NSCLC Patient NSCLC Tissue NSCLC Sample
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Snippet	Background Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of... Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of transcription... Background Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of... Abstract Background Tumor immune escape and angiogenesis contribute to tumor progression, and gangliosides and activation of signal transducer and activator of...
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StartPage	180
SubjectTerms	Biomedical and Life Sciences Biomedicine Cancer Research Carcinoma, Non-Small-Cell Lung - blood supply Carcinoma, Non-Small-Cell Lung - immunology Dendritic cells Dendritic Cells - immunology Dendritic Cells - pathology Female G(M3) Ganglioside - biosynthesis G(M3) Ganglioside - immunology Genetic aspects Genetic transcription Health Promotion and Disease Prevention Humans Immunohistochemistry Lung cancer, Non-small cell Lung Neoplasms - blood supply Lung Neoplasms - immunology Male Medicine/Public Health Microvessels - immunology Microvessels - pathology Middle Aged Neovascularization, Pathologic - immunology Neovascularization, Pathologic - pathology Oncology Physiological aspects Research Article Risk factors STAT3 Transcription Factor - biosynthesis STAT3 Transcription Factor - immunology Surgical Oncology Tissue Array Analysis Tissue microarrays
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Title	Tissue micro array analysis of ganglioside N-glycolyl GM3 expression and signal transducer and activator of transcription (STAT)-3 activation in relation to dendritic cell infiltration and microvessel density in non-small cell lung cancer
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