Tumour‐associated macrophages correlate with microvascular bed extension in colorectal cancer patients
Tumour‐associated macrophages (TAMs) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and invasion. In colorectal cancer (CRC), there are no conclusive data about the role of TAMs in angiogenesis‐mediated tumour progression. In this study, we aimed t...
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| Published in | Journal of cellular and molecular medicine Vol. 20; no. 7; pp. 1373 - 1380 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
John Wiley & Sons, Inc
01.07.2016
John Wiley and Sons Inc |
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| Online Access | Get full text |
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| Abstract | Tumour‐associated macrophages (TAMs) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and invasion. In colorectal cancer (CRC), there are no conclusive data about the role of TAMs in angiogenesis‐mediated tumour progression. In this study, we aimed to evaluate a correlation between TAMs, TAM immunostained area (TAMIA) microvascular density (MVD), endothelial area (EA) and cancer cells positive to VEGF‐A (CCP‐VEGF‐A) in primary tumour tissue of locally advanced CRC patients undergone to radical surgery. A series of 76 patients with CRC were selected and evaluated by immunohistochemistry and image analysis. An anti‐CD68 antibody was employed to assess TAMs and TAMIA expression, an anti‐CD34 antibody was utilized to detect MVD and EA expression, whereas an anti‐VEGF‐A antibody was used to detect CCP‐VEGF‐A; then, tumour sections were evaluated by image analysis methods. The mean ± S.D. of TAMs, MVD and CCP‐VEGF‐A was 65.58 ± 21.14, 28.53 ± 7.75 and 63% ± 37%, respectively; the mean ± S.D. of TAMIA and EA was 438.37 ± 124.14μ2 and 186.73 ± 67.22μ2, respectively. A significant correlation was found between TAMs, TAMIA, MVD and EA each other (r ranging from 0.69 to 0.84; P ranging from 0.000 to 0.004). The high level of expression of TAMs and TAMIA in tumour tissue and the significant correlation with both MVD and EA illustrate that TAMs could represent a marker that plays an important role in promoting angiogenesis‐mediated CRC. In this context, novel agents killing TAMs might be evaluated in clinical trials as a new anti‐angiogenic approach. |
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| AbstractList | Tumour‐associated macrophages (TAMs) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and invasion. In colorectal cancer (CRC), there are no conclusive data about the role of TAMs in angiogenesis‐mediated tumour progression. In this study, we aimed to evaluate a correlation between TAMs, TAM immunostained area (TAMIA) microvascular density (MVD), endothelial area (EA) and cancer cells positive to VEGF‐A (CCP‐VEGF‐A) in primary tumour tissue of locally advanced CRC patients undergone to radical surgery. A series of 76 patients with CRC were selected and evaluated by immunohistochemistry and image analysis. An anti‐CD68 antibody was employed to assess TAMs and TAMIA expression, an anti‐CD34 antibody was utilized to detect MVD and EA expression, whereas an anti‐VEGF‐A antibody was used to detect CCP‐VEGF‐A; then, tumour sections were evaluated by image analysis methods. The mean ± S.D. of TAMs, MVD and CCP‐VEGF‐A was 65.58 ± 21.14, 28.53 ± 7.75 and 63% ± 37%, respectively; the mean ± S.D. of TAMIA and EA was 438.37 ± 124.14μ2 and 186.73 ± 67.22μ2, respectively. A significant correlation was found between TAMs, TAMIA, MVD and EA each other (r ranging from 0.69 to 0.84; P ranging from 0.000 to 0.004). The high level of expression of TAMs and TAMIA in tumour tissue and the significant correlation with both MVD and EA illustrate that TAMs could represent a marker that plays an important role in promoting angiogenesis‐mediated CRC. In this context, novel agents killing TAMs might be evaluated in clinical trials as a new anti‐angiogenic approach. Tumour-associated macrophages (TAMs) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and invasion. In colorectal cancer (CRC), there are no conclusive data about the role of TAMs in angiogenesis-mediated tumour progression. In this study, we aimed to evaluate a correlation between TAMs, TAM immunostained area (TAMIA) microvascular density (MVD), endothelial area (EA) and cancer cells positive to VEGF-A (CCP-VEGF-A) in primary tumour tissue of locally advanced CRC patients undergone to radical surgery. A series of 76 patients with CRC were selected and evaluated by immunohistochemistry and image analysis. An anti-CD68 antibody was employed to assess TAMs and TAMIA expression, an anti-CD34 antibody was utilized to detect MVD and EA expression, whereas an anti-VEGF-A antibody was used to detect CCP-VEGF-A; then, tumour sections were evaluated by image analysis methods. The mean ± S.D. of TAMs, MVD and CCP-VEGF-A was 65.58 ± 21.14, 28.53 ± 7.75 and 63% ± 37%, respectively; the mean ± S.D. of TAMIA and EA was 438.37 ± 124.14μ(2) and 186.73 ± 67.22μ(2) , respectively. A significant correlation was found between TAMs, TAMIA, MVD and EA each other (r ranging from 0.69 to 0.84; P ranging from 0.000 to 0.004). The high level of expression of TAMs and TAMIA in tumour tissue and the significant correlation with both MVD and EA illustrate that TAMs could represent a marker that plays an important role in promoting angiogenesis-mediated CRC. In this context, novel agents killing TAMs might be evaluated in clinical trials as a new anti-angiogenic approach. Abstract Tumour‐associated macrophages ( TAM s) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and invasion. In colorectal cancer ( CRC ), there are no conclusive data about the role of TAM s in angiogenesis‐mediated tumour progression. In this study, we aimed to evaluate a correlation between TAM s, TAM immunostained area ( TAMIA ) microvascular density ( MVD ), endothelial area ( EA ) and cancer cells positive to VEGF ‐A ( CCP ‐ VEGF ‐A) in primary tumour tissue of locally advanced CRC patients undergone to radical surgery. A series of 76 patients with CRC were selected and evaluated by immunohistochemistry and image analysis. An anti‐ CD 68 antibody was employed to assess TAM s and TAMIA expression, an anti‐ CD 34 antibody was utilized to detect MVD and EA expression, whereas an anti‐ VEGF ‐A antibody was used to detect CCP ‐ VEGF ‐A; then, tumour sections were evaluated by image analysis methods. The mean ± S.D. of TAM s, MVD and CCP ‐ VEGF ‐A was 65.58 ± 21.14, 28.53 ± 7.75 and 63% ± 37%, respectively; the mean ± S.D. of TAMIA and EA was 438.37 ± 124.14μ 2 and 186.73 ± 67.22μ 2 , respectively. A significant correlation was found between TAM s, TAMIA , MVD and EA each other ( r ranging from 0.69 to 0.84; P ranging from 0.000 to 0.004). The high level of expression of TAM s and TAMIA in tumour tissue and the significant correlation with both MVD and EA illustrate that TAM s could represent a marker that plays an important role in promoting angiogenesis‐mediated CRC . In this context, novel agents killing TAM s might be evaluated in clinical trials as a new anti‐angiogenic approach. Tumour‐associated macrophages ( TAM s) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and invasion. In colorectal cancer ( CRC ), there are no conclusive data about the role of TAM s in angiogenesis‐mediated tumour progression. In this study, we aimed to evaluate a correlation between TAM s, TAM immunostained area ( TAMIA ) microvascular density ( MVD ), endothelial area ( EA ) and cancer cells positive to VEGF ‐A ( CCP ‐ VEGF ‐A) in primary tumour tissue of locally advanced CRC patients undergone to radical surgery. A series of 76 patients with CRC were selected and evaluated by immunohistochemistry and image analysis. An anti‐ CD 68 antibody was employed to assess TAM s and TAMIA expression, an anti‐ CD 34 antibody was utilized to detect MVD and EA expression, whereas an anti‐ VEGF ‐A antibody was used to detect CCP ‐ VEGF ‐A; then, tumour sections were evaluated by image analysis methods. The mean ± S.D. of TAM s, MVD and CCP ‐ VEGF ‐A was 65.58 ± 21.14, 28.53 ± 7.75 and 63% ± 37%, respectively; the mean ± S.D. of TAMIA and EA was 438.37 ± 124.14μ 2 and 186.73 ± 67.22μ 2 , respectively. A significant correlation was found between TAM s, TAMIA , MVD and EA each other ( r ranging from 0.69 to 0.84; P ranging from 0.000 to 0.004). The high level of expression of TAM s and TAMIA in tumour tissue and the significant correlation with both MVD and EA illustrate that TAM s could represent a marker that plays an important role in promoting angiogenesis‐mediated CRC . In this context, novel agents killing TAM s might be evaluated in clinical trials as a new anti‐angiogenic approach. Tumour‐associated macrophages (TAMs) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and invasion. In colorectal cancer (CRC), there are no conclusive data about the role of TAMs in angiogenesis‐mediated tumour progression. In this study, we aimed to evaluate a correlation between TAMs, TAM immunostained area (TAMIA) microvascular density (MVD), endothelial area (EA) and cancer cells positive to VEGF‐A (CCP‐VEGF‐A) in primary tumour tissue of locally advanced CRC patients undergone to radical surgery. A series of 76 patients with CRC were selected and evaluated by immunohistochemistry and image analysis. An anti‐CD68 antibody was employed to assess TAMs and TAMIA expression, an anti‐CD34 antibody was utilized to detect MVD and EA expression, whereas an anti‐VEGF‐A antibody was used to detect CCP‐VEGF‐A; then, tumour sections were evaluated by image analysis methods. The mean ± S.D. of TAMs, MVD and CCP‐VEGF‐A was 65.58 ± 21.14, 28.53 ± 7.75 and 63% ± 37%, respectively; the mean ± S.D. of TAMIA and EA was 438.37 ± 124.14μ2 and 186.73 ± 67.22μ2, respectively. A significant correlation was found between TAMs, TAMIA, MVD and EA each other (r ranging from 0.69 to 0.84; P ranging from 0.000 to 0.004). The high level of expression of TAMs and TAMIA in tumour tissue and the significant correlation with both MVD and EA illustrate that TAMs could represent a marker that plays an important role in promoting angiogenesis‐mediated CRC. In this context, novel agents killing TAMs might be evaluated in clinical trials as a new anti‐angiogenic approach. |
| Author | Luposella, Maria Sacco, Rosario Russo, Emilio Ammendola, Michele Zuccalà, Valeria Porcelli, Mariangela Zizzo, Nicola Ranieri, Girolamo Leporini, Christian Sammarco, Giuseppe Patruno, Rosa De Sarro, Giovambattista Filippelli, Gianfranco Marech, Ilaria Gadaleta, Cosmo Damiano |
| AuthorAffiliation | 1 Diagnostic and Interventional Radiology Unit with Integrated Section of Translational Medical Oncology National Cancer Research Centre, ‘Giovanni Paolo II’ Bari Italy 2 Chair of Clinical Surgery University of Catanzaro ‘Magna Graecia’ Medical School Catanzaro Italy 3 Chair of Pathology University of Bari Valenzano Italy 5 Medical Oncology Unit ‘S. Francesco di Paola’ Hospital Cosenza Italy 4 Department of Health Science Clinical Pharmacology and Pharmacovigilance Unit and Pharmacovigilance's Centre Calabria Region University of Catanzaro ‘Magna Graecia’ Medical School Catanzaro Italy |
| AuthorAffiliation_xml | – name: 1 Diagnostic and Interventional Radiology Unit with Integrated Section of Translational Medical Oncology National Cancer Research Centre, ‘Giovanni Paolo II’ Bari Italy – name: 5 Medical Oncology Unit ‘S. Francesco di Paola’ Hospital Cosenza Italy – name: 3 Chair of Pathology University of Bari Valenzano Italy – name: 4 Department of Health Science Clinical Pharmacology and Pharmacovigilance Unit and Pharmacovigilance's Centre Calabria Region University of Catanzaro ‘Magna Graecia’ Medical School Catanzaro Italy – name: 2 Chair of Clinical Surgery University of Catanzaro ‘Magna Graecia’ Medical School Catanzaro Italy |
| Author_xml | – sequence: 1 givenname: Ilaria surname: Marech fullname: Marech, Ilaria organization: National Cancer Research Centre, ‘Giovanni Paolo II’ – sequence: 2 givenname: Michele surname: Ammendola fullname: Ammendola, Michele organization: University of Catanzaro ‘Magna Graecia’ Medical School – sequence: 3 givenname: Rosario surname: Sacco fullname: Sacco, Rosario organization: University of Catanzaro ‘Magna Graecia’ Medical School – sequence: 4 givenname: Giuseppe surname: Sammarco fullname: Sammarco, Giuseppe organization: University of Catanzaro ‘Magna Graecia’ Medical School – sequence: 5 givenname: Valeria surname: Zuccalà fullname: Zuccalà, Valeria organization: University of Catanzaro ‘Magna Graecia’ Medical School – sequence: 6 givenname: Nicola surname: Zizzo fullname: Zizzo, Nicola organization: University of Bari – sequence: 7 givenname: Christian surname: Leporini fullname: Leporini, Christian organization: University of Catanzaro ‘Magna Graecia’ Medical School – sequence: 8 givenname: Maria surname: Luposella fullname: Luposella, Maria organization: University of Catanzaro ‘Magna Graecia’ Medical School – sequence: 9 givenname: Rosa surname: Patruno fullname: Patruno, Rosa organization: University of Bari – sequence: 10 givenname: Gianfranco surname: Filippelli fullname: Filippelli, Gianfranco organization: Medical Oncology Unit ‘S. Francesco di Paola’ Hospital – sequence: 11 givenname: Emilio surname: Russo fullname: Russo, Emilio organization: University of Catanzaro ‘Magna Graecia’ Medical School – sequence: 12 givenname: Mariangela surname: Porcelli fullname: Porcelli, Mariangela organization: National Cancer Research Centre, ‘Giovanni Paolo II’ – sequence: 13 givenname: Cosmo Damiano surname: Gadaleta fullname: Gadaleta, Cosmo Damiano organization: National Cancer Research Centre, ‘Giovanni Paolo II’ – sequence: 14 givenname: Giovambattista surname: De Sarro fullname: De Sarro, Giovambattista organization: University of Catanzaro ‘Magna Graecia’ Medical School – sequence: 15 givenname: Girolamo surname: Ranieri fullname: Ranieri, Girolamo organization: National Cancer Research Centre, ‘Giovanni Paolo II’ |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/27105577$$D View this record in MEDLINE/PubMed |
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| ContentType | Journal Article |
| Copyright | 2016 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. 2016. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. |
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| DOI | 10.1111/jcmm.12826 |
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| Keywords | tumour-associated macrophages colorectal cancer angiogenesis novel anti-angiogenic approach |
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| Snippet | Tumour‐associated macrophages (TAMs) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and invasion. In... Tumour-associated macrophages (TAMs) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and invasion. In... Abstract Tumour‐associated macrophages ( TAM s) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and... Tumour‐associated macrophages ( TAM s) represent pivotal components of tumour microenvironment promoting angiogenesis, tumour progression and invasion. In... |
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| StartPage | 1373 |
| SubjectTerms | Angiogenesis Biomarkers Cancer CD34 antigen Clinical trials Colorectal cancer Colorectal carcinoma Colorectal Neoplasms - blood supply Colorectal Neoplasms - pathology Endothelial Cells - pathology Ethics Female Growth factors Humans Hypoxia Image detection Image processing Immunohistochemistry Lymphatic system Macrophages Macrophages - pathology Male Metastasis Microvasculature Microvessels - pathology Neovascularization, Pathologic - pathology novel anti‐angiogenic approach Original Patients Studies Surgery Tumor microenvironment Tumor necrosis factor-TNF Tumors tumour‐associated macrophages Vascular endothelial growth factor Vascular Endothelial Growth Factor A - metabolism |
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| Title | Tumour‐associated macrophages correlate with microvascular bed extension in colorectal cancer patients |
| URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fjcmm.12826 https://www.ncbi.nlm.nih.gov/pubmed/27105577 https://www.proquest.com/docview/2290725510/abstract/ https://search.proquest.com/docview/1801425276 https://pubmed.ncbi.nlm.nih.gov/PMC4929299 |
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