Up-Regulation of Endothelial Delta-like 4 Expression Correlates with Vessel Maturation in Bladder Cancer
Purpose: Angiogenesis and vascular endothelial growth factor (VEGF) expression are associated with a poor outcome in bladder cancer. To understand more about the mechanisms, we studied the role of delta-like 4 (DLL4), an endothelial-specific ligand of the Notch signaling pathway, in bladder cancer a...
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Published in | Clinical cancer research Vol. 12; no. 16; pp. 4836 - 4844 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Philadelphia, PA
American Association for Cancer Research
15.08.2006
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Abstract | Purpose: Angiogenesis and vascular endothelial growth factor (VEGF) expression are associated with a poor outcome in bladder cancer.
To understand more about the mechanisms, we studied the role of delta-like 4 (DLL4), an endothelial-specific ligand of the
Notch signaling pathway, in bladder cancer angiogenesis.
Experimental Design: The expression of DLL4, CD34, and VEGF were studied in a cohort of 60 bladder tumors and 10 normal samples using quantitative
PCR. In situ hybridization was used to study the pattern of DLL4 expression in 22 tumor and 9 normal samples. Serial sections were also
stained for CD34 and α-smooth muscle actin (α-SMA) using conventional immunohistochemistry.
Results: The expression of DLL4 was significantly up-regulated in superficial ( P < 0.01) and invasive ( P < 0.05) bladder cancers. DLL4 expression significantly correlated with CD34 ( P < 0.001) and VEGF ( P < 0.001) expression. The in situ hybridization studies showed that DLL4 was highly expressed within bladder tumor vasculature. Additionally, DLL4 expression
significantly correlated with vessel maturation as judged by periendothelial cell expression of α-SMA, 98.7% of DLL4-positive
tumor vessels coexpressed α-SMA, compared with 64.5% of DLL4-negative tumor vessels ( P < 0.001). High DLL4 expression may have prognostic value in superficial and invasive bladder.
Conclusion: DLL4 expression is associated with vascular differentiation in bladder cancer; thus, targeting DLL4 may be a novel antiangiogenic
therapy. |
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AbstractList | Purpose: Angiogenesis and vascular endothelial growth factor (VEGF) expression are associated with a poor outcome in bladder cancer. To understand more about the mechanisms, we studied the role of delta-like 4 (DLL4), an endothelial-specific ligand of the Notch signaling pathway, in bladder cancer angiogenesis.
Experimental Design: The expression of DLL4, CD34, and VEGF were studied in a cohort of 60 bladder tumors and 10 normal samples using quantitative PCR. In situ hybridization was used to study the pattern of DLL4 expression in 22 tumor and 9 normal samples. Serial sections were also stained for CD34 and α-smooth muscle actin (α-SMA) using conventional immunohistochemistry.
Results: The expression of DLL4 was significantly up-regulated in superficial (P < 0.01) and invasive (P < 0.05) bladder cancers. DLL4 expression significantly correlated with CD34 (P < 0.001) and VEGF (P < 0.001) expression. The in situ hybridization studies showed that DLL4 was highly expressed within bladder tumor vasculature. Additionally, DLL4 expression significantly correlated with vessel maturation as judged by periendothelial cell expression of α-SMA, 98.7% of DLL4-positive tumor vessels coexpressed α-SMA, compared with 64.5% of DLL4-negative tumor vessels (P < 0.001). High DLL4 expression may have prognostic value in superficial and invasive bladder.
Conclusion: DLL4 expression is associated with vascular differentiation in bladder cancer; thus, targeting DLL4 may be a novel antiangiogenic therapy. PURPOSEAngiogenesis and vascular endothelial growth factor (VEGF) expression are associated with a poor outcome in bladder cancer. To understand more about the mechanisms, we studied the role of delta-like 4 (DLL4), an endothelial-specific ligand of the Notch signaling pathway, in bladder cancer angiogenesis.EXPERIMENTAL DESIGNThe expression of DLL4, CD34, and VEGF were studied in a cohort of 60 bladder tumors and 10 normal samples using quantitative PCR. In situ hybridization was used to study the pattern of DLL4 expression in 22 tumor and 9 normal samples. Serial sections were also stained for CD34 and alpha-smooth muscle actin (alpha-SMA) using conventional immunohistochemistry.RESULTSThe expression of DLL4 was significantly up-regulated in superficial (P < 0.01) and invasive (P < 0.05) bladder cancers. DLL4 expression significantly correlated with CD34 (P < 0.001) and VEGF (P < 0.001) expression. The in situ hybridization studies showed that DLL4 was highly expressed within bladder tumor vasculature. Additionally, DLL4 expression significantly correlated with vessel maturation as judged by periendothelial cell expression of alpha-SMA, 98.7% of DLL4-positive tumor vessels coexpressed alpha-SMA, compared with 64.5% of DLL4-negative tumor vessels (P < 0.001). High DLL4 expression may have prognostic value in superficial and invasive bladder.CONCLUSIONDLL4 expression is associated with vascular differentiation in bladder cancer; thus, targeting DLL4 may be a novel antiangiogenic therapy. Purpose: Angiogenesis and vascular endothelial growth factor (VEGF) expression are associated with a poor outcome in bladder cancer. To understand more about the mechanisms, we studied the role of delta-like 4 (DLL4), an endothelial-specific ligand of the Notch signaling pathway, in bladder cancer angiogenesis. Experimental Design: The expression of DLL4, CD34, and VEGF were studied in a cohort of 60 bladder tumors and 10 normal samples using quantitative PCR. In situ hybridization was used to study the pattern of DLL4 expression in 22 tumor and 9 normal samples. Serial sections were also stained for CD34 and α-smooth muscle actin (α-SMA) using conventional immunohistochemistry. Results: The expression of DLL4 was significantly up-regulated in superficial ( P < 0.01) and invasive ( P < 0.05) bladder cancers. DLL4 expression significantly correlated with CD34 ( P < 0.001) and VEGF ( P < 0.001) expression. The in situ hybridization studies showed that DLL4 was highly expressed within bladder tumor vasculature. Additionally, DLL4 expression significantly correlated with vessel maturation as judged by periendothelial cell expression of α-SMA, 98.7% of DLL4-positive tumor vessels coexpressed α-SMA, compared with 64.5% of DLL4-negative tumor vessels ( P < 0.001). High DLL4 expression may have prognostic value in superficial and invasive bladder. Conclusion: DLL4 expression is associated with vascular differentiation in bladder cancer; thus, targeting DLL4 may be a novel antiangiogenic therapy. Angiogenesis and vascular endothelial growth factor (VEGF) expression are associated with a poor outcome in bladder cancer. To understand more about the mechanisms, we studied the role of delta-like 4 (DLL4), an endothelial-specific ligand of the Notch signaling pathway, in bladder cancer angiogenesis. The expression of DLL4, CD34, and VEGF were studied in a cohort of 60 bladder tumors and 10 normal samples using quantitative PCR. In situ hybridization was used to study the pattern of DLL4 expression in 22 tumor and 9 normal samples. Serial sections were also stained for CD34 and alpha-smooth muscle actin (alpha-SMA) using conventional immunohistochemistry. The expression of DLL4 was significantly up-regulated in superficial (P < 0.01) and invasive (P < 0.05) bladder cancers. DLL4 expression significantly correlated with CD34 (P < 0.001) and VEGF (P < 0.001) expression. The in situ hybridization studies showed that DLL4 was highly expressed within bladder tumor vasculature. Additionally, DLL4 expression significantly correlated with vessel maturation as judged by periendothelial cell expression of alpha-SMA, 98.7% of DLL4-positive tumor vessels coexpressed alpha-SMA, compared with 64.5% of DLL4-negative tumor vessels (P < 0.001). High DLL4 expression may have prognostic value in superficial and invasive bladder. DLL4 expression is associated with vascular differentiation in bladder cancer; thus, targeting DLL4 may be a novel antiangiogenic therapy. |
Author | Mark Rochester Richard Poulsom Karena Le Monnier Adrian L. Harris Nilay S. Patel David W. Cranston Ji-Liang Li Michael S. Dobbie Graham Steers |
Author_xml | – sequence: 1 givenname: Nilay S surname: PATEL fullname: PATEL, Nilay S organization: Growth Factor Group. Cancer Research UK, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, United Kingdom – sequence: 2 givenname: Michael S surname: DOBBIE fullname: DOBBIE, Michael S organization: Growth Factor Group. Cancer Research UK, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, United Kingdom – sequence: 3 givenname: Mark surname: ROCHESTER fullname: ROCHESTER, Mark organization: Growth Factor Group. Cancer Research UK, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, United Kingdom – sequence: 4 givenname: Graham surname: STEERS fullname: STEERS, Graham organization: Growth Factor Group. Cancer Research UK, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, United Kingdom – sequence: 5 givenname: Richard surname: POULSOM fullname: POULSOM, Richard organization: In-situ Hybridization Service, Cancer Research UK London Research Institute, London, United Kingdom – sequence: 6 givenname: Karena surname: LE MONNIER fullname: LE MONNIER, Karena organization: Department of Urology, Churchill Hospital, University of Oxford, Oxford, United Kingdom – sequence: 7 givenname: David W surname: CRANSTON fullname: CRANSTON, David W organization: Department of Urology, Churchill Hospital, University of Oxford, Oxford, United Kingdom – sequence: 8 givenname: Ji-Liang surname: LI fullname: LI, Ji-Liang organization: Growth Factor Group. Cancer Research UK, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, United Kingdom – sequence: 9 givenname: Adrian L surname: HARRIS fullname: HARRIS, Adrian L organization: Growth Factor Group. Cancer Research UK, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, United Kingdom |
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Keywords | Endothelial cell Urinary system disease Blood vessel Bladder disease Circulatory system Malignant tumor Urinary tract disease Gene expression Bladder cancer Endothelium |
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Snippet | Purpose: Angiogenesis and vascular endothelial growth factor (VEGF) expression are associated with a poor outcome in bladder cancer.
To understand more about... Angiogenesis and vascular endothelial growth factor (VEGF) expression are associated with a poor outcome in bladder cancer. To understand more about the... Purpose: Angiogenesis and vascular endothelial growth factor (VEGF) expression are associated with a poor outcome in bladder cancer. To understand more about... PURPOSEAngiogenesis and vascular endothelial growth factor (VEGF) expression are associated with a poor outcome in bladder cancer. To understand more about the... |
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SubjectTerms | Actins - biosynthesis Actins - genetics Adult Aged Aged, 80 and over angiogenesis Antigens, CD34 - biosynthesis Antigens, CD34 - genetics Antineoplastic agents Biological and medical sciences bladder cancer Carcinoma, Transitional Cell - blood supply Carcinoma, Transitional Cell - genetics Carcinoma, Transitional Cell - metabolism Cohort Studies Female Humans Immunohistochemistry Intercellular Signaling Peptides and Proteins - biosynthesis Intercellular Signaling Peptides and Proteins - genetics Male Medical sciences Middle Aged Neovascularization, Pathologic - genetics Neovascularization, Pathologic - metabolism Nephrology. Urinary tract diseases Notch Pharmacology. Drug treatments Polymerase Chain Reaction Prognosis Tumors of the urinary system Up-Regulation Urinary Bladder Neoplasms - blood supply Urinary Bladder Neoplasms - genetics Urinary Bladder Neoplasms - metabolism Urinary system involvement in other diseases. Miscellaneous Urinary tract. Prostate gland Vascular Endothelial Growth Factor A - biosynthesis Vascular Endothelial Growth Factor A - genetics |
Title | Up-Regulation of Endothelial Delta-like 4 Expression Correlates with Vessel Maturation in Bladder Cancer |
URI | http://clincancerres.aacrjournals.org/content/12/16/4836.abstract https://www.ncbi.nlm.nih.gov/pubmed/16914569 https://search.proquest.com/docview/68752668 |
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