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Expression of the VEGF and angiopoietin genes in endometrial atypical hyperplasia and endometrial cancer.

Holland CM, Day K, Evans A, Smith SK - Br. J. Cancer (2003)

Bottom Line: Angiogenesis is critical for the growth and metastasis of endometrial cancer and is therefore an important therapeutic target.Vascular endothelial growth factor-A (VEGF-A) is a key molecule in angiogenesis, but the identification of related molecules and the angiopoietins suggests a more complex picture.We confirmed the presence of VEGF-A mRNA in the epithelial cells of cancers examined (13 out of 13), but not in benign endometrium or ACH.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB1 1QP, UK. cath.holland@obgyn.cam.ac.uk

ABSTRACT
Angiogenesis is critical for the growth and metastasis of endometrial cancer and is therefore an important therapeutic target. Vascular endothelial growth factor-A (VEGF-A) is a key molecule in angiogenesis, but the identification of related molecules and the angiopoietins suggests a more complex picture. We investigated the presence of transcripts for VEGF-A, VEGF-B, VEGF-C, VEGF-D, Angiopoietin-1 and Angiopoietin-2 in benign endometrium, atypical complex hyperplasia (ACH) and endometrioid endometrial carcinoma using in situ hybridisation. We confirmed the presence of VEGF-A mRNA in the epithelial cells of cancers examined (13 out of 13), but not in benign endometrium or ACH. We also demonstrate, using quantitative polymerase chain reaction, that levels of VEGF-B mRNA are significantly lower in endometrial cancer than benign endometrium. We conclude that loss of VEGF-B may contribute to the development of endometrial carcinoma by modulating availability of receptors for VEGF-A.

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Related in: MedlinePlus

Expression of mRNA encoding VEGF-D and Ang-2 in macrophages infiltrating a poorly differentiated (FIGO grade 3) endometrioid endometrial carcinoma. In situ hybridisation with VEGF-D antisense probe shown under dark-field (A) conditions and light-field conditions (C). In situ hybridisation with VEGF-D sense (control) probe shows no specific hybridisation (B) (scale bar applies to (A), (B), (E) and (F)). Immunostaining with anti-human CD68 in a serial section (D), localises the silver grains to tumour associated macrophages (TAMs) (scale bar applies to (C), (D), (G) and (H)). In situ hybridisation with Ang-2 antisense probe shown under dark-field (E) and light-field (G) conditions. In situ hybridisation with Ang-2 sense (control) probe (F) shows no specific hybridisation. Anti-human cytokeratin staining (H) localises the hybridisation to TAMs.
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fig3: Expression of mRNA encoding VEGF-D and Ang-2 in macrophages infiltrating a poorly differentiated (FIGO grade 3) endometrioid endometrial carcinoma. In situ hybridisation with VEGF-D antisense probe shown under dark-field (A) conditions and light-field conditions (C). In situ hybridisation with VEGF-D sense (control) probe shows no specific hybridisation (B) (scale bar applies to (A), (B), (E) and (F)). Immunostaining with anti-human CD68 in a serial section (D), localises the silver grains to tumour associated macrophages (TAMs) (scale bar applies to (C), (D), (G) and (H)). In situ hybridisation with Ang-2 antisense probe shown under dark-field (E) and light-field (G) conditions. In situ hybridisation with Ang-2 sense (control) probe (F) shows no specific hybridisation. Anti-human cytokeratin staining (H) localises the hybridisation to TAMs.

Mentions: Messenger RNA encoding VEGF-D was present in three of the five ACH specimens and in six of the 13 carcinomas (one moderately differentiated tumour and five poorly differentiated tumours). The distribution of silver grains did not correspond with epithelial tumour cells but did co-localise with tumour-associated macrophages (CD-68 positive cells) in serial sections (Figure 3Figure 3


Expression of the VEGF and angiopoietin genes in endometrial atypical hyperplasia and endometrial cancer.

Holland CM, Day K, Evans A, Smith SK - Br. J. Cancer (2003)

Expression of mRNA encoding VEGF-D and Ang-2 in macrophages infiltrating a poorly differentiated (FIGO grade 3) endometrioid endometrial carcinoma. In situ hybridisation with VEGF-D antisense probe shown under dark-field (A) conditions and light-field conditions (C). In situ hybridisation with VEGF-D sense (control) probe shows no specific hybridisation (B) (scale bar applies to (A), (B), (E) and (F)). Immunostaining with anti-human CD68 in a serial section (D), localises the silver grains to tumour associated macrophages (TAMs) (scale bar applies to (C), (D), (G) and (H)). In situ hybridisation with Ang-2 antisense probe shown under dark-field (E) and light-field (G) conditions. In situ hybridisation with Ang-2 sense (control) probe (F) shows no specific hybridisation. Anti-human cytokeratin staining (H) localises the hybridisation to TAMs.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2394472&req=5

fig3: Expression of mRNA encoding VEGF-D and Ang-2 in macrophages infiltrating a poorly differentiated (FIGO grade 3) endometrioid endometrial carcinoma. In situ hybridisation with VEGF-D antisense probe shown under dark-field (A) conditions and light-field conditions (C). In situ hybridisation with VEGF-D sense (control) probe shows no specific hybridisation (B) (scale bar applies to (A), (B), (E) and (F)). Immunostaining with anti-human CD68 in a serial section (D), localises the silver grains to tumour associated macrophages (TAMs) (scale bar applies to (C), (D), (G) and (H)). In situ hybridisation with Ang-2 antisense probe shown under dark-field (E) and light-field (G) conditions. In situ hybridisation with Ang-2 sense (control) probe (F) shows no specific hybridisation. Anti-human cytokeratin staining (H) localises the hybridisation to TAMs.
Mentions: Messenger RNA encoding VEGF-D was present in three of the five ACH specimens and in six of the 13 carcinomas (one moderately differentiated tumour and five poorly differentiated tumours). The distribution of silver grains did not correspond with epithelial tumour cells but did co-localise with tumour-associated macrophages (CD-68 positive cells) in serial sections (Figure 3Figure 3

Bottom Line: Angiogenesis is critical for the growth and metastasis of endometrial cancer and is therefore an important therapeutic target.Vascular endothelial growth factor-A (VEGF-A) is a key molecule in angiogenesis, but the identification of related molecules and the angiopoietins suggests a more complex picture.We confirmed the presence of VEGF-A mRNA in the epithelial cells of cancers examined (13 out of 13), but not in benign endometrium or ACH.

View Article: PubMed Central - PubMed

Affiliation: Department of Pathology, University of Cambridge, Tennis Court Road, Cambridge CB1 1QP, UK. cath.holland@obgyn.cam.ac.uk

ABSTRACT
Angiogenesis is critical for the growth and metastasis of endometrial cancer and is therefore an important therapeutic target. Vascular endothelial growth factor-A (VEGF-A) is a key molecule in angiogenesis, but the identification of related molecules and the angiopoietins suggests a more complex picture. We investigated the presence of transcripts for VEGF-A, VEGF-B, VEGF-C, VEGF-D, Angiopoietin-1 and Angiopoietin-2 in benign endometrium, atypical complex hyperplasia (ACH) and endometrioid endometrial carcinoma using in situ hybridisation. We confirmed the presence of VEGF-A mRNA in the epithelial cells of cancers examined (13 out of 13), but not in benign endometrium or ACH. We also demonstrate, using quantitative polymerase chain reaction, that levels of VEGF-B mRNA are significantly lower in endometrial cancer than benign endometrium. We conclude that loss of VEGF-B may contribute to the development of endometrial carcinoma by modulating availability of receptors for VEGF-A.

Show MeSH
Related in: MedlinePlus