Overexpression of vascular endothelial growth factor and its receptors in bronchial dypslasia demonstrated by quantitative RT-PCR analysis

Merrick, Daniel T.; Haney, Jerry; Petrunich, Sheila; Sugita, Michio; Miller, York E.; Keith, Robert L.; Kennedy, Timothy; Franklin, Wilbur A.

doi:10.1016/j.lungcan.2004.07.049

Cited by 46 publications

(23 citation statements)

References 43 publications

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“…In bronchial pre-malignant lesions, a progressive increase in MVD from hyperplastic/metaplastic lesion to dysplasia or in situ carcinoma has been demonstrated. Vascular endothelial growth factor mRNA and protein expression parallel the increased MVD in these lesions, with VEGF expression predominantly in the bronchial epithelium (Merrick et al, 2005). …”

Section: Respiratory Tractmentioning

confidence: 70%

Angiogenesis in pre-malignant conditions

et al. 2008

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Evidence from human studies suggests that angiogenesis commences during the pre-malignant stages of cancer. Inhibiting angiogenesis may, therefore, be of potential value in preventing progression to invasive cancer. Understanding the mechanisms inducing angiogenesis in these lesions and identification of those important in human tumourigenesis are necessary to develop translational strategies that will help realise the goal of angioprevention.

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Section: Respiratory Tractmentioning

confidence: 70%

Angiogenesis in pre-malignant conditions

et al. 2008

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“…Overexpression of angiogenic factors in human cancers has been described previously, for example, for VEGF-A in lung, breast and pancreas carcinoma (Yoshiji et al, 1996;Itakura et al, 2000;Merrick et al, 2005), for FGF-2 in pancreas carcinoma and prostate cancer (Yamanaka et al, 1993;Giri et al, 1999) and for ANG-1 and ANG-2 in gastric and hepatocellular carcinoma (Torimura et al, 2004;Wang et al, 2005). However, there are also reports that disagree with the concept that tumours produce higher amounts of angiogenic factors than their normal tissue counterparts: in breast cancer tissues the expression of FGF-2 was reduced (Luqmani et al, 1992) or did not differ from the expression in normal breast tissues (Colomer et al, 1997).…”

mentioning

confidence: 77%

Angiogenesis and lymphangiogenesis are downregulated in primary breast cancer

et al. 2009

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BACKGROUND: Angiogenesis and lymphangiogenesis are considered to play key roles in tumour growth, progression and metastasis. However, targeting tumour angiogenesis in clinical trials showed only modest efficacy. We therefore scrutinised the concept of tumour angiogenesis and lymphangiogenesis by analysing the expression of crucial markers involved in these processes in primary breast cancer. METHODS: We analysed the expression of angiogenic, lymphangiogenic or antiangiogenic factors, their respective receptors and specific markers for endothelial and lymphendothelial cells by quantitative real-time RT-PCR in primary breast cancer and compared the expression profiles to non-cancerous, tumour-adjacent tissues and breast tissues from healthy women. RESULTS: We found decreased mRNA amounts of major angiogenic and lymphangiogenic factors in tumour compared to healthy tissues, whereas antiangiogenic factors were upregulated. Concomitantly, angiogenic and lymphangiogenic receptors were downregulated in breast tumours. This antiangiogenic, antilymphangiogenic microenvironment was even more pronounced in aggressive tumours and accompanied by reduced amounts of endothelial and lymphatic endothelial cell markers. CONCLUSION: Primary breast tumours are not a site of highly active angiogenesis and lymphangiogenesis. Selection for tumour cells that survive with minimal vascular supply may account for this observation in clinical apparent tumours.

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“…Biological behavior differs between the 2 main histological types of NSCLC: adenocarcinoma has a higher metastatic potential than squamous cell carcinomas (16 ). Some studies report that VEGF expression is higher in adenocarcinomas than squamous cell carcinomas (16,21 ), but data also suggest that there is no difference in VEGF levels between those 2 subtypes (29,30 ). We observed that the 2 histological types of NSCLC not only displayed similar expression of VEGF and VEGF splice variants, but also showed similar relative expression of VEGF splice variants, and therefore we conclude that their different metastatic potential cannot be associated with VEGF.…”

Section: Discussionmentioning

confidence: 99%

Quantitative Real-Time Reverse Transcription–PCR Study of the Expression of Vascular Endothelial Growth Factor (VEGF) Splice Variants and VEGF Receptors (VEGFR-1 and VEGFR-2) in Non–Small Cell Lung Cancer

et al. 2007

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Background: Vascular endothelial growth factor (VEGF) is a major regulator of angiogenesis and its expression is increased in non–small cell lung cancer (NSCLC). We aimed to determine the expression pattern of VEGF splice variants in NSCLC and its correlation with the clinicopathological characteristics of tumors. Methods: We used real-time reverse transcription PCR to quantify the mRNA expression of total VEGF, 4 VEGF splice variants (VEGF121, VEGF165, VEGF183, and VEGF189), and 2 VEGF receptors (VEGFR-1 and VEGFR-2) in 27 pairs of cancerous and adjacent noncancerous tissues originating from patients with NSCLC. Results: Total VEGF, VEGF121, and VEGF165 were expressed in all specimens, whereas VEGF183 and VEGF189 were present in small amounts in certain samples. Total VEGF, VEGF121, and VEGF165 mRNA was upregulated in cancerous compared with healthy tissues, whereas VEGF183 and VEGF189 expression tended to be higher in healthy tissues. The expression of VEGFRs was similar between matched specimens. No correlation was found between the expression of total VEGF or VEGF splice variants and the clinicopathological characteristics of tumors. The expression patterns of VEGF splice variants differed between tissue pairs. VEGF121 was the major variant expressed in all samples; however, its relative expression was higher in cancerous tissues. The relative expression of VEGF183 and VEGF189 was upregulated in healthy lung tissues, whereas the ratio of VEGF165 to total VEGF was similar between matched specimens. Conclusions: The expression pattern of certain VEGF splice variants is altered during tumorigenesis. Our data support the hypothesis that during malignant progression an angiogenic switch favoring the shorter diffusible isoforms occurs.

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Overexpression of vascular endothelial growth factor and its receptors in bronchial dypslasia demonstrated by quantitative RT-PCR analysis

Cited by 46 publications

References 43 publications

Angiogenesis in pre-malignant conditions

Angiogenesis in pre-malignant conditions

Angiogenesis and lymphangiogenesis are downregulated in primary breast cancer

Quantitative Real-Time Reverse Transcription–PCR Study of the Expression of Vascular Endothelial Growth Factor (VEGF) Splice Variants and VEGF Receptors (VEGFR-1 and VEGFR-2) in Non–Small Cell Lung Cancer

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