Angiogenesis in Bladder Cancer: Relationship Between Microvessel Density and Tumor Prognosis

Bochner, Bernard H.; Côté, Richard J.; Weidner, Noel; Groshen, Susan; Chen, Su Chiu; Skinner, Donald G.; Nichols, Peter W.

doi:10.1093/jnci/87.21.1603

Cited by 385 publications

(217 citation statements)

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“…We showed striking luminal induction of VEGF in superficial bladder cancer (Turner et al, 2002). Vascular endothelial growth factor is a key angiogenic factor and microvessel density as a measure of angiogenesis has been shown to be highly associated with poor outcome in invasive bladder cancer (Bochner et al, 1995). Vascular endothelial growth factor is well recognised to be induced by hypoxia via hypoxia inducible factor (HIF) and this suggests that genes induced by hypoxia may be related to the aggressive phenotype.…”

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confidence: 82%

Comparison of hypoxia transcriptome in vitro with in vivo gene expression in human bladder cancer

et al. 2005

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Hypoxia-inducible genes have been linked to the aggressive phenotype of cancer. However, nearly all work on hypoxia-regulated genes has been conducted in vitro on cell lines. We investigated the hypoxia transcriptome in primary human bladder cancer using cDNA microarrays to compare genes induced by hypoxia in vitro in bladder cancer cell line EJ28 with genes upregulated in 39 bladder tumour specimens (27 superficial and 12 invasive). We correlated array mRNA fold changes with carbonic anhydrase 9 (CA IX) staining of tumours as a surrogate marker of hypoxia. Of 6000 genes, 32 were hypoxia inducible in vitro more than two-fold, five of which were novel, including lactate transporter SLC16A3 and RNAse 4. Eight of 32 hypoxia-inducible genes in vitro were also upregulated on the vivo array. Vascular endothelial growth factor mRNA was upregulated two-fold by hypoxia and 2 -18-fold in 31 out of 39 tumours. Glucose transporter 1 was also upregulated on both arrays mRNA, and fold changes on the in vivo array significantly correlated with CA IX staining of tumours (P ¼ 0.008). However, insulin-like growth factor binding protein 3 mRNA was the most strongly differentially expressed gene in both arrays and this confirmed its upregulation in urine of bladder cancer patients (n ¼ 157, Po0.01). This study defines genes suitable for an in vivo hypoxia 'profile', shows the heterogeneity of the hypoxia response and describes new hypoxia-regulated genes.

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confidence: 82%

Comparison of hypoxia transcriptome in vitro with in vivo gene expression in human bladder cancer

et al. 2005

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“…70 Using immunohistochemistry, increased microvascular density as a surrogate for angiogenesis has been found to be associated with tumor progression and decreased overall survival in BC patients. 71 Furthermore, increased urinary excretion of b-FGF, 70 angiogenic factors such as autocrine motility factor (AMF), 72 AMF receptor, 73 and hyaluronic acid and its degradation products 74 have been found in BC patients and have been proposed as means of detection and tumor monitoring.…”

Section: Angiogenesismentioning

confidence: 99%

Molecular Mechanisms and Pathways in Bladder Cancer Development and Progression

Jung

Messing

2000

Cancer Control

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Background: The basis for bladder cancer development and progression is complex and involves genetic abnormalities. These abnormalities yield phenotypic changes that allow normal transitional cells to becomeity of these new cases, approximately 75%, are limited to the mucosa (stage Ta or Tis) and lamina propria (T1) at presentation, and most of these tumors can be removed by transurethral resection. Recurrence rates are high (30% to 85%), and 10% to 30% of "superficial" tumors (T1 or less) will subsequently progress to muscle invasive disease (stages T2-T4), which has a poorer prognosis. 2 For the remaining 25%, the initial presentation involves muscle invasive disease that will usually relapse with metastases (as well as localized disease persistence) within a median of 2 years if managed only by transurethral resection and intravesical therapy. 3 These data support the heterogeneous nature and malignant potential of transitional cell carcinoma

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“…5 The induction of angiogenesis is mediated by positive and negative regulatory molecules released by tumor-associated epithelial cells, endothelial cells, mesothelial cells and leukocytes. 2,[6][7][8] The balance between these regulating molecules determines the extent of tissue vascularization. 9 The major endogenous inhibitors of angiogenesis include thrombospondin and interferons, [10][11][12] whereas the major endogenous promoters of angiogenesis include fibroblast growth factor (FGF), 13 vascular endothelial growth factor (VEGF), 14,15 interleukin 8 (IL-8, chemokine (C-X-C motif) ligand 8 (CXCL8)), 16,17 platelet-derived endothelial cell growth factor 18 and members of the matrix metalloproteinase family (MMP-2, MMP-9).…”

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confidence: 99%

“…19 In quiescent normal tissues, factors that inhibit angiogenesis predominate, whereas in rapidly dividing tissues (ie, tumors), the balance of angiogenic molecules favors stimulation, creation of neovasculature and tumor growth. 3,6 Previously, we reported on the increased angiogenic potential of human prostate cancer cells that overexpressed the Bcl-2 proto-oncogene. Specifically, increased Bcl-2 expression enhanced the tumorigenic and angiogenic ability of prostate cancer xenografts.…”

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confidence: 99%

Expression of CXCL1 in human endothelial cells induces angiogenesis through the CXCR2 receptor and the ERK1/2 and EGF pathways

Miyake¹,

Goodison

Urquidi³

et al. 2013

Laboratory Investigation

116

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Endothelial cell growth and proliferation are critical for angiogenesis; thus, greater insight into the regulation of pathological angiogenesis is greatly needed. Previous studies have reported on chemokine (C-X-C motif) ligand 1 (CXCL1) expression in epithelial cells and that secretion of CXCL1 from these epithelial cells induces angiogenesis. However, limited reports have demonstrated CXCL1 expression in endothelial cells. In this report, we present data that expand on the role of CXCL1 in human endothelial cells inducing angiogenesis. Specifically, CXCL1 is expressed and secreted from human endothelial cells. Interference of CXCL1 function using neutralizing antibodies resulted in a reduction in endothelial cell migration and viability/proliferation, the latter associated with a decrease in levels of cyclin D and cdk4. In vitro studies revealed that CXCL1 influenced neoangiogenesis through the regulation of epidermal growth factor and ERK1/2. In a xenograft angiogenesis model, interference of CXCL1 function resulted in inhibition of angiogenesis. A better understanding of the role of CXCL1 in the interactions between the endothelial and epithelial components will provide insight into how human tissues use CXCL1 to survive and thrive in a hostile environment.

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Angiogenesis in Bladder Cancer: Relationship Between Microvessel Density and Tumor Prognosis

Abstract: Tumor angiogenesis, as determined by microvessel density measurement, is an independent prognostic indicator for patients with invasive TCC of the bladder.

Cited by 385 publications

References 0 publications

Comparison of hypoxia transcriptome in vitro with in vivo gene expression in human bladder cancer

Comparison of hypoxia transcriptome in vitro with in vivo gene expression in human bladder cancer

Molecular Mechanisms and Pathways in Bladder Cancer Development and Progression

Expression of CXCL1 in human endothelial cells induces angiogenesis through the CXCR2 receptor and the ERK1/2 and EGF pathways

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