Angiogenesis in anal warts, anal intraepithelial neoplasia and anal squamous cell carcinoma

Mullerat, J; Fong, L.F. Wong Te; Davies, Susan; Winslet, M. C.; Perrett, CW

doi:10.1046/j.1463-1318.2003.00481.x

Cited by 15 publications

(11 citation statements)

References 26 publications

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“…Human papillomavirus infection is associated with increased angiogenesis, both in high‐risk HPV‐associated cervical dysplasia and cancer and in the more benign HPV‐associated warts . Although HPV mainly infects epithelial cells, the virus may stimulate neovascularization indirectly by increasing the secretion of angiogenic proteins, which can activate ECs in a paracrine manner (Table ).…”

Section: Human Tumour‐inducing Virusessupporting

confidence: 67%

Viruses as key regulators of angiogenesis

Vrancken

Vervaeke

Balzarini

et al. 2011

Reviews in Medical Virology

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Angiogenesis is an important physiological process that is controlled by a precise balance of growth and inhibitory factors in healthy tissues. However, environmental and genetic factors may disturb this delicate balance, resulting in the development of angiogenic diseases, tumour growth and metastasis. During the past decades, extensive research has led to the identification and characterization of genes, proteins and signalling pathways that are involved in neovascularization. Moreover, increasing evidence indicates that viruses may also regulate angiogenesis either directly, by (i) producing viral chemokines, growth factors and/or receptors or (ii) activating blood vessels as a consequence of endothelial cell tropism, or indirectly, by (iii) modulating the activity of cellular proteins and/or (iv) inducing a local or systemic inflammatory response, thereby creating an angiogenic microenvironment. As such, viruses may modulate several signal transduction pathways involved in angiogenesis leading to changes in endothelial cell proliferation, migration, adhesion, vascular permeability and/or protease production. Here, we will review different mechanisms that may be applied by viruses to deregulate the angiogenic balance in healthy tissues and/or increase the angiogenic potential of tumours.

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Section: Human Tumour‐inducing Virusessupporting

confidence: 67%

Viruses as key regulators of angiogenesis

Vrancken

Vervaeke

Balzarini

et al. 2011

Reviews in Medical Virology

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“…Investigations in our unit quantifying angiogenesis in the colorectal adenoma-carcinoma sequence using immunohistochemical staining for CD31 antigen suggest that a significant increase in MVD is induced with the onset of dysplasia, parallelled by a significant increase in VEGF expression at the same stage of progression (Staton et al, 2007). Microvessel density and VEGF expression also increase in a linear manner with the progression of transformation in anal intraepithelial neoplasia, the precursor of anal SCC (Mullerat et al, 2003). Angiogenesis, as defined by the extent of sinusoidal capillarisation detected by CD34 antibodies, increases with progression towards hepatocellular carcinoma (HCC) commencing at the low-grade dysplastic nodule stage with a concomitant increase in VEGF expression (Park et al, 2000).…”

Section: Gastrointestinal Tractmentioning

confidence: 96%

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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“…Nevertheless, although endothelial cells are permissive to the HIVentry, is still debated whether HIV can replicate in these cells [22][23][24][25]. From the clinical point of view, HIV-infected individuals show a high prevalence of Kaposi's sarcoma, hemangioma, and other angioproliferative diseases [26][27][28], but growing evidences suggest that, in this setting of patients, vascular repair processes are in reality defective. In fact, as the cART prolongs their survival, novel comorbidities, including atherosclerosis, coronary artery disease and thrombosis have emerged [13,14].…”

Section: Characterization Of Infected Cfu-ecmentioning

confidence: 99%