Vascular contribution to metastasis

Research output: Contribution to journalArticle

Michael Sax, Prue N. Plummer, Vivek Mittal, Albert S. Mellick

It has been 40 years since Folkman's seminal paper [Cancer Res 1974. 34:2109-13], proposing the presence of a tumour associated angiogenic factor, which could be targeted as an anticancer therapy. There are currently a handful of drugs in trial or use that have been marketed as targeting angiogenesis. Unfortunately, the most widely used of these, bevacizumab (Avastin™, Roche), has met with limited success clinically. For this reason and based on a calculation of cost benefit, bevacizumab is now only publically subsidised for use in a limited range of solid tumours. That the contribution of vasculature to malignancy remains poorly understood is increasingly clear. At the same time, the traditional view that vascularisation is a passive participant in the process of malignancy, and that endothelium merely provides a conduit by which tumour cells spread, is being replaced with an understanding that vasculature is a key player in the process of metastasis. Furthermore, the identification of non-traditional sources of vasculature has complicated our understanding of the tumour endothelium as a unique population that can be simply targeted as an anticancer therapy. The following review seeks to provide an up-to-date view of vascular contribution to metastasis and implications for new vasculature-targeted anticancer treatments.

Original languageEnglish
Pages (from-to)103-107
Number of pages5
JournalCancer Forum
Volume38
Issue number2
StatePublished - Jan 1 2014

Cite this

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Vascular contribution to metastasis. / Sax, Michael; Plummer, Prue N.; Mittal, Vivek; Mellick, Albert S.

In: Cancer Forum, Vol. 38, No. 2, 01.01.2014, p. 103-107.

Research output: Contribution to journalArticle

Harvard

Sax, M, Plummer, PN, Mittal, V & Mellick, AS 2014, 'Vascular contribution to metastasis' Cancer Forum, vol. 38, no. 2, pp. 103-107.

APA

Sax, M., Plummer, P. N., Mittal, V., & Mellick, A. S. (2014). Vascular contribution to metastasis. Cancer Forum, 38(2), 103-107.

Vancouver

Sax M, Plummer PN, Mittal V, Mellick AS. Vascular contribution to metastasis. Cancer Forum. 2014 Jan 1;38(2):103-107.

Author

Sax, Michael ; Plummer, Prue N. ; Mittal, Vivek ; Mellick, Albert S. / Vascular contribution to metastasis. In: Cancer Forum. 2014 ; Vol. 38, No. 2. pp. 103-107.

BibTeX

@article{25fc2c3dff5e4d0eb723c7b2b064f2d9,
title = "Vascular contribution to metastasis",
abstract = "It has been 40 years since Folkman's seminal paper [Cancer Res 1974. 34:2109-13], proposing the presence of a tumour associated angiogenic factor, which could be targeted as an anticancer therapy. There are currently a handful of drugs in trial or use that have been marketed as targeting angiogenesis. Unfortunately, the most widely used of these, bevacizumab (Avastin™, Roche), has met with limited success clinically. For this reason and based on a calculation of cost benefit, bevacizumab is now only publically subsidised for use in a limited range of solid tumours. That the contribution of vasculature to malignancy remains poorly understood is increasingly clear. At the same time, the traditional view that vascularisation is a passive participant in the process of malignancy, and that endothelium merely provides a conduit by which tumour cells spread, is being replaced with an understanding that vasculature is a key player in the process of metastasis. Furthermore, the identification of non-traditional sources of vasculature has complicated our understanding of the tumour endothelium as a unique population that can be simply targeted as an anticancer therapy. The following review seeks to provide an up-to-date view of vascular contribution to metastasis and implications for new vasculature-targeted anticancer treatments.",
author = "Michael Sax and Plummer, {Prue N.} and Vivek Mittal and Mellick, {Albert S.}",
year = "2014",
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RIS

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AU - Sax, Michael

AU - Plummer, Prue N.

AU - Mittal, Vivek

AU - Mellick, Albert S.

PY - 2014/1/1

Y1 - 2014/1/1

N2 - It has been 40 years since Folkman's seminal paper [Cancer Res 1974. 34:2109-13], proposing the presence of a tumour associated angiogenic factor, which could be targeted as an anticancer therapy. There are currently a handful of drugs in trial or use that have been marketed as targeting angiogenesis. Unfortunately, the most widely used of these, bevacizumab (Avastin™, Roche), has met with limited success clinically. For this reason and based on a calculation of cost benefit, bevacizumab is now only publically subsidised for use in a limited range of solid tumours. That the contribution of vasculature to malignancy remains poorly understood is increasingly clear. At the same time, the traditional view that vascularisation is a passive participant in the process of malignancy, and that endothelium merely provides a conduit by which tumour cells spread, is being replaced with an understanding that vasculature is a key player in the process of metastasis. Furthermore, the identification of non-traditional sources of vasculature has complicated our understanding of the tumour endothelium as a unique population that can be simply targeted as an anticancer therapy. The following review seeks to provide an up-to-date view of vascular contribution to metastasis and implications for new vasculature-targeted anticancer treatments.

AB - It has been 40 years since Folkman's seminal paper [Cancer Res 1974. 34:2109-13], proposing the presence of a tumour associated angiogenic factor, which could be targeted as an anticancer therapy. There are currently a handful of drugs in trial or use that have been marketed as targeting angiogenesis. Unfortunately, the most widely used of these, bevacizumab (Avastin™, Roche), has met with limited success clinically. For this reason and based on a calculation of cost benefit, bevacizumab is now only publically subsidised for use in a limited range of solid tumours. That the contribution of vasculature to malignancy remains poorly understood is increasingly clear. At the same time, the traditional view that vascularisation is a passive participant in the process of malignancy, and that endothelium merely provides a conduit by which tumour cells spread, is being replaced with an understanding that vasculature is a key player in the process of metastasis. Furthermore, the identification of non-traditional sources of vasculature has complicated our understanding of the tumour endothelium as a unique population that can be simply targeted as an anticancer therapy. The following review seeks to provide an up-to-date view of vascular contribution to metastasis and implications for new vasculature-targeted anticancer treatments.

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