The not-so innocent bystander: The microenvironment as a therapeutic target in cancer
The microenvironment in which cancer arises is often regarded as a bystander to the clonal expansion and acquisition of malignant characteristics of the tumour. However, a major function of the microenvironment is to suppress cancer, and its disruption is required for the establishment of cancer. In addition, tumour cells can further distort the microenvironment to promote growth, recruit non-malignant cells that provide physiological resources, and facilitate invasion. In this review, the authors discuss the contribution of the microenvironment, i.e., the stroma and its resident vasculature, inflammatory cells, growth factors and the extracellular matrix (ECM), in the development of cancer, and focus on two components as potential therapeutic targets in breast cancer. First, the ECM, which imparts crucial signaling via integrins and other receptors, is a first-line barrier to invasion, modulates aggressive behavior and may be manipulated to provide novel impediments to tumour growth. Second, the authors discuss the involvement of TGF-beta1 as an example of one of many growth factors that can regulate ECM composition and degradation and that play complex roles in cancer. Compared to the variable routes taken by cells to become cancers, the response of tissues to cancer is relatively consistent. Therefore, controlling and eliminating cancer may be more readily achieved indirectly via the tissue microenvironment.
- Research Organization:
- Lawrence Berkeley National Lab. (LBNL), Berkeley, CA (United States)
- Sponsoring Organization:
- USDOE Director, Office of Science. Office of Biological and Environmental Research. Life Sciences Division; National Aeronautics and Space Administration (US)
- DOE Contract Number:
- AC03-76SF00098
- OSTI ID:
- 812893
- Report Number(s):
- LBNL-53067; R&D Project: 80HR01; TRN: US200315%%147
- Journal Information:
- Expert Opinion on Therapeutic Targets, Vol. 7, Issue 1; Other Information: Journal Publication Date: February 2003; PBD: 19 Jun 2003
- Country of Publication:
- United States
- Language:
- English
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