Angiogenesis in breast carcinoma--clinicopathologic relevance and potential use as a quantifiable surrogate endpoint biomarker.

Although stochastic acquisition of structural genetic aberrations has become the dominant paradigm for progression of solid tumors, the process of tumor cell invasion and metastasis in large part represents a cooperative interaction with host tissues. Such interactions occur at multiple levels and include the exchange of cytokines/growth factors, the induction of neovascularization (angiogenesis), proteolytic degradation and synthetic alterations of the native extracellular matrix, and fibroblast/inflammatory cell chemotaxis. Many classical histologic and mammographic features of breast carcinoma, such as desmoplasia, are a direct reflection of these tumor-host relationships. Further, sustained growth is not possible without a coordinated interaction between diverse neoplastic and native cell populations. In recent years, quantifiable parameters of tumor-host interaction, such as protease elaboration, have been shown to correlate with intrinsic properties of neoplastic cells and to predict clinical outcome. It is thus reasonable to propose that functional cellular alterations imposed by chemopreventive agents may be reflected in tumor-host interaction parameters. The objective of this review is to briefly summarize the literature addressing one parameter of tumor-host interaction--angiogenesis--emphasizing its applicability as a quantifiable biomarker in breast neoplasia.