Publication

Publisher	ESMO, Lugano
ISBN	978-88-906359-7-7

Tumour initiation and progression are not simple cell autonomous events limited to the malignant cells, but rather complex conditions involving reciprocal and dynamic heterotypic interactions between cancer cells and normal cells present in their immediate vicinity. Hence, the concepts of tumour microenvironment and tumour-host interactions were introduced to denote this novel complexity. The tumour microenvironment contains many different cell types, including endothelial cells, carcinoma-associated fibroblasts and immune/inflammatory cells, either derived from preexisting resident cells or recruited from the bone marrow. Changes in the tumour microenvironment are largely orchestrated by the cancer cells themselves. In some circumstances, however, they can be initiated and maintained by the microenvironment itself, for example as part of chronic inflammatory or tissue remodelling processes induced by infections, chemical or physical damages preceding or accompanying tumorigenesis. Collectively, reciprocal heterotypic interactions in the tumour microenvironment dynamically contribute to promote cancer cell survival, proliferation, motility, invasion and metastasis. Thereby, they determine local tumour progression, distant metastasis formation and response (or resistance) to therapy and eventually disease outcome. Tumour angiogenesis, invasion and metastasis involve profound and complex tumour-host interactions. While tumour angiogenesis has been therapeutically targeted to provide some survival benefits, tumour invasion and metastasis are conditions still orphan of a valid treatment. Recent advances in metastasis research, however, have shed new light on mechanisms that may open unprecedented opportunities for clinical therapies. In this chapter we will summarize the essentials of tumour angiogenesis and metastasis and highlight open questions and new opportunities for future therapies.