"Cancers develop in complex tissue environments, which they depend on for sustained growth, invasion and metastasis. Unlike tumor cells, stromal cell types within the tumor microenvironment (TME) are genetically stable and thus represent an attractive therapeutic target with reduced risk of resistance and tumor recurrence. However, specifically disrupting the pro-tumorigenic TME is a challenging undertaking, as the TME has diverse capacities to induce both beneficial and adverse consequences for tumorigenesis. Furthermore, many studies have shown that the microenvironment is capable of normalizing tumor cells, suggesting that re-education of stromal cells, rather than targeted ablation per se, may be an effective strategy for treating cancer. Here we discuss the paradoxical roles of the TME during specific stages of cancer progression and metastasis, as well as recent therapeutic attempts to re-educate stromal cells within the TME to have anti-tumorigenic effects."
Bidirectional communication between cells and their microenvironment is critical for both normal tissue homeostasis and tumor growth. In particular, interactions between tumor cells and the associated stroma represent a powerful relationship that influences disease initiation and progression and patient prognosis. The link between chronic inflammation and tumorigenesis was first proposed by Rudolf Virchow in 1863 after the observation that infiltrating leukocytes are a hallmark of tumors. Since then, a plethora of studies have contributed to the characterization of the TME, further complicating the already challenging task of understanding and treating cancer. Whereas cancer was previously viewed as a heterogeneous disease involving aberrant mutations in tumor cells, it is now evident that tumors are also diverse by nature of their microenvironmental composition and their stromal cell proportions or activation states. In response to evolving environmental conditions and oncogenic signals from growing tumors, the TME continually changes over the course of cancer progression, underscoring the need to consider the influences of the TME on metastasis as a dynamic process and understand how tumor cells drive the construction of their own niche.
Via Cancer Commons, Gilbert Faure au nom de l'ASSIM