from animal models provides further support for the idea that paracrine interactions may also attract nontumor (e.g., bone marrow–derived) and tumor cells to establish a premetastatic niche. 2,3 The ac-tive dysadhesion of local tissues to allow tumor-cell invasion (e.g., via E-cadherin, dysadherin, or both) is also probably triggered by paracrine sig-naling, as Batistatou et al. point out. Finally, the complex roles played by the host-site microenviron-ment and by the immune system in metastatic dormancy are not yet fully understood, although recent intriguing results point to tumor-specific T-cell suppression of multistage carcinogenesis through cytokine signaling. 4
CITATION STYLE
Jonkman, M. F., & Pasmooij, A. M. G. (2009). Revertant Mosaicism — Patchwork in the Skin. New England Journal of Medicine, 360(16), 1680–1682. https://doi.org/10.1056/nejmc0809896
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