Anoikis is defined broadly as apoptosis that is inhibited by appropriate cell-matrix interactions.  Normal and tumor cells vary widely in their sensitivity to anoikis, but, in general, metastatic tumor cells are inevitably anoikis-resistant.  In particular, tumor cells that possess a cancer stem cell or mesenchymal phenotype, arising from the oncogenic Epithelial-Mesenchymal Transition (EMT), are transcriptionally re-programmed to resist anoikis.  While the anoikis response occurs through the mitochondrial pathway typically found in other apoptotic responses (e.g., DNA damage, death receptors, oxidative stress), the regulation of anoikis by cell-matrix signalling is unique and only partially characterized.  The uniqueness of anoikis is: a. regulation by integrins, non-integrin matrix receptors, and the signaling complexes associated with them; b. regulation by metabolic changes occurring in response to attachment/detachment;  c. regulation by oncogenes and tumor suppressor genes d. regulation by tumor microenvironment;  e. regulation by EMT.

Preface.- Introduction.- The intersection of anoikis resistance and fatty acid metabolism in cancer.- Anoikis resistance in melanoma.- Anoikis mediated by stress-activated MAPK signaling pathways.- Metabolic Regulation of Anoikis.- Metabolic Reprogramming contributes to Anoikis resistance in Cancer Cells.- Role of the nuclear receptors in anoikis.- The roles of anoikis in cervical cancer.- Shc and the control of small GTPase dynamics in cellular anchorage.- Anoikis and the Human Gut Epithelium in Health and Disease.- Epithelial cell extrusion:  the prelude to anoikis.- Microtubule modifications and mitochondria:  role in anoikis.