Local and systemic processes defining cancer are summarized in the classic and modified 'hallmarks of cancer', providing a conceptual tool to visualize a multi-pathway system (Figure 1). 1 Over the previous two decades, a mechanistic link between the family of structural proteins known as Tensins and primary malignancies has been proposed. [2][3][4][5] The initial hypotheses on the four members of the Tensin family focussed on their role as either structural support or focal adhesion adaptor proteins, providing a critical link between the extracellular matrix (ECM) and intracellular cytoskeleton. 6,7 However, this was likely an oversimplification with more recent evidence suggesting additional signal transduction roles. Furthermore, the dysregulation of focal adhesion complexes is one recognized mechanism behind the ability of cancer cells to metastasise. A clear role or mechanism of action in oncogenesis for Tensins has not been elucidated, and findings appear tumour type-specific. 2 The growing body of evidence for a diagnostic, prognostic and potential therapeutic role for these proteins mandates a clearer understanding of their molecular biology and oncogenic function. Tensin 4 (CTEN) has received the most focus in the literature and was recently reviewed in Liao et al (2021). 8 The remaining three Tensin family members share
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