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In vitro engineering of tumor milieus is complex because cancer progression and metastasis involve spatio-temporally evolving cell-matrix interactions, myriad interactions between tumor cells and auxiliary cells, hypoxic cores, leaky... more
In vitro engineering of tumor milieus is complex because cancer progression and metastasis involve spatio-temporally evolving cell-matrix interactions, myriad interactions between tumor cells and auxiliary cells, hypoxic cores, leaky unorganized vasculature and a host of signaling molecules. Recent advances in 3D printing approaches enable the precise placement of cells, bioactive factors and biomaterials, thus permitting the recapitulation of several features associated with the in vivo tumor microenvironment. 3D printed in vitro tumor models can serve as robust platforms to study mechanisms of disease progression, enable high throughput screening of drugs and aid the development of next generation molecular therapies. This focused review discusses the importance and relevance of 3D printing technologies in building 3D tumor models in vitro. Several recent 3D printed cancer models are discussed, as also the evolution and features of next-generation models.
Biofilm formation has been demonstrated for several pathogens and is evidently a significant microbial survival strategy. They have immense clinical relevance for their role in various infectious diseases and a range of device-related... more
Biofilm formation has been demonstrated for several pathogens and is evidently a significant microbial survival strategy. They have immense clinical relevance for their role in various infectious diseases and a range of device-related infections because of their increased tolerance to antibiotics. Intra- and inter-species interactions play an important role in the population dynamics and distribution of species within the biofilm community, thereby altering the course of infections and response to antimicrobial therapy. For instance, P. aeruginosa in the cystic fibrosis airway produces an exoproduct, 4-Hydroxy-2-heptylquinoline N-oxide (HQNO), that causes wild-type cells of S. aureus to phenotypically switch to small colony variants (SCVs). SCVs are problematic in chronic infections; even though they comprise a minor proportion of the population, they persist by virtue of their inherent resilience and host adaptability.