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The cancer microenvironment, or tumour microenvironment, describes the non-cancerous cells present in the tumour. These include fibroblasts, immune cells and cells that comprise the blood vessels. It also includes the proteins produced by all of the cells present in the tumour that support the growth of the cancer cells.
The interaction between colon cancer cells and colonic epithelial cells (CECs) is critical yet not well-known. Here, the authors show that tumor extracellular vesicles mediate mitochondrial DNA transfer to CECs, initiating mitochondrial activation and RelA-induced TGFβ1 expression, leading to tumor progression.
In patient with glioblastoma, a major cause of resistance to chemotherapy and radiotherapy is the high degree to intratumoral heterogeneity and cell plasticity. Here, the authors demonstrate that chemoradiation induces the reprograming of glioblastoma cells into an invasive and vessel co-opting state, termed VC-Resist, capable of promoting resistance to therapy.
Assessing tumour microenvironment-targeted drug candidates remains challenging. Here, the authors develop a comprehensive screening platform that allows for monitoring, quantifying, and ranking drug-induced effects in self-organizing, vascularized tumour spheroids.
An inflammatory-fibrotic tumor microenvironment supports metastatic disease progression in pancreatic ductal adenocarcinoma (PDAC). Here the authors show that metastasis-infiltrating macrophages influence metastasis-associated fibroblast (MAF) heterogeneity in liver metastatic PDAC, by promoting JAK/STAT signalling pathway activation in MAFs.
In this Tools of the Trade article, Zuzana Tatarova describes the development of MIMA, an integrated analytical platform providing the quantitative information on tumour microenvironment drug responses required for effective treatment design.
In this recent study, He et al. establish that chronic stress promotes metastasis through stress-induced formation of neutrophil extracellular traps (NETs).
Cancer cells adjust the composition of their glycocalyx to increase its thickness and create a physical barrier that shields them from immune recognition and engagement.