Why don’t we get more cancer? A proposed role of the microenvironment in restraining cancer progression

By Mina J. Bissell, W. C. Hines. Nature Medicine, 2011

1,473 citations recorded by the source corpus.

Tumors are like new organs and are made of multiple cell types and components. The tumor competes with the normal microenvironment to overcome antitumorigenic pressures. Before that battle is won, the tumor may exist within the organ unnoticed by the host, referred to as 'occult cancer'. We review how normal tissue homeostasis and architecture inhibit progression of cancer and how changes in the microenvironment can shift the balance of these signals to the procancerous state. We also include a discussion of how this information is being tailored for clinical use.

Subfields: Cancer Research, Oncology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/4fb0aaf572b558fa72f08208fca0fbfce3756cc0

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Citations in the corpus

New horizons in tumor microenvironment biology: challenges and opportunities (2015, background): “Cancer cells first breach the basement membrane, a specialized ECM structure in the TME, by co-opting the EMT program, which allows dissolution of tight junctions, loss of cell polarity, and acquisition of multiple mesenchymal attributes [81].”
Recent developments in myofibroblast biology: paradigms for connective tissue remodeling. (2012, background): “Patients with breast cancer whose tumors express this wound-response signature have a markedly reduced overall survival and distant metastasis-free survival compared with those with tumors that do not express this signature.(80) Immunohistochemical analysis of breast tumors also reveals that many of”
In Vivo Imaging Reveals Extracellular Vesicle-Mediated Phenocopying of Metastatic Behavior (2015, background): “Together with the diverging microenvironment surrounding tumor cells, this leads to intercellular differences in epigenetic profiles and, subsequently, to differential cellular behavior (Bissell and Hines, 2011; Postovit et al., 2006).”
Exosome-Based Cell-Cell Communication in the Tumor Microenvironment (2018, background): “In its intricacy, the tumor microenvironment has emerged to be a key modulator of tumor progression by providing inhibitory or stimulatory growth signals (Bissell and Hines, 2011).”
Vitamin D Receptor-Mediated Stromal Reprogramming Suppresses Pancreatitis and Enhances Pancreatic Cancer Therapy (2014, neutral): “The notion that cellular and structural components of a ‘‘normal’’ microenvironment exert tumor-suppressive forces and signals has been discussed previously (Bissell and Hines, 2011), although this has not been demonstrated in the pancreas and leaves in question the potential benefits of reprogramme”
YAP/TAZ at the roots of cancer (2016, background): “In normal epithelial organs, tissue architecture has been suggested as an overarching tumor suppressor (Bissell and Hines, 2011), strictly confining mechanical strains only to specific tissue niches.”
Fibroblast heterogeneity in the cancer wound (2014, background): “Indeed, this has been proposed as one reason why certain tumors found in autopsy studies appear dormant and nonprogressing (Bissell and Hines, 2011).”
Cancer Evolution: Mathematical Models and Computational Inference (2014, background): “…heterogeneity with analyses of tumor tissue architecture to account for genetic variation and epigenetic variation of cancer cells as well as their interactions with surrounding cells (Marusyk et al. 2012; Barcellos-Hoff et al. 2013; Frank and Rosner 2012; Bissell and Hines 2011; Cairns 1975).”