Year: 2017
Type: review
Abstract: Historically, it has been widely presumed that differentiated cells are determined during development and become irreversibly committed to their designated fates. In certain circumstances, however, differentiated cells can display plasticity by changing their identity, either by dedifferentiation to a progenitor-like state or by transdifferentiation to an alternative differentiated cell type. Such cellular plasticity can be triggered by physiological or oncogenic stress, or it can be experimentally induced through cellular reprogramming. Notably, physiological stresses that promote plasticity, such as severe tissue damage, inflammation, or senescence, also represent hallmarks of cancer. Furthermore, key drivers of cellular plasticity include major oncogenic and tumor suppressor pathways and can be exacerbated by drug treatment. Thus, plasticity may help cancer cells evade detection and treatment. We propose that cancer can be considered as a disease of excess plasticity, a notion that has important implications for intervention and treatment.
Source: Annual Review of Cancer Biology
Language: English
Topic: Cancer Cells and Metastasis
Subfield: Oncology
Field: Medicine
Domain: Health Sciences
Open Access status: bronze
Awards: Progenitor cells of the mouse prostate epithelium, Analysis of drug response in organoids and mouse models, Roles for Nkx3.1 in prostate cancer initiation, Roles for Nkx3.1 in prostate cancer initiation, Topology of Cancer Evolution and Heterogeneity, Investigating the cell of origin for bladder cancer, Molecular mechanisms of prostate cancer metastasis, Preclinical analyses of advanced prostate cancer in genetically-engineered mice
OpenAlex ID: W2632214275