Targeting Ferroptosis to Iron Out Cancer.
By Behrouz Hassannia, Peter Vandenabeele, T. Vanden Berghe. Cancer Cell, 2019
2,119 citations recorded by the source corpus.
One of the key challenges in cancer research is how to effectively kill cancer cells while leaving the healthy cells intact. Cancer cells often have defects in cell death executioner mechanisms, which is one of the main reasons for therapy resistance. To enable growth, cancer cells exhibit an increased iron demand compared with normal, non-cancer cells. This iron dependency can make cancer cells more vulnerable to iron-catalyzed necrosis, referred to as ferroptosis. The identification of FDA-approved drugs as ferroptosis inducers creates high expectations for the potential of ferroptosis to be a new promising way to kill therapy-resistant cancers.
Subfields: Cancer Research, Molecular Biology, Pulmonary and Respiratory Medicine
View Paper: https://www.semanticscholar.org/paper/483179f4d0c0704dea2a05376d6902e0de5bf2b3
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Cancer Research
In Molecular Biology
In Pulmonary and Respiratory Medicine
Citations in the corpus
- CD8+ T cells and fatty acids orchestrate tumor ferroptosis and immunity via ACSL4 (2022, background): “Ferroptosis is regulated by fatty acid metabolism (Kagan et al., 2017) (Hassannia et al., 2019; Magtanong et al., 2019).”
- Targeting cell death pathways for cancer therapy: recent developments in necroptosis, pyroptosis, ferroptosis, and cuproptosis research (2022, background): “RT-generated ROS remove electrons from PUFAs, resulting in the formation of PUFA radicals (PUFAs-OH).”