Journal
CANCER CELL
Volume 33, Issue 5, Pages 890-+Publisher
CELL PRESS
DOI: 10.1016/j.ccell.2018.03.017
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Funding
- NIH/NCI grants [P01 CA168585, R21 CA169993, R35 CA197633, R01 CA170689]
- Parker Institute for Cancer Immunotherapy
- American Cancer Society Research Scholar Award [RSG-12-257-01-TBE]
- Melanoma Research Alliance Established Investigator Award [20120279]
- UCLA Jonsson Cancer Center Foundation
- National Center for Advancing Translational Sciences UCLA CTSI Grant [UL1TR000124]
- Concern Foundation CONquer CanCER Now Award
- Dr. Robert Vigen Memorial Fund
- Garcia-Corsini Family Fund
- Ressler Family Fund
- Grimaldi Family Fund
- NIH Ruth L. Kirschstein Institutional National Research Service Award [T32-CA009120]
- V Foundation-Gil Nickel Family Endowed Fellowship in Melanoma Research
- Spanish Society of Medical Oncology (SEOM) for Translational Research in Reference Centers
- UCLA Medical Scientist Training Program [NIH NIGMS TG GM08042]
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Malignant transformation can result in melanoma cells that resemble different stages of their embryonic development. Our gene expression analysis of human melanoma cell lines and patient tumors revealed that melanoma follows a two-dimensional differentiation trajectory that can be subclassified into four progressive subtypes. This differentiation model is associated with subtype-specific sensitivity to iron-dependent oxidative stress and cell death known as ferroptosis. Receptor tyrosine kinase-mediated resistance to mitogen-activated protein kinase targeted therapies and activation of the inflammatory signaling associated with immune therapy involves transitions along this differentiation trajectory, which lead to increased sensitivity to ferroptosis. Therefore, ferroptosis-inducing drugs present an orthogonal therapeutic approach to target the differentiation plasticity of melanoma cells to increase the efficacy of targeted and immune therapies.
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