Thank you so much Geert!

Thank you so much Pedro and Ancely for highlighting our study 🙏

Thank you so much Antonio!

Thank you Alex!

Thank you Geert!

Thank you so much Jessalyn!

* Modulation of EMCS’s integrity and function emerges as a therapeutic strategy to control ferroptosis susceptibility in ferroptosis-resistant cancer cells.

*The vulnerability of triple-negative breast cancer cell phenotypes to ferroptosis directly correlates with EMCS’s structural integrity and contact site density.

* Oxi-lipidomics analysis of EMCS fractions reveals that these membranes are enriched in ferroptosis-prone phospholipid species, making these sites hotspots for initial phospholipid peroxidation.

* Phospholipid peroxide accumulation triggers expansion of EMCSs, facilitating the spreading of lipid-ROS to the mitochondria and inducing their fragmentation.

Highlights of the study
* Phospholipid peroxidation initiates within 5 minutes of ferroptosis induction, specifically at subdomains of the ER membrane in close contact with the mitochondria, called ER-mitochondria contact sites or EMCSs.

how it controls the melanoma drug tolerant persister state and the consequences of its perturbation on ferroptosis 2/2