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Nevertheless, this adaptive evolution, which frequently takes the form of a highly plastic, partial EMT (p-EMT) state, induces a profound lipidomic reconfiguration and iron dysregulation, thereby inadvertently revealing a targetable metabolic vulnerability: ferroptosis. In this Perspective, we outline the hierarchical molecular logic that governs this susceptibility, emphasizing the manner in which progressive p53 mutations (ranging from loss-of-function to gain-of-function) transform p-EMT cells from passive sensitization to an extreme \u201cmetabolic addiction.\u201d We argue that conventional \u201coccupancy-driven\u201d kinase inhibitors are unable to eliminate these resistant populations because they are unable to dismantle the essential non-catalytic scaffolding functions of core EMT-induced kinases (EIKs). As a result, we suggest a paradigm shift toward a chemical biology approach that is \u201cevent-driven.\u201d The p-EMT infrastructure can be irreversibly destroyed and resistant cells can be compelled to undergo catastrophic lipid peroxidation by deploying proteolysis targeting chimeras (PROTACs) against concealed scaffold super-hubs, particularly AXL and lemur tail kinase 3 (LMTK3), which are indispensable for stabilizing the hybrid p-EMT infrastructure. Additionally, we investigate the spatiotemporal modulation of this synthetic lethal axis by the tumor microenvironment (TME) through matrix mechanics and extracellular vesicles (EVs). Ultimately, we suggest a multimodal liquid biopsy strategy that couples specific oxidized phospholipid signatures with circulating tumor DNA (ctDNA) kinetics to precisely monitor in vivo ferroptotic events. This approach offers a transformative roadmap for eradicating minimal residual disease (MRD) and surmounting BC dormancy.<\/jats:p>","DOI":"10.1038\/s41420-026-03217-5","type":"journal-article","created":{"date-parts":[[2026,7,4]],"date-time":"2026-07-04T12:14:25Z","timestamp":1783167265000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Unlocking the ferroptotic window: Lipidomic rewiring and metabolic addiction in EMT-driven breast cancer resistance"],"prefix":"10.1038","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-6090-2490","authenticated-orcid":false,"given":"Jian","family":"Lu","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chrysa","family":"Filippopoulou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Junjie","family":"Sun","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pengtao","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chaoyue","family":"Pan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaoyan","family":"Wu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xidong","family":"Gu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xiaohong","family":"Xie","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qijin","family":"Shu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4417-2707","authenticated-orcid":false,"given":"Georgios","family":"Giamas","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2026,7,4]]},"reference":[{"key":"3217_CR1","doi-asserted-by":"publisher","DOI":"10.1016\/j.drup.2026.101353","volume":"85","author":"B Cerci","year":"2026","unstructured":"Cerci B, Saatci O, Basik M, Sahin O. 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