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Matthew Welsch

Researcher at Columbia University

Publications -  18
Citations -  6158

Matthew Welsch is an academic researcher from Columbia University. The author has contributed to research in topics: Cancer & Cell. The author has an hindex of 9, co-authored 18 publications receiving 3681 citations. Previous affiliations of Matthew Welsch include Yale University & Howard Hughes Medical Institute.

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Regulation of Ferroptotic Cancer Cell Death by GPX4

TL;DR: Targeted metabolomic profiling and chemoproteomics revealed that GPX4 is an essential regulator of ferroptotic cancer cell death and sensitivity profiling in 177 cancer cell lines revealed that diffuse large B cell lymphomas and renal cell carcinomas are particularly susceptible to GPx4-regulated ferroPTosis.
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Privileged Scaffolds for Library Design and Drug Discovery

TL;DR: This review explores the concept of using privileged scaffolds to identify biologically active compounds through building chemical libraries by revealing through four selected examples the present state of the art in privileged scaffold library synthesis.
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Pharmacological inhibition of cystine–glutamate exchange induces endoplasmic reticulum stress and ferroptosis

TL;DR: Dixon, Patel, et al. as mentioned in this paper found that erastin is a very effective inhibitor of system xc− function and that it is over 1000 times more potent than the previously known best inhibitor, sulfasalazine.
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Multivalent Small-Molecule Pan-RAS Inhibitors

TL;DR: The synthesis and testing of potential small-molecule pan-RAS ligands are described, which were designed to interact with adjacent sites on the surface of oncogenic KRAS and suggest that pan- RAS inhibition may be an effective therapeutic strategy for some cancers.
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Modulatory profiling identifies mechanisms of small molecule-induced cell death

TL;DR: Modulatory profiling of compounds correctly predicted three previously uncharacterized compounds to be microtubule-destabilizing agents, classified numerous compounds that act nonspecifically, and identified compounds that cause cell death through a mechanism that is morphologically and biochemically distinct from previously established ones.