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Nicholas I Bartschat on Muck Rack

Nicholas I Bartschat

As seen in: BioRxiv, Cell Press
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Articles

Sumoylated Etv1 establishes mouse mammary cancer stem cells that support tumorigenesis by non-stem cancer cells

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By Zhijie Li, Kelsey E. Koch, Dakota Thompson, Jeremy Chang, Christopher Franke, Mohammed O. Suraju, Anna Beck, Allison Lorenzen, Jeffrey White, Nicholas I Bartschat, Mikhail V. Kulak, David Meyerholz, Colin Kenny, Ronald Weigel
| Cell Press Verified
Keywords mammary oncogenesis stem cells Etv1 sumoylation transcription tumorigenesis cancer stem cell mouse mammary carcinoma neu breast cancer Get full text access Log in, subscribe or purchase for full access. References 1. Siegel, R.L. ∙ Miller, K.D. ∙ Fuchs, H.E. ... Cancer Statistics, 2021 CA Cancer J. Clin. 2021; 71:7-33 2. Colleoni, M. ∙ Munzone, E. Extended adjuvant chemotherapy in endocrine non-responsive disease Breast. 2013; 22:S161-S164 3. Morrow, M.
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Antagonistic Roles for MITF and TFE3 in Melanoma Plasticity

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By Jeremy T. Chang, Katelyn R Campbell-Hanson, Marion Vanneste, Nicholas I Bartschat
| BioRxiv
Abstract Melanoma cells have the ability to switch from a melanocytic and proliferative state to a mesenchymal and invasive state and back again. This plasticity drives intra-tumoral heterogeneity, progression, and therapeutic resistance. Microphthalmia-associated Transcription Factor (MITF) promotes the melanocytic/proliferative phenotype, but factors that drive the mesenchymal/invasive phenotype and the mechanisms that effect the switch between cell states are unclear.
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