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Marianne Koritzinsky

Researcher at Princess Margaret Cancer Centre

Publications -  89
Citations -  7701

Marianne Koritzinsky is an academic researcher from Princess Margaret Cancer Centre. The author has contributed to research in topics: Unfolded protein response & Cancer. The author has an hindex of 38, co-authored 76 publications receiving 6899 citations. Previous affiliations of Marianne Koritzinsky include Maastricht University & Maastricht University Medical Centre.

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Hypoxia signalling through mTOR and the unfolded protein response in cancer

TL;DR: Growing evidence suggests that HIF-, mTOR- and UPR-dependent responses to hypoxia act in an integrated way, influencing each other and common downstream pathways that affect gene expression, metabolism, cell survival, tumorigenesis and tumour growth.
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ER stress‐regulated translation increases tolerance to extreme hypoxia and promotes tumor growth

TL;DR: It is demonstrated that cells cultured under hypoxic/anoxic conditions and transformed cells in hypoxic areas of tumors activate a translational control program known as the integrated stress response (ISR), which adapts cells to endoplasmic reticulum (ER) stress and suggests that this pathway is an attractive target for antitumor modalities.
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Regulation of protein synthesis by hypoxia via activation of the endoplasmic reticulum kinase perk and phosphorylation of the translation initiation factor eif2alpha

TL;DR: Results indicate that adaptation of cells to hypoxic stress requires activation of PERK and phosphorylation of eIF2α and suggest that the mechanism of hypoxia-induced translational attenuation may be linked to ER stress and the unfolded-protein response.
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Hypoxia-mediated down-regulation of Bid and Bax in tumors occurs via hypoxia-inducible factor 1-dependent and -independent mechanisms and contributes to drug resistance.

TL;DR: The contribution of Bid and/or Bax down-regulation to drug responsiveness was demonstrated by the relative resistance of normoxic cells that had no or reduced expression of Bid or Bax and by the finding that forcedexpression of Bid in hypoxic cells resulted in increased sensitivity to the topoisomerase II inhibitor etoposide.