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Anika Nagelkerke

Researcher at Imperial College London

Publications -  47
Citations -  6963

Anika Nagelkerke is an academic researcher from Imperial College London. The author has contributed to research in topics: Cancer & Breast cancer. The author has an hindex of 19, co-authored 41 publications receiving 5983 citations. Previous affiliations of Anika Nagelkerke include University of Groningen & Radboud University Nijmegen.

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Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

Daniel J. Klionsky, +2522 more
- 21 Jan 2016 - 
TL;DR: In this paper, the authors present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macro-autophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Hypoxia Stimulates Migration of Breast Cancer Cells via the PERK/ATF4/LAMP3-arm of the Unfolded Protein Response

TL;DR: The PERK/ATF4/LAMP3-arm of the UPR is an additional pathway mediating hypoxia-induced breast cancer cell migration and is found to be optimal in stimulating migration of MDA-MB-231 cells.
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The mechanical microenvironment in cancer: How physics affects tumours.

TL;DR: Overall, tumour mechanics are significantly different from normal tissue, and this feature should be further explored for use in cancer prevention, detection and treatment.
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Hypoxic Activation of the PERK/eIF2α arm of the Unfolded Protein Response Promotes Metastasis through Induction of LAMP3

TL;DR: Hypoxia is a potent activator of the PERK/eIF2α signaling pathway, a component of the unfolded protein response (UPR) and an important mediator of hypoxia tolerance and tumor growth, and the importance of this pathway in the metastasis of human cervix carcinoma was investigated.
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The unfolded protein response as a target for cancer therapy

TL;DR: Factors associated with the unfolded protein response that represent potential therapeutic targets are discussed, indicating increased dependence on the UPR in multiple cancers, and can confer resistance to anti-cancer treatment.