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Nicholas J. S. Perry

Researcher at Institute of Cancer Research

Publications -  11
Citations -  1187

Nicholas J. S. Perry is an academic researcher from Institute of Cancer Research. The author has contributed to research in topics: Cancer & Cell signaling. The author has an hindex of 7, co-authored 11 publications receiving 810 citations. Previous affiliations of Nicholas J. S. Perry include Imperial College London.

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Perioperative events influence cancer recurrence risk after surgery.

TL;DR: The rationale and early evidence for the adaptation of anaesthetic techniques and the strategic use of anti-adrenergic, anti-inflammatory, and/or antithrombotic therapies hold promise as affordable, readily available interventions that will improve the postoperative recurrence-free survival of patients with cancer.
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Cancer recurrence after surgery: Direct and indirect effects of anesthetic agents*

TL;DR: A review examines the most widely postulated mechanisms for the impact of anesthesia on neuroendocrine and immune function, and proposes that an upregulation of HIFs in tumor cells by these anesthetics may contribute to a tumor's recurrence by stimulating cytoprotective or protumorigenic behavior in residual cells.
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Prostate cancer cell malignancy via modulation of HIF-1α pathway with isoflurane and propofol alone and in combination.

TL;DR: The findings suggest that modulation of HIF-1α activity by anaesthetics may affect cancer recurrence following surgery, and isoflurane but not propofol should be avoided for use in cancer surgery.
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Isoflurane, a commonly used volatile anesthetic, enhances renal cancer growth and malignant potential via the hypoxia-inducible factor cellular signaling pathway in vitro.

TL;DR: Evidence is provided that a frequently used anesthetic can exert a protumorigenic effect on a human cancer cell line, and this may represent an important contributory factor to high recurrence rates observed after surgery.
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DNA Damage, Repair, and Cancer Metabolism.

TL;DR: links between cancer metabolism and DNA damage/DNA repair are increasingly apparent, yielding opportunities to investigate the mechanistic basis behind potential metabolic vulnerabilities of a substantial fraction of tumors.