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Efficacy of Recombinant Methioninase (rMETase) on Recalcitrant Cancer Patient-Derived Orthotopic Xenograft (PDOX) Mouse Models: A Review

1
AntiCancer, Inc., San Diego, CA 92111, USA
2
Department of Surgery, University of California, San Diego, CA 92093, USA
3
Department of Surgery, Graduate School of Medicine, Tohoku University, Sendai, Miyagi 9808575, Japan
*
Author to whom correspondence should be addressed.
Cells 2019, 8(5), 410; https://doi.org/10.3390/cells8050410
Received: 2 April 2019 / Revised: 13 April 2019 / Accepted: 17 April 2019 / Published: 2 May 2019
PDF [689 KB, uploaded 2 May 2019]

Abstract

An excessive requirement for methionine (MET), termed MET dependence, appears to be a general metabolic defect in cancer and has been shown to be a very effective therapeutic target. MET restriction (MR) has inhibited the growth of all major cancer types by selectively arresting cancer cells in the late-S/G2 phase, when they also become highly sensitive to cytotoxic agents. Recombinant methioninase (rMETase) has been developed to effect MR. The present review describes the efficacy of rMETase on patient-derived orthotopic xenograft (PDOX) models of recalcitrant cancer, including the surprising result that rMETase administrated orally can be highly effective.
Keywords: recombinant methioninase; methionine dependence; nude mice; orthotopic implantation; patient-derived tumor recombinant methioninase; methionine dependence; nude mice; orthotopic implantation; patient-derived tumor
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Kawaguchi, K.; Han, Q.; Li, S.; Tan, Y.; Igarashi, K.; Murakami, T.; Unno, M.; Hoffman, R.M. Efficacy of Recombinant Methioninase (rMETase) on Recalcitrant Cancer Patient-Derived Orthotopic Xenograft (PDOX) Mouse Models: A Review. Cells 2019, 8, 410.

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