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
(This article belongs to the Special Issue Patient-Derived Cancer Models from Basic Study to Clinical Application)
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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
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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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