Article
Targeting methionine with oral recombinant methioninase (o-rMETase) arrests a patient-derived orthotopic xenograft (PDOX) model of BRAF-V600E mutant melanoma: implications for chronic clinical cancer therapy and prevention.
Cell cycle (Georgetown, Tex.) - 1 Jan 2018
Kawaguchi Kei, Han Qinghong, Li Shukuan, Tan Yuying, Igarashi Kentaro, Kiyuna Tasuku, Miyake Kentaro, Miyake Masuyo, Chmielowski Bartosz, Nelson Scott D, Russell Tara A, Dry Sarah M, Li Yunfeng, Singh Arun S, Eckardt Mark A, Unno Michiaki, Eilber Fritz C, Hoffman Robert M
Abstract excerpt
The elevated methionine (MET) use by cancer cells is termed MET dependence and may be the only known general metabolic defect in cancer. Targeting MET by recombinant methioninase (rMETase) can arrest the growth of cancer cells in vitro and in vivo. We previously reported that rMETase, administrated by intra-peritoneal injection (ip-rMETase), could inhibit tumor growth in a patient-derived orthotopic xenograft...
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