期刊
BRITISH JOURNAL OF CANCER
卷 127, 期 3, 页码 377-378出版社
SPRINGERNATURE
DOI: 10.1038/s41416-022-01905-4
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Colorectal peritoneal metastases (CRPM) can develop resistance to oxaliplatin, a commonly used chemotherapy agent for hyperthermic intraperitoneal chemotherapy (HIPEC). However, genomic deletion or pharmacological inhibition of glutamate-cysteine ligase in CRPM tumors can effectively reduce the inactivation of oxaliplatin mediated by glutathione. These findings may reignite interest in combining HIPEC with cytoreductive surgery for the management of this previously considered incurable stage-IV disease.
Colorectal peritoneal metastases (CRPM) can be resistant to the chemotherapy agent (oxaliplatin) most employed, up until recently, as hyperthermic intraperitoneal chemotherapy (HIPEC). Glutathione-mediated inactivation of oxaliplatin can be substantially reduced by genomic deletion of the gene or pharmacological inhibition of glutamate-cysteine ligase in CRPM tumouroids. These discoveries may rekindle the enthusiasm for HIPEC in concert with cytoreductive surgery, which has been employed to manage patients with this once-nihilistic form of stage-IV disease.
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