From paradox to target: IFN-β hijacks MEK signaling to drive a cell death-evading dormant phenotype in colorectal cancer.

A paradoxical immune signal keeps metastatic cancer dormant, revealing a vulnerability that blocking could prevent cancer's return.

IFN-β paradoxically promotes colorectal cancer dormancy by hijacking MEK signaling to establish a cell death-resistant dormant state; co-targeting the IFN-β/MEK axis may prevent metastatic dormancy escape and represents a novel therapeutic vulnerability in CRC.

What the study was

Study design

translational

Category

novel_therapeutics

Maturity

preclinical

Journal

Journal of Experimental & Clinical Cancer Research

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