IFNγ Mutations Prompt CTLA-4 Inhibitor Resistance
Copyright policy )IFNγ Mutations Prompt CTLA-4 Inhibitor Resistance
Abstract A recent study pinpoints loss of IFNγ signaling as one reason why many patients do not respond to the CTLA-4 inhibitor ipilimumab. Analyzing whole-exome tumor sequencing data from 16 patients with melanoma, the researchers found multiple copy-number alterations that led to the loss of key IFNγ pathway genes in 12 ipilimumab nonresponders. Mice bearing melanoma tumors that lacked one of these genes, IFNGR1, also had an impaired response to anti–CTLA-4 therapy and significantly reduced overall survival, compared with their counterparts whose tumors had intact IFNGR1.
Skin Neoplasms, Antibodies, Monoclonal, Sequence Analysis, DNA, Prognosis, Ipilimumab, Interferon-gamma, Mice, Drug Resistance, Neoplasm, Mutation, Animals, Humans, Melanoma, Signal Transduction
Skin Neoplasms, Antibodies, Monoclonal, Sequence Analysis, DNA, Prognosis, Ipilimumab, Interferon-gamma, Mice, Drug Resistance, Neoplasm, Mutation, Animals, Humans, Melanoma, Signal Transduction
selected citations These citations are derived from selected sources.This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).3 popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network.Average influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically).Average impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network.Average
Citations provided by BIP!Popularity provided by BIP!