Publications by authors named "K A Cohen-Solal"

Interferon (IFN)-λ, a type III interferon (IFN), is a member of a new family of pleotropic cytokines that share high similarity with classical IFNs α and β (IFN-α/β), type I IFNs. IFN-λ acts as an antiviral agent and displays distinct biological functions, including tumor suppression. Although it activates the common Janus kinase (JAK) and signal transducer and activator of transcription (STAT) pathways, similar to IFN-α/β, IFN-λ differentially induces the expression of IFN-stimulated genes (ISGs).

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Resistance to targeted therapy in cancer is often coupled with the acquisition of a pro-invasive phenotype by tumors cells and a highly permissive tumor microenvironment promoting drug resistance. Transcription factors are frequently shown as major points of convergence of multiple dysregulated receptors and signaling pathways in cancer. Several transcription factors are now incriminated as drivers of both drug resistance and invasiveness.

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IFN-λ is the newly established type III IFN with unique immunomodulatory functions. In contrast to the IFN-α/β family and to some extent IFN-γ, IFN-λ is apparently acting in specific areas of the body to activate resident immune cells and induces a local immunity, instrumental in preventing particular infections and also keeping transformed cells under control. Mucosal areas of lung and gastrointestinal tracts are now under scrutiny to elucidate the immune mechanisms triggered by IFN-λ and leading to viral protection.

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Hepatocellular carcinoma (HCC) is the most prevalent type of liver cancer. No significant improvement has been reported with currently available systemic therapies. IFN-α has been tested in both clinic and animal models and only moderate benefits have been observed.

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