For the longest time in Melanoma therapy, only DTIC and interferon were cited in Melanoma therapy. Interferon was given in adjuvant setting Mostly and DTIC in Metastatic diseases from Melanoma. Despite our understanding of the working of Interferon, there no clear biomarker that would predict which melanoma would be more snsitive to Interferon. Therefore integration of Interferon into new combinations with new Target therapies such as Ipilimumab and Vemurafenib, remains a hot topic of investigation.
Interferons can act on tumor cell through the direct JAK-STAT pathway, but for some other reasons, go through the ISGF/GAS/PE-1/p91 pathways. The interferon can recruit stimulation of the IRF pathways as well as activating the MHC class I to immunologically block progression in Melanoma. How this will impact the effects of newly found pathways of Ipilimumab and Vemurafenib is anybody guess and a matter of current trials. It appears that we now have to play catch-up, since earlier investigations to define predictive biomarkers for interferon/DTIC responses were not timely completed. Turning and returning a old stone needs once again to be completed!
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