Erlotinib augmentation with dapsone for rash mitigation and increased anti-cancer effectiveness.

摘要: Background The epidermal growth factor receptor tyrosine kinase inhibitor erlotinib has failed in many ways to be as potent the anti-cancer role pre-clinical studies would have suggested. This paper traces some aspects of this failure a compensatory erlotinib-mediated increase interleukin-8. Many other-but not all- cancer chemotherapeutic cytotoxic drugs also provoke malignant clone’s interleukin-8 synthesis. Untreated glioblastoma and other cells themselves natively synthesize Interleukin-8 tumor promoting, mobility metastasis formation enhancing, effects well pro-angiogenesis effects.