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Cancer therapeutic resistance occurs as cancers develop resistance to treatments such as chemotherapy, radiotherapy and targeted therapies, through many different mechanisms. These include specific genetic and epigenetic changes in the cancer cell and/or the microenvironment in which the cancer cell resides.
Transferrin receptor targeting chimeras have been developed that enable targeting of drug resistance in epidermal growth factor receptor-driven lung cancer and reversible control of human primary chimeric antigen receptor T cells, representing a promising new family of bifunctional antibodies for targeted cancer therapy.
Hata and colleagues discuss the complexity and clinical importance of cancer persister cells, as well as existing methods for studying and eliminating them, expanding on challenges and opportunities in this area of research.
Leighow et al. develop a strategy called the dual-switch selection gene drive platform, which enables the evolutionary dynamics of acquired resistance to be manipulated for therapeutic ends.
