RNA interference in the clinics: where are we standing now?

Over the last decade, the field of cancer therapy and the mode of action of approved cancer drugs have dramatically changed across the globe. The struggle against cancer in clinical trials shifted from the testing of cytotoxic ‘classical’ chemotherapeutic drugs toward agents with clearly defined molecular targets [1]. A deeper understanding of the underlying molecular and cellular mechanisms in cancer cells including cancer stem cells, miRNAs and circulating tumor DNA [2,3], which has been exponentially generated within the last 50 years, enabled the development of new drugs. This new class of targeted agents can essentially be divided into two groups of cancer therapeutics: small orally available molecules directed against intracellular (multiple) tyrosine kinases or mTOR pathway and ‘big’ monoclonal antibodies that are mainly directed against extracellular targets including membranous and soluble proteins [4].

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