DOI 10.1007/s00280-015-2903-8 REVIEW ARTICLE Antimitotic drugs in the treatment of cancer

have unlimited replicative potential via the upregulation of telomerase (a specialized deoxyribonucleic acid (DNA) polymerase) expression that counters telomerase erosion (Fig. 1) [4]. In addition, cancer cells have the ability to evade tumor suppressor genes, resulting in sustained chronic prolifera-tion. These cells may avoid apoptosis induction by the loss of protein p53 (TP53) tumor suppressor function, or in the case of necrosis, proinflammatory signals that recruit cells of the immune system, which may promote malignancy and invasion [3, 5]. Cancer cells may also produce their own growth factor ligands such as Bombesin-like peptides (secreted by human small cell lung cancer) or signal to non-tumorigenic surrounding tissue to supply cancer cells with growth factors (Fig. 1) [6]. These cells may activat