Guest Editors
Dr. Chen Li, Department of Biology, Chemistry, Pharmacy, Free University of Berlin, Germany.
E-mail:chen.li.scholar@gmail.com; chen.li@fu-berlin.de
Dr. Ayman Moawad Mahmoud, Department of Life Sciences, Manchester Metropolitan University, Manchester, United Kingdom. E-mail:a.mahmoud@mmu.ac.uk
Summary
Although progress in anticancer therapy advancements was made somehow in the last decade, drug resistance of chemotherapy and immunotherapy with the subsequent spreading of metastases are the leading causes of failure in the treatment of multiple cancers. Drug resistance development involves dynamic changes of cancer heterogeneity as cancer evolves, as well as drug-induced physiological changes, specifically amplification/activation of oncogenes, loss/inactivation of tumor suppressor genes, dysregulation of transcriptional networks, altered metabolism, and microenvironment. Various clinical strategies, including combination therapies and epigenetic drugs, have been used to avoid or reverse drug resistance. Identifying both when the loss of efficacy in cancer drugs begins, and also the mechanism by which this resistance develops is of vital importance to clinicians and researchers tasked with identifying the issue, theorizing solutions, and implementing new treatments in the wake of resistance. The ultimate goal in these instances must be that of treating cancer and preventing further resistance development further down the line. By identifying these often unpredictable mechanisms of resistance, new refined drug molecules or drug delivery methods can be developed to avoid cancer drug resistance and ensure patient therapy is optimum.
Keywords
Drug resistance; Cancer chemotherapy; cancer immunotherapy; Epigenetics
Published Papers