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dc.contributor.authorAdamska, Aleksandra
dc.contributor.authorElaskalani, Omar
dc.contributor.authorEmmanouilidi, Aikaterini
dc.contributor.authorKim, Minkypung
dc.contributor.authorAbdol Razak, Norbaini Binti
dc.contributor.authorMetharom, Pat
dc.contributor.authorFalasca, Marco
dc.identifier.citationAdamska, A. and Elaskalani, O. and Emmanouilidi, A. and Kim, M. and Abdol Razak, N. and Metharom, P. and Falasca, M. 2018. Molecular and cellular mechanisms of chemoresistance in pancreatic cancer. Advances in Biological Regulation. 68: pp. 77-87.

Pancreatic Ductal Adenocarcinoma (PDAC) is one of the most chemoresistant cancers, and current therapies targeting cancer-associated molecular pathways have not given satisfactory results, owing in part to rapid upregulation of alternative compensatory pathways. Most of the available treatments are palliative, focussing on improving the quality of life. At present, available options are surgery, embolization, radiation, chemotherapy, immunotherapy and use of other more targeted drugs. In this review, we describe the cellular and molecular effects of current chemotherapy drugs such as gemcitabine, FOLFIRINOX (5-fluorouracil [5-FU], oxaliplatin, irinotecan, and leucovorin) and ABRAXANE (nab-Paclitaxel), which have shown a survival benefit, although modest, for pancreatic cancer patients. Nevertheless, gemcitabine remains the standard first-line option for advanced-stage pancreatic cancer patients and, as resistance to the drug has attracted an increasing scientific interest, we deliberate on the main intracellular processes and proteins vital in acquired chemoresistance to gemcitabine. Lastly, our review examines various microenvironmental factors capable of instigating PDAC to develop resistance to chemotherapeutic drugs.

dc.titleMolecular and cellular mechanisms of chemoresistance in pancreatic cancer
dc.typeJournal Article
dcterms.source.titleAdvances in Biological Regulation
curtin.departmentSchool of Pharmacy and Biomedical Sciences
curtin.accessStatusFulltext not available

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