Molecular and cellular mechanisms of chemoresistance in pancreatic cancer
(2018) In Advances in Biological Regulation 68. p.77-87- Abstract
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... (More)
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.
(Less)
- author
- Adamska, Aleksandra LU ; Elaskalani, Omar ; Emmanouilidi, Aikaterini ; Kim, Minkyoung ; Abdol Razak, Norbaini Binti ; Metharom, Pat and Falasca, Marco
- publishing date
- 2018
- type
- Contribution to journal
- publication status
- published
- keywords
- Animals, Deoxycytidine/analogs & derivatives, Drug Resistance, Neoplasm, Fluorouracil/therapeutic use, Humans, Pancreatic Neoplasms/drug therapy, Gemcitabine
- in
- Advances in Biological Regulation
- volume
- 68
- pages
- 77 - 87
- publisher
- Elsevier
- external identifiers
-
- pmid:29221990
- scopus:85044939171
- pmid:29221990
- DOI
- 10.1016/j.jbior.2017.11.007
- language
- English
- LU publication?
- no
- id
- b68df963-559b-452e-80cd-73f3d7152ff7
- date added to LUP
- 2023-05-22 10:06:51
- date last changed
- 2024-04-19 22:57:03
@article{b68df963-559b-452e-80cd-73f3d7152ff7,
abstract = {{<p>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.</p>}},
author = {{Adamska, Aleksandra and Elaskalani, Omar and Emmanouilidi, Aikaterini and Kim, Minkyoung and Abdol Razak, Norbaini Binti and Metharom, Pat and Falasca, Marco}},
keywords = {{Animals; Deoxycytidine/analogs & derivatives; Drug Resistance, Neoplasm; Fluorouracil/therapeutic use; Humans; Pancreatic Neoplasms/drug therapy; Gemcitabine}},
language = {{eng}},
pages = {{77--87}},
publisher = {{Elsevier}},
series = {{Advances in Biological Regulation}},
title = {{Molecular and cellular mechanisms of chemoresistance in pancreatic cancer}},
url = {{http://dx.doi.org/10.1016/j.jbior.2017.11.007}},
doi = {{10.1016/j.jbior.2017.11.007}},
volume = {{68}},
year = {{2018}},
}