Guest Editor(s)
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- Prof. Enrico Mini
Università degli Studi di Firenze, Florence, Italy.
Website | E-mail
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- Prof. Godefridus J. (Frits) Peters
Amsterdam UMC, location VUMC, Laboratory Medical Oncology, Cancer Center, Amsterdam, The Netherlands.
Department of Biochemistry, Medical University of Gdansk, Gdansk, Poland.
Website | E-mail
Special Issue Introduction
Gastrointestinal cancers comprise a wide range of neoplasms affecting all the organs of the digestive system. Overall, they represent about 30% of all diagnosed neoplasms and about 38% of cancer related deaths. They mainly comprise carcinomas of the esophagus, stomach, liver and biliary tract, pancreas, and colon-rectum, but other types of neoplasms are also included such as small bowel carcinomas, primary gastric and intestinal lymphomas, neuroendocrine tumors of the gastrointestinal tract, gastrointestinal stromal tumors and anal canal cancer.
Despite early diagnostic tools for the most frequent neoplasms, a substantial percentage of cases displays metastasis at diagnosis or develops it following primary surgery. Under these circumstances, pharmacological anticancer therapy represents the primary treatment.
Recently, clinical improvements in efficacy outcomes of patients with gastrointestinal neoplasms have been obtained with a variety of anticancer agents, including cytotoxic agents, so called targeted-agents and immune active drugs. However, both intrinsic and acquired tumor drug resistance are still a major obstacle toward cure of these patients.
Knowledge of the mechanisms underlying these phenomena is thus pivotal to develop pharmacological strategies able to circumvent tumor drug resistance. Several determinants have been identified in all human cancers. They comprise mechanisms occurring at the genome, epigenome, transcriptome, and protein levels as well as at the oncometabolite level.
Cancer stem cells, embryonic transcription factors, epithelial mesenchymal transition, deleterious changes in proteins/enzymes involved in the absorption, distribution, metabolism, and excretion of anticancer drugs, as well as dysregulated metabolism in cancer and immune cells represent relevant examples of cancer genotypic/phenotypic alterations responsible for drug resistance.
This Special Issue is aimed at summarizing current advanced knowledge and latest acquisitions in this field, to provide guidance to further research for a more extensive understanding of drug resistance and for the development of pharmacological approaches to overcome it.
Submission Deadline
30 Sep 2022
Cancer Drug Resistance
