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Special Issue "Combating Drug Resistance in Cancer—from Novel Biomarkers to Enhanced Therapeutic Efficacy"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 31 August 2022 | Viewed by 576

Special Issue Editors

Dr. Mirela Sedic
E-Mail Website
Guest Editor
Centre for Applied Bioanthropology, Institute for Anthropological Research Ljudevita Gaja 32, 10000 Zagreb, Croatia
Interests: chemotherapy; chemoresistance; cancer biology; colon cancer; cell signaling; proteomics; lipidomics; sphingolipids; biomarkers; personalised medicine
Special Issues, Collections and Topics in MDPI journals
Dr. Miran Čoklo
E-Mail Website
Guest Editor
Centre for Applied Bioanthropology, Institute for Anthropological Research, Zagreb, Croatia
Interests: personalised medicine; colon cancer; biomarkers; head and neck cancer; lipidomics; pharmacogenomics

Special Issue Information

Dear Colleagues,

The development of chemoresistance represents a major hurdle for the successful treatment of cancer. A multitude of scientific findings from recent preclinical and clinical studies have undoubtedly broadened our current knowledge of the mechanisms underlying the development of cancer drug resistance and have paved the way for the design of novel therapeutic strategies for patients with refractory cancer. In particular, numerous genomics studies have already been conducted in different cancer types to uncover major molecular players governing cancer progression and treatment response, with these data being publicly available in different cancer databases and repositories. However, the more comprehensive characterisation of cancer drug resistance encompassing different layers of molecular information (e.g., transcriptomics, proteomics, metabolomics, lipidomics, microRNAs, long non-coding RNAs, medical/mass-spectrometry imaging, etc.) and the integration and analysis of data from public cancer data repositories and newly obtained experimental data using artificial intelligence tools would facilitate the data-driven identification of the key molecular features of chemoresistance. In addition, the discovery of novel biomarkers that would enable treatment response to be monitored for a timely identification of cancer patients with an increased risk for disease recurrence holds promise to improve the management of cancer patients. In this Special Issue of the IJMS, we welcome basic and translational studies that address all issues pertinent to cancer drug resistance, including the following: the discovery of novel molecular mechanisms and druggable targets for chemoresistance; the identification of novel prognostic and predictive biomarkers of chemoresistance to enable patient stratification and to tailor treatment; the application of bioinformatics and artificial intelligence tools for drug response prediction, risk stratification and the elucidation of the chemoresistance mechanisms by integrating different molecular information; and the discovery of novel combinations of clinically approved anticancer drugs with chemotherapy-sensitising agents to overcome chemoresistance in cancer patients.

Dr. Mirela Sedic
Dr. Miran Čoklo
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • chemoresistance
  • biomarker
  • artificial intelligence
  • bioinformatics
  • -omics
  • anti-cancer drug response prediction
  • risk stratification
  • rational cancer treatment combinations

Published Papers (1 paper)

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Research

Article
Antigen Peptide Transporter 1 (TAP1) Promotes Resistance to MEK Inhibitors in Pancreatic Cancers
Int. J. Mol. Sci. 2022, 23(13), 7168; https://doi.org/10.3390/ijms23137168 - 28 Jun 2022
Viewed by 373
Abstract
Mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitors show limited benefit in Kirsten rat sarcoma (KRAS) mutant pancreatic cancer due to drug resistance. To identify mechanisms of resistance to MEK inhibitor (MEKi), we employed a differential expression analysis of MEKi-sensitive versus MEKi-resistant [...] Read more.
Mitogen-activated protein kinase (MAPK) kinase (MEK) inhibitors show limited benefit in Kirsten rat sarcoma (KRAS) mutant pancreatic cancer due to drug resistance. To identify mechanisms of resistance to MEK inhibitor (MEKi), we employed a differential expression analysis of MEKi-sensitive versus MEKi-resistant KRAS-mutant pancreatic cancer cell lines. Here, we report that the antigen peptide transporter 1 (TAP1) expression levels of MEKi-resistant cell lines were notably higher than those of MEKi-sensitive cell lines. Suppression of TAP1 significantly sensitized the MEKi-resistant pancreatic ductal adenocarcinoma (PDAC) cells to MEKi and induced higher apoptotic rate in vitro. Moreover, knockdown of TAP1 in MEKi-resistant tumor significantly decreased tumor growth in vivo. Consistently, overexpression of TAP1 in sensitive PDAC cells resulted in increased resistance to MEKi, both in vitro and in vivo. Mechanistic studies demonstrated that TAP1 promoted chemoresistance by enhancing the transport of MEKi out of PDAC cells, leading to reduced intracellular MEKi concentration and attenuated inhibition of KRAS signaling pathways. Moreover, TAP1 expression increased spheroid formation abilities of PDAC cells. These findings suggest that TAP1 could serve as a potential marker for predicting the response of patients to MEKi. Combination of TAP1 suppression and MEKi may provide a novel therapeutic strategy for PDAC treatment. Full article
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