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Cancers
Special Issues
Overcoming Chemoresistance in Cancer: Identifying Biomarkers and Novel Targets
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Overcoming Chemoresistance in Cancer: Identifying Biomarkers and Novel Targets

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Cancer Therapy".

Deadline for manuscript submissions: 1 March 2025 | Viewed by 1818

Special Issue Editors

Dr. Annapina Russo

E-Mail Website
Guest Editor
Department of Pharmacy, University of Naples “Federico II”, 80131 Naples, Italy
Interests: cancer; chemoresistance; nucleolar stress; extra-ribosomal function of ribosomal proteins; cell cycle
Special Issues, Collections and Topics in MDPI journals
Dr. Giulia Russo

E-Mail Website
Guest Editor
Department of Pharmacy, University of Naples “Federico II”, 80131 Naples, Italy
Interests: tumorigenesis; cancer therapy; TP53; ribosomal stress; extra-ribosomal function of ribosomal proteins
Special Issues, Collections and Topics in MDPI journals
Dr. Annalisa Pecoraro

E-Mail Website
Guest Editor
Department of Pharmacy, University of Naples “Federico II”, 80131 Naples, Italy
Interests: chemoresistance; targeted therapy; nucleolar stress; ribosomal proteins; signaling pathways in cancer

Special Issue Information

Dear Colleagues,

The development of chemoresistance remains the main obstacle in the successful treatment of cancer. There is no doubt that a great deal of work has been done in the last few years to increase our understanding of the mechanisms behind the development of drug resistance in cancer. However, the identification of new targets is crucial for the development of personalized therapeutic strategies aiming to overcome chemoresistance.

In this Special Issue of Cancers, original research articles and reviews are welcome. Research areas may include (but are not limited to) the following: the identification of novel molecular mechanisms of chemoresistance; the discovery of novel molecular biomarkers to allow cancer patient stratification and personalized treatment; the discovery of new drug targets; and the development of novel combined treatments targeting multiple signaling pathways.

We look forward to receiving your contributions.

Dr. Annapina Russo
Dr. Giulia Russo
Dr. Annalisa Pecoraro
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 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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • cancer treatment
  • chemoresistance
  • tumor microenvironment
  • cancer signaling pathways
  • targeted therapy
  • personalized anti-cancer therapies
  • biomarker
  • anti-cancer drug response prediction

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Published Papers (2 papers)

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Research

20 pages, 3056 KiB  
Article
Deciphering the Role of ASPM in Breast Cancer: A Comprehensive Multicohort Study
by Asmaa Ibrahim, Nehal M. Atallah, Shorouk Makhlouf, Michael S. Toss, Andrew Green and Emad Rakha
Cancers 2024, 16(22), 3814; https://doi.org/10.3390/cancers16223814 - 13 Nov 2024
Viewed by 491
Abstract
Background: Assembly factor for spindle microtubules (ASPM) has gained significant attention in cancer research due to its association with tumor growth and progression. Through the analysis of large-scale genomic datasets, ASPM has been identified as the top upregulated gene in breast cancer (BC), [...] Read more.
Background: Assembly factor for spindle microtubules (ASPM) has gained significant attention in cancer research due to its association with tumor growth and progression. Through the analysis of large-scale genomic datasets, ASPM has been identified as the top upregulated gene in breast cancer (BC), characterized by high proliferation. This multicohort study aimed to investigate the clinicopathological and prognostic significance of ASPM mRNA and protein expression in BC. Methods: ASPM mRNA expression was assessed using the Cancer Genome Atlas (TCGA) BC cohort and has been further validated in the Molecular Taxonomy of BC International Consortium (METABRIC) (n = 1980), The Uppsala cohort (n = 249), in addition to the combined multicentric cohort (n = 7252). ASPM protein expression was evaluated in a large BC cohort (n = 1300) using immunohistochemistry. The correlations between ASPM expression, clinicopathological parameters, molecular subtypes and outcome were assessed. The response to taxane treatment was compared to the clinical prognosis of ASPM using the ROC plotter. Results: High ASPM mRNA and protein expression were significantly associated with aggressive BC features and poor survival across all cohorts. The association with poor outcomes was maintained in the adjuvant chemotherapy and radio-therapy-treated patients. Responders to taxane treatment showed significantly elevated ASPM levels compared to non-responders. Conclusions: High ASPM expression predicts poor prognosis in BC. It may play a role in treatment resistance within a specific subgroup of patients. Further clinical trials are warranted to explore the potential of ASPM as a target for therapeutic interventions in cancer. Full article
(This article belongs to the Special Issue Overcoming Chemoresistance in Cancer: Identifying Biomarkers and Novel Targets)
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18 pages, 3914 KiB  
Article
Overcoming Irinotecan Resistance by Targeting Its Downstream Signaling Pathways in Colon Cancer
by Shashank Saurav, Sourajeet Karfa, Trung Vu, Zhipeng Liu, Arunima Datta, Upender Manne, Temesgen Samuel and Pran K. Datta
Cancers 2024, 16(20), 3491; https://doi.org/10.3390/cancers16203491 - 15 Oct 2024
Viewed by 1094
Abstract
Among the most popular chemotherapeutic agents, irinotecan, regarded as a prodrug belonging to the camptothecin family that inhibits topoisomerase I, is widely used to treat metastatic colorectal cancer (CRC). Although immunotherapy is promising for several cancer types, only microsatellite-instable (~7%) and not microsatellite-stable [...] Read more.
Among the most popular chemotherapeutic agents, irinotecan, regarded as a prodrug belonging to the camptothecin family that inhibits topoisomerase I, is widely used to treat metastatic colorectal cancer (CRC). Although immunotherapy is promising for several cancer types, only microsatellite-instable (~7%) and not microsatellite-stable CRCs are responsive to it. Therefore, it is important to investigate the mechanism of irinotecan function to identify cellular proteins and/or pathways that could be targeted for combination therapy. Here, we have determined the effect of irinotecan treatment on the expression/activation of tumor suppressor genes (including p15Ink4b, p21Cip1, p27Kip1, and p53) and oncogenes (including OPN, IL8, PD-L1, NF-κB, ISG15, Cyclin D1, and c-Myc) using qRT-PCR, Western blotting, immunofluorescence (IF), and RNA sequencing of tumor specimens. We employed stable knockdown, neutralizing antibodies (Abs), and inhibitors of OPN, p53, and NF-κB to establish downstream signaling and sensitivity/resistance to the cytotoxic activities of irinotecan. Suppression of secretory OPN and NF-κB sensitized colon cancer cells to irinotecan. p53 inhibition or knockdown was not sufficient to block or potentiate SN38-regulated signaling, suggesting p53-independent effects. Irinotecan treatment inhibited tumor growth in syngeneic mice. Analyses of allograft tumors from irinotecan-treated mice validated the cell culture results. RNA-seq data suggested that irinotecan-mediated activation of NF-κB signaling modulated immune and inflammatory genes in mice, which may compromise drug efficacy and promote resistance. In sum, these results suggest that, for CRCs, targeting OPN, NF-κB, PD-L1, and/or ISG15 signaling may provide a potential strategy to overcome resistance to irinotecan-based chemotherapy. Full article
(This article belongs to the Special Issue Overcoming Chemoresistance in Cancer: Identifying Biomarkers and Novel Targets)
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