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Biomedicines
Special Issues
Understanding the Mechanisms behind Cancer Therapy Resistance and Finding Solutions
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Understanding the Mechanisms behind Cancer Therapy Resistance and Finding Solutions

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Molecular and Translational Medicine".

Deadline for manuscript submissions: closed (31 January 2024) | Viewed by 7061

Special Issue Editors

Dr. Carlo Cenciarelli

E-Mail Website
Guest Editor
Institute of Translational Pharmacology, National Research Council of Italy, Rome, Italy
Interests: cancer; glioblastoma; T cell therapy; mAbs; signal transduction; cell growth
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Hany E. Marei

E-Mail Website
Guest Editor
Faculty of Veterinary Medicine, Department of Cytology and Histology, Mansoura University, Mansoura, Egypt
Interests: CAR T; scRNAseq for GBM; ribosome sequence for GBM; unannotated ORF for detection of neoantigens
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Current cancer research is facing several challenges, including resistance to chemotherapy, radiotherapy, immunotherapy, and molecularly targeted treatments. The mechanisms of resistance to cancer treatments have been found to be selective for molecular targets and in many cases share common resistance strategies. For example, the drug target may change, prosurvival pathways could become active, and inducing cell death could not work as intended. It is now possible to understand and treat drug resistance through the clinical evaluation of sensible therapeutic drug combinations and the use of predictive biomarkers to enable patient stratification. All of this is made feasible by the growing arsenal of anticancer drugs, developing preclinical models, and creating effective high-throughput screening methods.

We therefore welcome submissions of original research, systematic reviews, clinical trials, and brief research reports, which explore the role of drug resistance in the context of cancer or identify cutting-edge approaches to combating therapeutic resistance.

Potential topics include but are not limited to:

  • Mechanisms of resistance for cancer chemotherapy, radiotherapy, targeted therapy, and immunotherapy for solid and hematological malignancies;
  • Novel markers of cancer resistance;
  • Use of multi-omics as a strategy for deciphering novel cancer drug resistance;
  • Innovative approaches to overcoming cancer therapeutic resistance.

Special consideration will be given to new multimodal therapeutic strategies for combating molecular targets linked to multidrug resistance (MDR) and cancer immunotherapies.

Dr. Carlo Cenciarelli
Prof. Dr. Hany E. Marei
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. Biomedicines is an international peer-reviewed open access monthly 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 2600 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

  • biomarkers
  • cancer
  • chemotherapy
  • cancer radiotherapy
  • cancer targeted therapy
  • cancer immunotherapy
  • mechanisms
  • multidrug resistance (MDR)
  • overcoming cancer drug resistance

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Published Papers (4 papers)

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Research

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14 pages, 2186 KiB  
Article
New Insights into Chemoresistance Mediated by Mdm2 Inhibitors: The Benefits of Targeted Therapy over Common Cytostatics
by Tatyana Grigoreva, Aleksandra Sagaidak, Daria Novikova and Vyacheslav Tribulovich
Biomedicines 2024, 12(3), 547; https://doi.org/10.3390/biomedicines12030547 - 29 Feb 2024
Cited by 1 | Viewed by 1251
Abstract
The inhibition of the Mdm2-p53 protein–protein interaction is a promising strategy for anticancer therapy. However, the problem of developing secondary chemoresistance in tumors treated with such drugs has not yet been sufficiently studied. In this work, we compared the properties of a drug-resistant [...] Read more.
The inhibition of the Mdm2-p53 protein–protein interaction is a promising strategy for anticancer therapy. However, the problem of developing secondary chemoresistance in tumors treated with such drugs has not yet been sufficiently studied. In this work, we compared the properties of a drug-resistant cell line obtained during long-term cultivation in the presence of an Mdm2 inhibitor, Nutlin-3a, with a similarly obtained line insensitive to the cytostatic drug paclitaxel. We first confirmed the higher safety levels of Mdm2 inhibitors when compared with cytostatics in terms of the development of secondary chemoresistance. We showed that Nutlin-3a affects both the targeted p53-mediated cellular machinery and the universal ABC-mediated efflux mechanism. While both targeted and general defense mechanisms are activated by the Mdm2 inhibitor, it still increases the susceptibility of tumor cells to other drugs. The results obtained indicate that the risks of developing chemoresistance under the therapy with a targeted agent are fundamentally lower than during cytotoxic therapy. Full article
(This article belongs to the Special Issue Understanding the Mechanisms behind Cancer Therapy Resistance and Finding Solutions)
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8 pages, 2341 KiB  
Communication
Co-Targeting Nucleus Accumbens Associate 1 and NF-κB Signaling Synergistically Inhibits Melanoma Growth
by Lixiang Gu, Xingcong Ren, Chrispus Ngule, Xiaofang Xiong, Jianxun Song, Zhiguo Li and Jin-Ming Yang
Biomedicines 2023, 11(8), 2221; https://doi.org/10.3390/biomedicines11082221 - 8 Aug 2023
Viewed by 1211
Abstract
Nucleus-accumbens-associated protein-1 (NAC1) is a cancer-related transcriptional factor encoded by the NACC1 gene, which is amplified and overexpressed in various human cancers and has been appreciated as one of the top potential cancer driver genes. NAC1 has therefore been explored as a potential [...] Read more.
Nucleus-accumbens-associated protein-1 (NAC1) is a cancer-related transcriptional factor encoded by the NACC1 gene, which is amplified and overexpressed in various human cancers and has been appreciated as one of the top potential cancer driver genes. NAC1 has therefore been explored as a potential therapeutic target for managing malignant tumors. Here, we show that NAC1 is a negative regulator of NF-κB signaling, and NAC1 depletion enhances the level of the nuclear NF-κB in human melanoma. Furthermore, the inhibition of NF-κB signaling significantly potentiates the antineoplastic activity of the NAC1 inhibition in both the cultured melanoma cells and xenograft tumors. This study identifies a novel NAC1-NF-κB signaling axis in melanoma, offering a promising new therapeutic option to treat melanoma. Full article
(This article belongs to the Special Issue Understanding the Mechanisms behind Cancer Therapy Resistance and Finding Solutions)
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Review

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22 pages, 4166 KiB  
Review
The Role of Long Noncoding RNAs (lncRNAs) in Esophageal Cancer Therapy Resistance and Metastasis
by Zong-Ping Weng, Shen-Kai Hsu, Hui-Min David Wang, Kuo-Jen Chen, Po-Yen Lee, Chien-Chih Chiu and Kai-Chun Cheng
Biomedicines 2024, 12(3), 660; https://doi.org/10.3390/biomedicines12030660 - 15 Mar 2024
Viewed by 1700
Abstract
Esophageal cancer (EC) is one of the most aggressive gastrointestinal cancers. Despite improvements in therapies, the survival rate of patients with EC remains low. Metastasis accounts for up to 90% of cancer-related deaths, and resistance to anti-neoplastic therapeutics is also a main cause [...] Read more.
Esophageal cancer (EC) is one of the most aggressive gastrointestinal cancers. Despite improvements in therapies, the survival rate of patients with EC remains low. Metastasis accounts for up to 90% of cancer-related deaths, and resistance to anti-neoplastic therapeutics is also a main cause of poor survival. Thus, metastasis and drug resistance are undoubtedly the two main challenges in cancer treatment. Among the different categories of noncoding RNAs, lncRNAs have historically drawn less attention. However, lncRNAs have gradually become a research hotspot, and increasing research has demonstrated that lncRNAs participate in the tumorigenesis of multiple types of cancer, including EC. Long noncoding RNAs (lncRNAs) are RNA transcripts longer than 200 nucleotides in length that play important roles in epigenetics, transcription regulation, and posttranscriptional processing. In this review, we elucidated the role of lncRNAs in the metastasis and drug resistance of EC and discussed their potential clinical applications and related limitations. With a better understanding of the underlying mechanisms of lncRNAs, we can identify therapeutic targets for EC in the future. Full article
(This article belongs to the Special Issue Understanding the Mechanisms behind Cancer Therapy Resistance and Finding Solutions)
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Other

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10 pages, 2356 KiB  
Brief Report
FGF1 Protects MCF-7 Cells against Taltobulin through Both the MEKs/ERKs and PI3K/AKT Signaling Pathway
by Jakub Szymczyk, Aleksandra Czyrek, Jacek Otlewski and Malgorzata Zakrzewska
Biomedicines 2023, 11(7), 1856; https://doi.org/10.3390/biomedicines11071856 - 29 Jun 2023
Cited by 4 | Viewed by 1572
Abstract
Breast cancer is a widespread and complex disease characterized by abnormal signaling pathways that promote tumor growth and progression. Despite significant medical advances and the development of increasingly effective therapies for breast cancer, drug resistance and reduced sensitivity to prior therapies remain persistent [...] Read more.
Breast cancer is a widespread and complex disease characterized by abnormal signaling pathways that promote tumor growth and progression. Despite significant medical advances and the development of increasingly effective therapies for breast cancer, drug resistance and reduced sensitivity to prior therapies remain persistent challenges. Dysregulation of growth factors such as FGFs and EGF and their receptors is a contributing factor to reduced response to treatment, promoting cell survival and proliferation, metastasis, EMT or increased expression of ABC transporters. Our study demonstrates a protective role for FGF1 in MCF-7 breast cancer cells against taltobulin-induced cytotoxicity, mediated by activation of its receptors and compares its activity to EGF, another growth factor involved in breast cancer development and progression. The mechanisms of action of these two proteins are different: FGF1 exerts its effects through the activation of both ERKs and AKT, whereas EGF acts only through ERKs. FGF1 action in the presence of the drug promotes cell viability, reduces apoptosis and increases cell migration. Although EGF and its receptors have received more attention in breast cancer research to date, our findings highlight the key role played by FGFs and their receptors in promoting drug resistance to tubulin polymerization inhibitors in FGFR-positive tumors. Full article
(This article belongs to the Special Issue Understanding the Mechanisms behind Cancer Therapy Resistance and Finding Solutions)
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