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Novel Drug Targets for Cancer Management
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Novel Drug Targets for Cancer Management

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Oncology".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 6934

Special Issue Editors

Prof. Shailendra Anoopkumar-Dukie

E-Mail Website
Guest Editor
School of Pharmacy and Medical Sciences, Griffith University, Gold Coast, QLD 4215, Australia
Interests: oxidative stress; cell signaling; inflammation; cancer research; neuroscience; lipid peroxidation; antioxidants; cytotoxicity; neuroinflammation; cancer treatment; treatment resistance; pharmacokinetic drug interactions; anticoagulant therapy; warfarin; atrial fibrillation therapy; chemotherapy; adverse drug effects
Special Issues, Collections and Topics in MDPI journals
Dr. Catherine McDermott

E-Mail Website
Guest Editor
Faculty of Health Sciences & Medicine, Bond University, Robina, QLD, Australia
Interests: physiology; toxicology; oncology

Special Issue Information

Dear Colleagues,

Cancer remains a leading cause of death worldwide, making the investigation of novel drug targets for cancer management essential. Finding new agents to treat cancer can be a long and expensive task. The repurposing of existing drugs that display anti-cancer properties can expedite this process and result in significant cost savings. The aim of this Special Issue is to present a collection of reviews and original contributions on the currently available evidence on novel drug targets and the cytotoxic and anti-cancer properties of novel or repurposed agents, the mechanisms behind these properties, and how these novel approaches might fit within current cancer therapies. Furthermore, this Special Issue aims to gather together the available evidence that illustrates the clinical potential of these novel approaches.

Dr. Shailendra Anoopkumar-Dukie
Dr. Catherine McDermott
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. Journal of Clinical Medicine 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 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

  • cancer
  • repurposing
  • novel drug targets

Published Papers (4 papers)

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Research

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19 pages, 6029 KiB  
Article
Low Doses of Celecoxib Might Promote Phenotype Switching in Cutaneous Melanoma Treated with Dabrafenib—Preliminary Study
by Diana Valentina Tudor, Adrian Florea, Mihai Cenariu, Diana Elena Olteanu, Marius Farcaș, Andreea Hopârtean, Simona Valeria Clichici and Gabriela Adriana Filip
J. Clin. Med. 2022, 11(15), 4560; https://doi.org/10.3390/jcm11154560 - 4 Aug 2022
Viewed by 1544
Abstract
Background: Cutaneous melanoma is a heterogeneous tumor with a rapidly switching molecular and cellular phenotype. The invasive phenotype switching characterized by MITFlow/AXLhigh predicts early resistance to multiple targeted drugs in melanoma. Celecoxib proved to be a valuable adjuvant in cutaneous [...] Read more.
Background: Cutaneous melanoma is a heterogeneous tumor with a rapidly switching molecular and cellular phenotype. The invasive phenotype switching characterized by MITFlow/AXLhigh predicts early resistance to multiple targeted drugs in melanoma. Celecoxib proved to be a valuable adjuvant in cutaneous melanoma in preclinical studies. Our in vitro study evaluated for the first time whether celecoxib could prevent phenotype switching in two human melanoma cell lines treated with dabrafenib. Methods: All in vitro experiments were carried out on BRAF-V600E-positive A375 and SK-MEL-28 human melanoma cell lines, and subjected to a celecoxib and dabrafenib drug combination for 72 h. Melanoma cells were already in the MITFlow/AXLhigh end of the spectrum. Of main interest was the evaluation of the key proteins expressed in phenotype switching (TGF-β, MITF, AXL, YAP, TAZ), as well as cell death mechanisms correlated with oxidative stress production. Results: Celecoxib significantly enhanced the apoptotic effect of dabrafenib in each melanoma cell line compared to the dabrafenib group (p < 0.0001). Even though celecoxib promoted low MITF expression, this was correlated with high receptor tyrosine kinase AXL levels in A375 and SK-MEL-28 cell lines (p < 0.0001), a positive marker for the phenotype switch to an invasive state. Conclusion: This preliminary study highlighted that celecoxib might promote MITFlow/AXLhigh expression in cutaneous melanoma treated with dabrafenib, facilitating phenotype switching in vitro. Our results need further confirmation, as this finding could represent an important limitation of celecoxib as an antineoplastic drug. Full article
(This article belongs to the Special Issue Novel Drug Targets for Cancer Management)
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13 pages, 49713 KiB  
Article
Staphylococcus aureus-Derived Extracellular Vesicles Enhance the Efficacy of Endocrine Therapy in Breast Cancer Cells
by Jeongshin An, Hyungju Kwon, Woosung Lim and Byung-In Moon
J. Clin. Med. 2022, 11(7), 2030; https://doi.org/10.3390/jcm11072030 - 5 Apr 2022
Cited by 14 | Viewed by 2524
Abstract
The microbiome involved in the human estrogen metabolism is known as the estrobolome. This study aimed to show that the estrobolome can be used in breast cancer treatment. We first analyzed the blood microbiome composition of healthy controls and patients with breast cancer. [...] Read more.
The microbiome involved in the human estrogen metabolism is known as the estrobolome. This study aimed to show that the estrobolome can be used in breast cancer treatment. We first analyzed the blood microbiome composition of healthy controls and patients with breast cancer. In particular, we investigated the bacteria producing β−glucuronidase and/or β−galactosidase, which are involved in estrogen metabolism in the human body. Staphylococcus species were more abundant in healthy controls than in breast cancer patients and therefore were selected for further analyses. The effect of Staphylococcus aureus on endocrine therapy was analyzed by a combination treatment with tamoxifen. Analysis of the microbiome of blood samples showed that species producing β−glucuronidase were more abundant in breast cancer patients than in healthy controls. Further experiments confirmed that the efficacy of tamoxifen increased when administered in conjugation with the extracellular vesicles (EVs) of S. aureus. Based on our results, we deduced that S. aureus EVs could potentially be used as adjuvants for breast cancer treatment in the future. Full article
(This article belongs to the Special Issue Novel Drug Targets for Cancer Management)
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18 pages, 4313 KiB  
Article
Treatment Efficacy of Immune Checkpoint Inhibitors for Patients with Advanced or Metastatic Colorectal Cancer: A Systematic Review and Meta-Analysis
by Junhee Pyo and Hyo-Jung Park
J. Clin. Med. 2021, 10(16), 3599; https://doi.org/10.3390/jcm10163599 - 16 Aug 2021
Cited by 4 | Viewed by 2155
Abstract
The treatment efficacy of immune checkpoint inhibitors (ICIs) in colorectal cancer (CRC) has been reported heterogeneously across clinical trials. We conducted a systematic review and meta-analysis to evaluate the efficacy of ICIs in patients with advanced/metastatic CRC. Ovid-Medline was searched to identify clinical [...] Read more.
The treatment efficacy of immune checkpoint inhibitors (ICIs) in colorectal cancer (CRC) has been reported heterogeneously across clinical trials. We conducted a systematic review and meta-analysis to evaluate the efficacy of ICIs in patients with advanced/metastatic CRC. Ovid-Medline was searched to identify clinical trials providing the efficacy outcomes of overall response rate (ORR) or disease control rate (DCR). The pooled ORR and DCR were estimated across all studies and subgroups. Meta-regression was performed to find the influencing factors for treatment efficacy. A total of thirty studies (1870 patients) were eligible. The overall ORR and DCR were 20.1% and 58.5%, respectively, but these results were heterogeneous across studies. Multivariate meta-regression revealed that microsatellite phenotype (odds ratio of MSI-H/dMMR versus MSS/pMMR: 1.67, p < 0.001) and drug regimen (odds ratio of monotherapy versus combination therapy: 1.07, p = 0.019) were the source of heterogeneity and also significantly influenced factors for the efficacy of the treatment. Although the efficacy of ICIs as a first-line therapy was higher than that of ICIs as the second- or more-line therapy (ORR: 51.5% vs. 13.4%, DCR: 85% vs. 49.5%), multivariate regression showed that the line of therapy was not a significant factor for the treatment efficacy. Our study suggests that the microsatellite phenotype and drug regimen, rather than the line of treatment, are the primary factors influencing the treatment response among advanced/metastatic CRC patients treated with an ICI-based regimen. Full article
(This article belongs to the Special Issue Novel Drug Targets for Cancer Management)
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Review

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13 pages, 622 KiB  
Review
Drivers of Radioresistance in Prostate Cancer
by Liam King, Nijole Bernaitis, David Christie, Russ Chess-Williams, Donna Sellers, Catherine McDermott, Wendy Dare and Shailendra Anoopkumar-Dukie
J. Clin. Med. 2022, 11(19), 5637; https://doi.org/10.3390/jcm11195637 - 24 Sep 2022
Cited by 5 | Viewed by 2026
Abstract
Prostate cancer (PCa) is the second most commonly diagnosed cancer worldwide. Radiotherapy remains one of the first-line treatments in localised disease and may be used as monotherapy or in combination with other treatments such as androgen deprivation therapy or radical prostatectomy. Despite advancements [...] Read more.
Prostate cancer (PCa) is the second most commonly diagnosed cancer worldwide. Radiotherapy remains one of the first-line treatments in localised disease and may be used as monotherapy or in combination with other treatments such as androgen deprivation therapy or radical prostatectomy. Despite advancements in delivery methods and techniques, radiotherapy has been unable to totally overcome radioresistance resulting in treatment failure or recurrence of previously treated PCa. Various factors have been linked to the development of tumour radioresistance including abnormal tumour vasculature, oxygen depletion, glucose and energy deprivation, changes in gene expression and proteome alterations. Understanding the biological mechanisms behind radioresistance is essential in the development of therapies that are able to produce both initial and sustained response to radiotherapy. This review will investigate the different biological mechanisms utilised by PCa tumours to drive radioresistance. Full article
(This article belongs to the Special Issue Novel Drug Targets for Cancer Management)
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