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Cancers
Special Issues
Feature Review for Cancer Therapy
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Feature Review for Cancer Therapy

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

Deadline for manuscript submissions: 15 May 2024 | Viewed by 16976

Special Issue Editors

Dr. Robert Kleszcz

E-Mail Website
Guest Editor
Department of Pharmaceutical Biochemistry, Poznan University of Medical Sciences, Święcicki 4 Str., 60-781 Poznań, Poland
Interests: head and neck cancer; hepatocellular cancer; pancreatic cancer; CNS cancer; colorectal cancer; targeted therapy; Wnt signaling pathway; metabolism of cancer cells Social media account
Dr. Jarosław Paluszczak

E-Mail Website
Guest Editor
Department of Pharmaceutical Biochemistry, Poznan University of Medical Sciences, Święcicki 4 Str., 60-781 Poznań, Poland
Interests: head and neck cancer; epigenetics; CNS cancer; colorectal cancer; targeted therapy; Wnt signaling pathway; metabolism of cancer cells; metronomic therapy; biomarkers
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The molecular diversity in cancers is reflected by the lack of universal treatment options. However, the understanding of the molecular and cellular hallmarks of cancer, presented by Hanahan and Weinberg, has contributed to significant progress in oncological therapies. It has allowed researchers to improve the clinical efficacy of classical cytostatic drugs but has also resulted in the development of new targeted therapeutics. Additionally, our growing comprehension of the role of stem-like cancer cells holds promise for a more robust eradication of tumors by targeting the sub-population of cells responsible for self-renewal and chemo-radio-resistance. Moreover, the growing understanding of the cross-talk between various cell types which are present in the tumor microenvironment translates into current immunomodulatory and other therapies.

This Special Issue aims to address the recent findings of research devoted to the improvement in oncological therapies, both at the experimental and clinical levels.

Potential topics include, but are not limited to:

  • Current standard treatment of cancer;
  • Current and potential targeted therapy of cancer;
  • Combinations of different therapeutic options;
  • Biomarkers for the improvement in therapy;
  • Natural compounds and their derivatives in cancer therapy;
  • Drug-repurposing for cancer therapy;
  • Nanomaterials in cancer treatment;
  • Perspectives for the de-escalation of anticancer therapy.

Dr. Robert Kleszcz
Dr. Jarosław Paluszczak
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. 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 therapy
  • chemotherapy
  • targeted therapy
  • cancer co-treatment
  • biomarkers
  • natural compounds
  • drug-repurposing
  • nanomaterials

Published Papers (8 papers)

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Review

23 pages, 2949 KiB  
Review
Low-Dose Naltrexone as an Adjuvant in Combined Anticancer Therapy
by Marianna Ciwun, Anna Tankiewicz-Kwedlo and Dariusz Pawlak
Cancers 2024, 16(6), 1240; https://doi.org/10.3390/cancers16061240 - 21 Mar 2024
Viewed by 1186
Abstract
Naltrexone (NTX) is a non-selective antagonist of opioid receptors, primarily used in the therapy of opioid and alcohol dependence. Low-dose naltrexone (LDN) exhibits antagonistic action against the opioid growth factor receptor (OGFr), whose signaling is associated with the survival, proliferation, and invasion of [...] Read more.
Naltrexone (NTX) is a non-selective antagonist of opioid receptors, primarily used in the therapy of opioid and alcohol dependence. Low-dose naltrexone (LDN) exhibits antagonistic action against the opioid growth factor receptor (OGFr), whose signaling is associated with the survival, proliferation, and invasion of cancer cells. The mechanism of action of LDN depends on the dose and duration of the OGFr blockade, leading to a compensatory increase in the synthesis of the opioid growth factor (OGF), which has an inhibitory effect on carcinogenesis. Numerous studies on in vitro and in vivo models provide evidence of LDN’s positive impact on inhibiting the OGF–OGFr axis in cancers. LDN’s unique mechanism of action on cancer cells, lack of direct cytotoxic effect, and immunomodulating action form the basis for its use as an adjuvant in chemotherapy and immunotherapy of cancerous lesions. Full article
(This article belongs to the Special Issue Feature Review for Cancer Therapy)
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24 pages, 1648 KiB  
Review
Targeting STAT3 and NF-κB Signaling Pathways in Cancer Prevention and Treatment: The Role of Chalcones
by Violetta Krajka-Kuźniak, Marta Belka and Katarzyna Papierska
Cancers 2024, 16(6), 1092; https://doi.org/10.3390/cancers16061092 - 08 Mar 2024
Viewed by 666
Abstract
Chalcones are a type of natural flavonoid compound that have been found to possess promising anticancer properties. Studies have shown that chalcones can inhibit the growth and proliferation of cancer cells, induce apoptosis, and suppress tumor angiogenesis. In addition to their potential therapeutic [...] Read more.
Chalcones are a type of natural flavonoid compound that have been found to possess promising anticancer properties. Studies have shown that chalcones can inhibit the growth and proliferation of cancer cells, induce apoptosis, and suppress tumor angiogenesis. In addition to their potential therapeutic applications, chalcones have also been studied for their chemopreventive effects, which involve reducing the risk of cancer development in healthy individuals. Overall, the anticancer properties of chalcones make them a promising area of research for developing new cancer treatments and preventative strategies. This review aims to provide a thorough overview of the central studies reported in the literature concerning cancer prevention and the treatment of chalcones. Although chalcones target many different mechanisms, the STAT and NF-κB signaling pathways are the ones this review will focus on, highlighting the existing crosstalk between these two pathways and considering the potential therapeutic opportunities for chalcone combinations. Full article
(This article belongs to the Special Issue Feature Review for Cancer Therapy)
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30 pages, 2609 KiB  
Review
Impact of Complex Apoptotic Signaling Pathways on Cancer Cell Sensitivity to Therapy
by Ryungsa Kim, Takanori Kin and William T. Beck
Cancers 2024, 16(5), 984; https://doi.org/10.3390/cancers16050984 - 28 Feb 2024
Viewed by 973
Abstract
Anticancer drugs induce apoptotic and non-apoptotic cell death in various cancer types. The signaling pathways for anticancer drug-induced apoptotic cell death have been shown to differ between drug-sensitive and drug-resistant cells. In atypical multidrug-resistant leukemia cells, the c-Jun/activator protein 1 (AP-1)/p53 [...] Read more.
Anticancer drugs induce apoptotic and non-apoptotic cell death in various cancer types. The signaling pathways for anticancer drug-induced apoptotic cell death have been shown to differ between drug-sensitive and drug-resistant cells. In atypical multidrug-resistant leukemia cells, the c-Jun/activator protein 1 (AP-1)/p53 signaling pathway leading to apoptotic death is altered. Cancer cells treated with anticancer drugs undergo c-Jun/AP-1–mediated apoptotic death and are involved in c-Jun N-terminal kinase activation and growth arrest- and DNA damage-inducible gene 153 (Gadd153)/CCAAT/enhancer-binding protein homologous protein pathway induction, regardless of the p53 genotype. Gadd153 induction is associated with mitochondrial membrane permeabilization after anticancer drug treatment and involves a coupled endoplasmic reticulum stress response. The induction of apoptosis by anticancer drugs is mediated by the intrinsic pathway (cytochrome c, Cyt c) and subsequent activation of the caspase cascade via proapoptotic genes (e.g., Bax and Bcl-xS) and their interactions. Anticancer drug-induced apoptosis involves caspase-dependent and caspase-independent pathways and occurs via intrinsic and extrinsic pathways. The targeting of antiapoptotic genes such as Bcl-2 enhances anticancer drug efficacy. The modulation of apoptotic signaling by Bcl-xS transduction increases the sensitivity of multidrug resistance-related protein-overexpressing epidermoid carcinoma cells to anticancer drugs. The significance of autophagy in cancer therapy remains to be elucidated. In this review, we summarize current knowledge of cancer cell death-related signaling pathways and their alterations during anticancer drug treatment and discuss potential strategies to enhance treatment efficacy. Full article
(This article belongs to the Special Issue Feature Review for Cancer Therapy)
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18 pages, 3641 KiB  
Review
Targeted Therapeutic Strategies for the Treatment of Cancer
by Benjamin Victoir, Cécile Croix, Fabrice Gouilleux and Gildas Prié
Cancers 2024, 16(2), 461; https://doi.org/10.3390/cancers16020461 - 22 Jan 2024
Cited by 1 | Viewed by 1492
Abstract
Extensive research is underway to develop new therapeutic strategies to counteract therapy resistance in cancers. This review presents various strategies to achieve this objective. First, we discuss different vectorization platforms capable of releasing drugs in cancer cells. Second, we delve into multitarget therapies [...] Read more.
Extensive research is underway to develop new therapeutic strategies to counteract therapy resistance in cancers. This review presents various strategies to achieve this objective. First, we discuss different vectorization platforms capable of releasing drugs in cancer cells. Second, we delve into multitarget therapies using drug combinations and dual anticancer agents. This section will describe examples of multitarget therapies that have been used to treat solid tumors. Full article
(This article belongs to the Special Issue Feature Review for Cancer Therapy)
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20 pages, 1432 KiB  
Review
The Role of Macrophages in Sarcoma Tumor Microenvironment and Treatment
by Agnieszka E. Zając, Anna M. Czarnecka and Piotr Rutkowski
Cancers 2023, 15(21), 5294; https://doi.org/10.3390/cancers15215294 - 05 Nov 2023
Cited by 2 | Viewed by 7887
Abstract
Sarcomas are a heterogeneous group of malignant mesenchymal tumors, including soft tissue and bone sarcomas. Macrophages in the tumor microenvironment, involved in immunosuppression and leading to tumor development, are called tumor-associated macrophages (TAMs). TAMs are very important in modulating the microenvironment of sarcomas [...] Read more.
Sarcomas are a heterogeneous group of malignant mesenchymal tumors, including soft tissue and bone sarcomas. Macrophages in the tumor microenvironment, involved in immunosuppression and leading to tumor development, are called tumor-associated macrophages (TAMs). TAMs are very important in modulating the microenvironment of sarcomas by expressing specific markers and secreting factors that influence immune and tumor cells. They are involved in many signaling pathways, such as p-STAT3/p-Erk1/2, PI3K/Akt, JAK/MAPK, and JAK/STAT3. TAMs also significantly impact the clinical outcomes of patients suffering from sarcomas and are mainly related to poor overall survival rates among bone and soft tissue sarcomas, for example, chondrosarcoma, osteosarcoma, liposarcoma, synovial sarcoma, and undifferentiated pleomorphic sarcoma. This review summarizes the current knowledge on TAMs in sarcomas, focusing on specific markers on sarcoma cells, cell–cell interactions, and the possibly involved molecular pathways. Furthermore, we discuss the clinical significance of macrophages in sarcomas as a potential target for new therapies, presenting clinical relevance, possible new treatment options, and ongoing clinical trials using TAMs in sarcoma treatment. Full article
(This article belongs to the Special Issue Feature Review for Cancer Therapy)
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13 pages, 699 KiB  
Review
Making the Case for Autophagy Inhibition as a Therapeutic Strategy in Combination with Androgen-Targeted Therapies in Prostate Cancer
by Ahmed M. Elshazly and David A. Gewirtz
Cancers 2023, 15(20), 5029; https://doi.org/10.3390/cancers15205029 - 18 Oct 2023
Cited by 1 | Viewed by 1221
Abstract
Androgen receptor targeting remains the primary therapeutic strategy in prostate cancer, encompassing androgen biosynthesis inhibitors and androgen receptor antagonists. While both androgen-receptor-positive and “castration-resistant” prostate cancer are responsive to these approaches, the development of resistance is an almost inevitable outcome leading to the [...] Read more.
Androgen receptor targeting remains the primary therapeutic strategy in prostate cancer, encompassing androgen biosynthesis inhibitors and androgen receptor antagonists. While both androgen-receptor-positive and “castration-resistant” prostate cancer are responsive to these approaches, the development of resistance is an almost inevitable outcome leading to the castration-resistant form of the disease. Given that “cytoprotective” autophagy is considered to be a predominant mechanism of resistance to various chemotherapeutic agents as well as to radiation in the cancer literature, the purpose of this review is to evaluate whether autophagy plays a central role in limiting the utility of androgen deprivation therapies in prostate cancer. Unlike most of our previous reports, where multiple functional forms of autophagy were identified, making it difficult if not impossible to propose autophagy inhibition as a therapeutic strategy, the cytoprotective form of autophagy appears to predominate in the case of androgen deprivation therapies. This opens a potential pathway for improving the outcomes for prostate cancer patients once effective and reliable pharmacological autophagy inhibitors have been developed. Full article
(This article belongs to the Special Issue Feature Review for Cancer Therapy)
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20 pages, 2081 KiB  
Review
Unraveling the Anticancer Potential of Statins: Mechanisms and Clinical Significance
by Mohamed Y. Zaky, Chuanwen Fan, Huan Zhang and Xiao-Feng Sun
Cancers 2023, 15(19), 4787; https://doi.org/10.3390/cancers15194787 - 29 Sep 2023
Cited by 5 | Viewed by 1423
Abstract
Statins are an essential medication class in the treatment of lipid diseases because they inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. They reduce cholesterol levels and reduce the risk of cardiovascular disease in both primary and secondary prevention. In addition to their powerful pharmacologic suppression [...] Read more.
Statins are an essential medication class in the treatment of lipid diseases because they inhibit 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase. They reduce cholesterol levels and reduce the risk of cardiovascular disease in both primary and secondary prevention. In addition to their powerful pharmacologic suppression of cholesterol production, statins appear to have pleitropic effects in a wide variety of other diseases by modulating signaling pathways. In recent years, statins have seen a large increase in interest due to their putative anticancer effects. Statins appear to cause upregulation or inhibition in key pathways involved in cancer such as inhibition of proliferation, angiogenesis, and metastasis as well as reducing cancer stemness. Further, statins have been found to induce oxidative stress, cell cycle arrest, autophagy, and apoptosis of cancer cells. Interestingly, clinical studies have shown that statin use is associated with a decreased risk of cancer formation, lower cancer grade at diagnosis, reduction in the risk of local reoccurrence, and increasing survival in patients. Therefore, our objective in the present review is to summarize the findings of the publications on the underlying mechanisms of statins’ anticancer effects and their clinical implications. Full article
(This article belongs to the Special Issue Feature Review for Cancer Therapy)
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24 pages, 2304 KiB  
Review
Advantages of the Combinatorial Molecular Targeted Therapy of Head and Neck Cancer—A Step before Anakoinosis-Based Personalized Treatment
by Robert Kleszcz
Cancers 2023, 15(17), 4247; https://doi.org/10.3390/cancers15174247 - 24 Aug 2023
Cited by 3 | Viewed by 1182
Abstract
The molecular initiators of Head and Heck Squamous Cell Carcinoma (HNSCC) are complex. Human Papillomavirus (HPV) infection is linked to an increasing number of HNSCC cases, but HPV-positive tumors generally have a good prognosis. External factors that promote the development of HPV-negative HNSCC [...] Read more.
The molecular initiators of Head and Heck Squamous Cell Carcinoma (HNSCC) are complex. Human Papillomavirus (HPV) infection is linked to an increasing number of HNSCC cases, but HPV-positive tumors generally have a good prognosis. External factors that promote the development of HPV-negative HNSCC include tobacco use, excessive alcohol consumption, and proinflammatory poor oral hygiene. On a molecular level, several events, including the well-known overexpression of epidermal growth factor receptors (EGFR) and related downstream signaling pathways, contribute to the development of HNSCC. Conventional chemotherapy is insufficient for many patients. Thus, molecular-based therapy for HNSCC offers patients a better chance at a cure. The first molecular target for therapy of HNSCC was EGFR, inhibited by monoclonal antibody cetuximab, but its use in monotherapy is insufficient and induces resistance. This article describes attempts at combinatorial molecular targeted therapy of HNSCC based on several molecular targets and exemplary drugs/drug candidates. The new concept of anakoinosis-based therapy, which means treatment that targets the intercellular and intracellular communication of cancer cells, is thought to be the way to improve the clinical outcome for HNSCC patients. The identification of a link between molecular targeted therapy and anakoinosis raises the potential for further progress in HPV-negative HNSCC therapy. Full article
(This article belongs to the Special Issue Feature Review for Cancer Therapy)
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