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Special Issue "Advances in the Treatment and Prevention of Chemotherapy Toxicity"

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

Deadline for manuscript submissions: closed (31 January 2021).

Special Issue Editors

Dr. José L. Quiles
grade E-Mail Website
Guest Editor
Department of Physiology, Institute of Nutrition and Food Technology “Jose Mataix”, Biomedical Research Center, University of Granada, Avda. Conocimiento s/n, 18100 Armilla, Granada, Spain
Interests: cancer biology; antioxidants; oxidative stress; food chemistry; nutrition; reactive oxygen species
Special Issues, Collections and Topics in MDPI journals
Dr. Alfonso Varela-López
E-Mail Website
Co-Guest Editor

Special Issue Information

Dear Colleagues,

Chemotherapy is still one of the most important treatments against cancer. Its effectiveness continues to grow thanks to new approaches and the combination of products and application guidelines. However, the side-effect of chemotherapy, i.e., its toxicity, is something that slows its application to some extent. The scientific community continues to investigate ways to reduce the side-effects of the different chemotherapeutic agents from diverse and novel points of view. The Special Issue presented here is aimed at gathering the latest knowledge about existing treatments to reduce the toxicity of different chemotherapeutic treatments. Contributions from many different approaches and based on one or more side-effects are expected. An eminently molecular approach to the problem of alterations such as cardiotoxicity of some treatments or peripheral neuropathy induced by others is expected, for example. New routes and forms of application of both chemotherapeutic agents and molecules that prevent toxicity are also welcome.

Prof. Dr. José L. Quiles
Dr. Alfonso Varela-López
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 papers will be 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

  • Advance
  • Alkylating agents
  • Anthracyclines
  • Anticancer
  • Antioxidants
  • Apoptosis
  • Bioactive compounds
  • Cancer
  • Cardiotoxicity
  • Cell cycle
  • Chemoprevention
  • Chemotherapy-induced neuropathy
  • Chemotherapy-induced toxicity
  • Combinatory therapy
  • Cytoskeletal disruptors (taxanes)
  • Cytoskeleton
  • Histone deacetylase inhibitors
  • Hyperthermia
  • Inhibitors of topoisomerase
  • Kinase inhibitors
  • Liposomes
  • Mitochondria
  • Mitrotubules
  • Nanocarriers
  • Nanomedicine
  • Nanoparticles
  • Neoadyuvance
  • Neurotoxicity
  • Nucleotide analogs and precursor analogs
  • Oxidative stress
  • Peptide antibiotics Platinum-based agents Reactive oxygen species Retinoids Vinca alkaloids

Published Papers (6 papers)

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Research

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Article
Inhibition of NUPR1–Karyopherin β1 Binding Increases Anticancer Drug Sensitivity
Int. J. Mol. Sci. 2021, 22(6), 2794; https://doi.org/10.3390/ijms22062794 - 10 Mar 2021
Viewed by 602
Abstract
Background: Nuclear protein-1 (NUPR1, also known as p8/Com-1) is a transcription factor involved in the regulation of cellular stress responses, including serum starvation and drug stimulation. Methods: We investigated the mechanism of NUPR1 nuclear translocation involving karyopherin β1 (KPNB1), using a single-molecule binding [...] Read more.
Background: Nuclear protein-1 (NUPR1, also known as p8/Com-1) is a transcription factor involved in the regulation of cellular stress responses, including serum starvation and drug stimulation. Methods: We investigated the mechanism of NUPR1 nuclear translocation involving karyopherin β1 (KPNB1), using a single-molecule binding assay and confocal microscopy. The cellular effects associated with NUPR1–KPNB1 inhibition were investigated by gene expression profiling and cell cycle analysis. Results: The single-molecule binding assay revealed that KPNB1 bound to NUPR1 with a binding affinity of 0.75 nM and that this binding was blocked by the aminothiazole ATZ-502. Following doxorubicin-only treatment, NUPR1 was translocated to the nucleus in more than 90% and NUPR1 translocation was blocked by the ATZ-502 combination treatment in MDA-MB-231 with no change in NUPR1 expression, providing strong evidence that NUPR1 nuclear translocation was directly inhibited by the ATZ-502 treatment. Inhibition of KPNB1 and NUPR1 binding was associated with a synergistic anticancer effect (up to 19.6-fold) in various cancer cell lines. NUPR1-related genes were also downregulated following the doxorubicin–ATZ-502 combination treatment. Conclusion: Our current findings clearly demonstrate that NUPR1 translocation into the nucleus requires karyopherin β1 binding. Inhibition of the KPNB1 and NUPR1 interaction may constitute a new cancer therapeutic approach that can increase the drug efficacy while reducing the side effects. Full article
(This article belongs to the Special Issue Advances in the Treatment and Prevention of Chemotherapy Toxicity)
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Article
A Smart Hyperthermia Nanofiber-Platform-Enabled Sustained Release of Doxorubicin and 17AAG for Synergistic Cancer Therapy
Int. J. Mol. Sci. 2021, 22(5), 2542; https://doi.org/10.3390/ijms22052542 - 03 Mar 2021
Cited by 4 | Viewed by 896
Abstract
This study demonstrates the rational fabrication of a magnetic composite nanofiber mesh that can achieve mutual synergy of hyperthermia, chemotherapy, and thermo-molecularly targeted therapy for highly potent therapeutic effects. The nanofiber is composed of biodegradable poly(ε-caprolactone) with doxorubicin, magnetic nanoparticles, and 17-allylamino-17-demethoxygeldanamycin. The [...] Read more.
This study demonstrates the rational fabrication of a magnetic composite nanofiber mesh that can achieve mutual synergy of hyperthermia, chemotherapy, and thermo-molecularly targeted therapy for highly potent therapeutic effects. The nanofiber is composed of biodegradable poly(ε-caprolactone) with doxorubicin, magnetic nanoparticles, and 17-allylamino-17-demethoxygeldanamycin. The nanofiber exhibits distinct hyperthermia, owing to the presence of magnetic nanoparticles upon exposure of the mesh to an alternating magnetic field, which causes heat-induced cell killing as well as enhanced chemotherapeutic efficiency of doxorubicin. The effectiveness of hyperthermia is further enhanced through the inhibition of heat shock protein activity after hyperthermia by releasing the inhibitor 17-allylamino-17-demethoxygeldanamycin. These findings represent a smart nanofiber system for potent cancer therapy and may provide a new approach for the development of localized medication delivery. Full article
(This article belongs to the Special Issue Advances in the Treatment and Prevention of Chemotherapy Toxicity)
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Article
Drinking Ice-Cold Water Reduces the Severity of Anticancer Drug-Induced Taste Dysfunction in Mice
Int. J. Mol. Sci. 2020, 21(23), 8958; https://doi.org/10.3390/ijms21238958 - 25 Nov 2020
Cited by 2 | Viewed by 997
Abstract
Taste disorders are common adverse effects of cancer chemotherapy that can reduce quality of life and impair nutritional status. However, the molecular mechanisms underlying chemotherapy-induced taste disorders remain largely unknown. Furthermore, there are no effective preventive measures for chemotherapy-induced taste disorders. We investigated [...] Read more.
Taste disorders are common adverse effects of cancer chemotherapy that can reduce quality of life and impair nutritional status. However, the molecular mechanisms underlying chemotherapy-induced taste disorders remain largely unknown. Furthermore, there are no effective preventive measures for chemotherapy-induced taste disorders. We investigated the effects of a combination of three anticancer drugs (TPF: docetaxel, cisplatin and 5-fluorouracil) on the structure and function of mouse taste tissues and examined whether the drinking of ice-cold water after TPF administration would attenuate these effects. TPF administration significantly increased the number of cells expressing apoptotic and proliferative markers. Furthermore, TPF administration significantly reduced the number of cells expressing taste cell markers and the magnitudes of the responses of taste nerves to tastants. The above results suggest that anticancer drug-induced taste dysfunction may be due to a reduction in the number of taste cells expressing taste-related molecules. The suppressive effects of TPF on taste cell marker expression and taste perception were reduced by the drinking of ice-cold water. We speculate that oral cryotherapy with an ice cube might be useful for prophylaxis against anticancer drug-induced taste disorders in humans. Full article
(This article belongs to the Special Issue Advances in the Treatment and Prevention of Chemotherapy Toxicity)
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Article
Enhanced Activity of P4503A4 and UGT1A10 Induced by Acridinone Derivatives C-1305 and C-1311 in MCF-7 and HCT116 Cancer Cells: Consequences for the Drugs’ Cytotoxicity, Metabolism and Cellular Response
Int. J. Mol. Sci. 2020, 21(11), 3954; https://doi.org/10.3390/ijms21113954 - 31 May 2020
Cited by 2 | Viewed by 815
Abstract
Activity modulation of drug metabolism enzymes can change the biotransformation of chemotherapeutics and cellular responses induced by them. As a result, drug-drug interactions can be modified. Acridinone derivatives, represented here by C-1305 and C-1311, are potent anticancer drugs. Previous studies in non-cellular systems [...] Read more.
Activity modulation of drug metabolism enzymes can change the biotransformation of chemotherapeutics and cellular responses induced by them. As a result, drug-drug interactions can be modified. Acridinone derivatives, represented here by C-1305 and C-1311, are potent anticancer drugs. Previous studies in non-cellular systems showed that they are mechanism-based inhibitors of cytochrome P4503A4 and undergo glucuronidation via UDP-glucuronosyltranspherase 1A10 isoenzyme (UGT1A10). Therefore, we investigated the potency of these compounds to modulate P4503A4 and UGT1A10 activity in breast MCF-7 and colon HCT116 cancer cells and their influence on cytotoxicity and cellular response in cells with different expression levels of studied isoenzymes. We show that C-1305 and C-1311 are inducers of not only P4503A4 but also UGT1A10 activity. MCF-7 and HCT116 cells with high P4503A4 activity are more sensitive to acridinone derivatives and undergo apoptosis/necrosis to a greater extent. UGT1A10 was demonstrated to be responsible for C-1305 and C-1311 glucuronidation in cancer cells and glucuronide products were excreted outside the cell very fast. Finally, we show that glucuronidation of C-1305 antitumor agent enhances its pro-apoptotic properties in HCT116 cells, while the cytotoxicity and cellular response induced by C-1311 did not change after drug glucuronidation in both cell lines. Full article
(This article belongs to the Special Issue Advances in the Treatment and Prevention of Chemotherapy Toxicity)
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Review

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Review
Advances in the Treatment and Prevention of Chemotherapy-Induced Ovarian Toxicity
Int. J. Mol. Sci. 2020, 21(20), 7792; https://doi.org/10.3390/ijms21207792 - 21 Oct 2020
Cited by 6 | Viewed by 1037
Abstract
Due to improvements in chemotherapeutic agents, cancer treatment efficacy and cancer patient survival rates have greatly improved, but unfortunately gonadal damage remains a major complication. Gonadotoxic chemotherapy, including alkylating agents during reproductive age, can lead to iatrogenic premature ovarian insufficiency (POI), and loss [...] Read more.
Due to improvements in chemotherapeutic agents, cancer treatment efficacy and cancer patient survival rates have greatly improved, but unfortunately gonadal damage remains a major complication. Gonadotoxic chemotherapy, including alkylating agents during reproductive age, can lead to iatrogenic premature ovarian insufficiency (POI), and loss of fertility. In recent years, the demand for fertility preservation has increased dramatically among female cancer patients. Currently, embryo and oocyte cryopreservation are the only established options for fertility preservation in women. However, there is growing evidence for other experimental techniques including ovarian tissue cryopreservation, oocyte in vitro maturation, artificial ovaries, stem cell technologies, and ovarian suppression. To prevent fertility loss in women with cancer, individualized fertility preservation options including established and experimental techniques that take into consideration the patient’s age, marital status, chemotherapy regimen, and the possibility of treatment delay should be provided. In addition, effective multidisciplinary oncofertility strategies that involve a highly skilled and experienced oncofertility team consisting of medical oncologists, gynecologists, reproductive biologists, surgical oncologists, patient care coordinators, and research scientists are necessary to provide cancer patients with high-quality care. Full article
(This article belongs to the Special Issue Advances in the Treatment and Prevention of Chemotherapy Toxicity)
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Review
Nephrotoxicity Associated with Novel Anticancer Agents (Aflibercept, Dasatinib, Nivolumab): Case Series and Nephrological Considerations
Int. J. Mol. Sci. 2020, 21(14), 4878; https://doi.org/10.3390/ijms21144878 - 10 Jul 2020
Cited by 4 | Viewed by 1362
Abstract
Cancer patients have an incidence of about 60% kidney disease development and are at elevated risk of acute renal damage. Kidney disease in these patients is frequently associated with nephrotoxicity from the ongoing oncological treatment. New anticancer therapeutic strategies, such as targeted therapies [...] Read more.
Cancer patients have an incidence of about 60% kidney disease development and are at elevated risk of acute renal damage. Kidney disease in these patients is frequently associated with nephrotoxicity from the ongoing oncological treatment. New anticancer therapeutic strategies, such as targeted therapies and immunotherapies, offer substantial benefits in the treatment of many neoplasms. However, their use is associated with significant nephrotoxicity, which qualitatively differs from that seen with traditional cytotoxic chemotherapy, while the underlying mechanisms are complex and still to be clearly defined. Nephrologists need to be knowledgeable about the array of such renal toxicities for effective collaboration with the oncologist in the prevention and management of kidney involvement. Renal adverse effects may range from asymptomatic proteinuria to renal failure, and their prompt identification and timely treatment is essential for optimal and safe care of the patient. In this article, after presenting clinical cases we discuss the differing renal toxicity of three novel anticancer agents (aflibercept, dasatinib, and nivolumab) and possible measures to counter it. Full article
(This article belongs to the Special Issue Advances in the Treatment and Prevention of Chemotherapy Toxicity)
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