Chemoprevention to Dwindle Tumor Development

A special issue of Biomedicines (ISSN 2227-9059). This special issue belongs to the section "Cancer Biology and Oncology".

Deadline for manuscript submissions: closed (30 April 2025) | Viewed by 513

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Department of Biotechnology and Food Technology, Southern Taiwan University of Science and Technology, Tainan 710, Taiwan
Interests: oncology proteomics; complementary medicine; oncology; ureteroscopy; punicalagin; proteins
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Dear Colleagues,

Cancer causes serious mortality every year. Researchers have devoted much effort and money to curing cancer. However, we have not achieved satisfactory results. There may be a better way to prevent cancer’s appearance rather than to cure it. Thus, cancer chemoprevention may emerge as one of the major strategies for lowering cancer morbidity. Cancer chemoprevention is a pharmacological intervention strategy with naturally present and/or synthetic compounds that may prevent or inhibit carcinogenesis and even suppress the progression of invasive cancer. Indeed, cancer chemoprevention prevents neoplasia progression by stalling neoplastic establishment and switching the formation of transformed cells before the appearance of malignant lesions.

The cornerstone of chemoprevention is uncovering the mechanism of carcinogenesis at the molecular, cellular and animal levels. Carcinogenesis is a multi-stage and multi-pathway process encompassing a series of epigenetic and genetic mutations usually compiled during several years or even decades that shift from normal to increasing grades of dysplasia, ultimately contributing to the emergence of an invasive and metastatic lesion. Thus, the most profound chemoprevention approach is to perform an intervention at an early stage of carcinogenesis using natural or synthetic agents in order to stunt, stop or even reverse the carcinogenesis.

We invite research manuscripts and reviews on the prevention of tumor development at the molecular, cellular or animal levels and clinical studies using natural or synthetic agents.

Prof. Dr. Ting-Feng Wu
Guest Editor

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Keywords

  • tumor
  • carcinogenesis
  • dysplasia
  • neoplasm
  • chemoprevention

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Published Papers (1 paper)

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Research

21 pages, 3245 KiB  
Article
Interactions of Nedaplatin with Nucleobases and Purine Alkaloids: Their Role in Cancer Therapy
by Kamil Szupryczyński and Beata Szefler
Biomedicines 2025, 13(7), 1551; https://doi.org/10.3390/biomedicines13071551 - 25 Jun 2025
Viewed by 314
Abstract
Background: Nedaplatin is a platinum-based anticancer drug that combines the benefits of Cisplatin and Carboplatin, retaining Cisplatin’s anticancer activity while reducing toxicity similar to Carboplatin. After hydrolysis, Nedaplatin targets purines in DNA and forms cross-links that induce cell death via apoptosis. However, [...] Read more.
Background: Nedaplatin is a platinum-based anticancer drug that combines the benefits of Cisplatin and Carboplatin, retaining Cisplatin’s anticancer activity while reducing toxicity similar to Carboplatin. After hydrolysis, Nedaplatin targets purines in DNA and forms cross-links that induce cell death via apoptosis. However, it is important to consider how the presence of other chemical compounds with structural similarities to Adenine or Guanine, such as aromatic, purine, or pyrimidine compounds containing a nitrogen atom with a free electron pair, might influence its activity at the cellular level. Alkaloids with structures similar to DNA nucleobases are common, and their influence on Nedaplatin’s activity requires investigation. Methods: In this study, the interactions between Nedaplatin (including its hydrolyzed forms, such as [Pt(NH3)2(H2O)2]2+ and [Pt(NH3)2(H2O)(OH)]+) and nucleobases (Adenine and Guanine) and purine alkaloids (Caffeine, Theobromine and Theophylline) were thoroughly investigated using theoretical (density functional theory, DFT) and experimental (UV-Vis spectroscopy) methods. DFT calculations were performed at the B3LYP/6-31G(d,p)/LANL2DZ and MN15/def2-TZVP levels, with structure optimization and harmonic analysis in the gas phase and aqueous solution (modeled using IEF-PCM). UV-Vis spectroscopy was used to verify theoretical findings by examining changes in absorption spectra. Results: Both theoretical and experimental studies confirmed that Nedaplatin forms complexes with both nucleobases and purine alkaloids. Nedaplatin was found to exhibit a higher affinity for nucleobases than for purine alkaloids. Furthermore, this affinity was dependent on the computational method used and on the hydrolyzed form of Nedaplatin. Theoretical calculations showed the formation of stable complexes through bonding with nitrogen atoms in the ligand molecules, which was confirmed by changes in UV-Vis spectra, indicating adduct formation. Conclusions: The results indicate that Nedaplatin readily forms complexes with both nucleobases and purine alkaloids, showing a stronger affinity for nucleobases. This finding highlights the potential importance of Nedaplatin’s interactions with other compounds present in the body, which may influence its effectiveness and mechanism of action in cancer therapy. These studies provide new insights into the molecular mechanisms of Nedaplatin’s action and may contribute to a better understanding of its pharmacological interactions. However, research requires confirmation not only in in vivo studies but also in clinical trials. Full article
(This article belongs to the Special Issue Chemoprevention to Dwindle Tumor Development)
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