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P. 9
Eurasian Journal of Medicine
and Oncology
EDITORIAL
From the Editor’s desk
Bernd Kaina*
Institute of Toxicology, University Medical Center, Mainz, Germany
Two articles have appeared in this volume of the Eurasian Journal of Medicine and
Oncology that I would like to address. The work by Rauf et al. describes two natural
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compounds isolated from Pistacia chinensis. This tree is found primarily in China
and is planted as a street tree in temperate zones worldwide due to its attractive fruit
and beautiful autumn foliage. Two flavonoids were extracted from the tree’s bark. The
flavonoids are polyphenols, and their chemical structures are described in the manuscript.
In silico analyses showed that the phytochemicals, designated as compound 1 and
compound 2, bind to several target proteins, including mechanistic target of rapamycin
(mTOR) and protein kinase B 1 (encoded by AKT1). They could therefore potentially
influence the phosphoinositide 3-kinase (PI3K)–AKT–mTOR pathway. If this binding
has an inhibitory effect, it could lead to reduced protein synthesis and, consequently,
inhibition of cell growth and proliferation. It could also contribute to increased levels
and activation of tumor suppressor protein p53 through targeting mouse double minute
2 homolog (MDM2), as well as to the activation of pro-apoptotic proteins such as BCL2,
thereby stimulating pro-apoptotic signaling. A third effect is based on the inhibition
of autophagy by mTORC1, which may also be inhibited. In summary, pro-apoptotic
processes could be promoted, and cells could be specifically driven to undergo cell death.
In light of this scenario, the authors also investigated cell death using the glioblastoma
cell line U87MG. In the 3-(4,5-di methyl thiazol-2-yl)-2,5-diphenyltetrazolium bromide
*Corresponding author: (MTT) assay, the flavonoids showed a positive effect, which is interpreted as anti-
Bernd Kaina cancer activity. However, it must be noted that the MTT assay is a metabolic assay and
(kaina@uni-mainz.de) reflects both proliferation inhibition and actual cell death. Unfortunately, these toxicity
Citation: Kaina B. From the Editor’s studies were not extended, and the authors did not assess apoptosis or, where applicable,
desk. Eurasian J Med Oncol. necroptosis. Therefore, it remains unclear whether the effects observed through the
2025;9(3):1-3. MTT assay are due to genuine cell death or simply reflect growth inhibition.
doi: 10.36922/EJMO025360369
Received: August 21, 2025 This is clearly a limitation of the work. Observing a growth-inhibitory or cytotoxic
effect on a tumor cell line should not immediately lead to the conclusion that a substance
Accepted: September 1, 2025 has “anti-cancer activity.” Such a conclusion requires evidence that the substance is
Published online: September 23, selectively active against tumor cells and not toxic to non-transformed cells. This implies
2025 that a broad panel of cell lines should be tested. Animal experiments are also necessary
Copyright: © 2025 Author(s). before claims of anti-cancer activity can be made. The term “activity on cancer cell lines”
This is an Open-Access article would be more precise and appropriate in this context.
distributed under the terms of the
Creative Commons Attribution Nevertheless, the study is interesting because it reports the identification of a new
License, permitting distribution,
and reproduction in any medium, group of natural compounds with potential relevance for cancer therapy. In future
provided the original work is research, it would be worthwhile to characterize the effects at both the cellular and
properly cited. molecular levels in detail, to answer important open questions. For example, in the
Publisher’s Note: AccScience toxicity prediction assay, one of the compounds tested positive in the Ames test. This
Publishing remains neutral with could indicate that at least one of the substances has genotoxic potential. Genotoxic
regard to jurisdictional claims in
published maps and institutional effects are clearly linked to cytotoxicity, as p53-dependent apoptotic signaling pathways
affiliations. are activated through DNA damage. In fact, some natural compounds that exert
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Volume 9 Issue 3 (2025) 1 doi: 10.36922/EJMO025360369

