Anti-cancer agents in medicinal chemistry最新文献

{"title":"Evaluation of Anticancer Potential in Human Colorectal Carcinoma HCT-116 Cells by Fungal-Mediated Zinc Oxide Nanoparticles.","authors":"Yaser E Alqurashi, Sami G Almalki, Ibrahim M Ibrahim, Aisha O Mohammed, Amal E Abd El Hady, Mehnaz Kamal, Faria Fatima, Danish Iqbal","doi":"10.2174/0118715206395334250707063019","DOIUrl":"https://doi.org/10.2174/0118715206395334250707063019","url":null,"abstract":"<p><strong>Introduction: </strong>Chemotherapy faces limitations such as toxicity and resistance, necessitating novel cancer treatments. Green-synthesized zinc oxide nanoparticles (ZnO-NPs) have attracted attention for their safety, biocompatibility, and therapeutic potential. This study investigates the anticancer efficacy of ZnO-NPs synthesized using the extracellular matrix of Aspergillus biplanus against colorectal cancer cell lines (HCT-116).</p><p><strong>Methods: </strong>ZnO-NPs were synthesized extracellularly using A. biplanus fungal extract. The nanoparticles were characterized through UV-Vis spectrophotometry, showing an absorbance peak at 375 nm, and scanning electron microscopy (SEM), which determined their morphology and size. The anticancer activity was evaluated in vitro using HCT-116 cells. Reactive oxygen species (ROS) generation and mitochondrial membrane potential (MMP) were assessed to understand the mechanism of cytotoxicity. In vivo studies were proposed for further validation.</p><p><strong>Results: </strong>The synthesized ZnO-NPs appeared pale white and exhibited a characteristic absorbance at 375 nm. SEM revealed spherical particles ranging from 35-150 nm. The ZnO-NPs showed strong anticancer activity with an IC50 value of 40.6 μg/mL. ROS levels increased significantly in treated cells, while the MMP decreased to 77.25% compared to 100% in controls.</p><p><strong>Discussion: </strong>ZnO-NPs exerted cytotoxic effects via ROS generation and mitochondrial dysfunction. These results underscore the nanoparticles' ability to induce apoptosis in cancer cells through oxidative stress pathways.</p><p><strong>Conclusion: </strong>Biogenically synthesized ZnO-NPs from A. biplanus show promise as eco-friendly anticancer agents. Further in vivo studies are recommended to confirm their therapeutic potential.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144999407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ursolic Acid Inhibits Triple-Negative Breast Cancer Progression by Modulating the FGFR1/AKT/ERK Pathway: Evidence from Network Pharmacology and Experimental Validation.","authors":"Ziming Chen, Weiqiang Guo, Yahan Gao, Pu Zhao, Xin Liu, Min Qian, Shuhui You, Xiaoxiao Wang, Min Xiang","doi":"10.2174/0118715206379579250722053647","DOIUrl":"https://doi.org/10.2174/0118715206379579250722053647","url":null,"abstract":"<p><strong>Introduction: </strong>Ursolic acid (UA) exhibits antitumor activity; however, its effects and mechanisms on triple-negative breast cancer (TNBC) cells are not well understood. The present study aimed to explore the anti- TNBC mechanisms of UA by network pharmacology and experimental validation.</p><p><strong>Methods: </strong>TNBC cell lines MDA-MB-231 and BT-549 cells were treated with UA. A CCK-8 assay was performed to detect cell growth, while flow cytometry assessed cell cycle arrest and apoptosis. The underlying mechanism and potential targets of UA for TNBC treatment were investigated by network pharmacology, including PharmMapper database, GO, KEGG enrichment, and PPI analysis. The protein expressions and phosphorylation levels of FGFR1, AKT, and ERK were measured by western blot. Pull-down assay, cellular thermal shift assay (CETSA), and molecular docking were used to analyze the interaction between UA and FGFR1. Xenograft models were established to examine the effect of UA on TNBC tumor growth.</p><p><strong>Results: </strong>UA effectively reduced cell viability, induced apoptosis, and arrested cell cycle in TNBC cells. Moreover, UA significantly regulated the expression of Bcl-2 and Bax to induce apoptosis. The results of network pharmacology and western blot suggested that UA reduced FGFR1/AKT/ERK pathway. Furthermore, pull-down, CETSA, and molecular docking results revealed that UA directly bound to FGFR1. In the xenograft model, UA inhibited the growth by suppressing FGFR1.</p><p><strong>Discussion: </strong>In this study, we employed network pharmacology and experimental approaches to elucidate the mechanism of UA on TNBC. The results demonstrated that UA targeted FGFR1 to inhibit TNBC via mediating FGFR1/AKT/ERK pathway.</p><p><strong>Conclusions: </strong>Our findings demonstrate that UA inhibits the FGFR1/AKT/ERK pathway by directly targeting FGFR1, thereby suppressing TNBC progression and supporting its potential as a therapeutic agent for TNBC treatment.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939500","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic and Molecular Determinants of Immunotherapy Response in Recurrent Ovarian Cancer.","authors":"Hamid Noori, Sana Aqil Khan, Mohamed Hisham Alamin, Komal Zulfiqar, Ishak Alibhai, Abdullah Sultany, Saurav Kumar Mishra","doi":"10.2174/0118715206402903250809112441","DOIUrl":"https://doi.org/10.2174/0118715206402903250809112441","url":null,"abstract":"<p><p>Ovarian cancer remains a significant public health challenge. It originates in the ovaries and presents in various histological subtypes. Surgery and chemotherapy are the most suitable treatments to combat this disease. This study aims to provide insights into the mechanisms and biological complexity needed to understand the pathogenesis of recurrent ovarian cancer. A thorough review of the relevant literature on recurrent ovarian cancer and immunotherapy was conducted to gather information on genetic factors, immune responses, therapeutic strategies, and other pertinent data. The findings were analyzed and discussed to provide an in-depth understanding aligned with the study's objectives. Recurrent ovarian cancer is a major clinical challenge that occurs when the disease returns after initial treatment and a period of remission. Recurrence typically arises when residual cancer cells remain in the body after treatment, eventually leading to disease progression. Genetic factors, including mutations in BRCA1/BRCA2 and other genetic markers, play a crucial role in ovarian cancer recurrence and influence responses to therapies. The immune system's response to cancer cells is also critical, with therapeutic interventions either enhancing or reducing efficacy. The complex mechanisms underlying ovarian cancer and its recurrence have left many aspects of the disease pathway still to be fully understood. In conclusion, a comprehensive understanding of genetic and immune factors is crucial for developing effective and personalized treatments.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-08-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939506","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Design, Synthesis, Antimicrobial and Antitumor Activities of Benzo[f]chromene Derivatives: DFT and Molecular Docking.","authors":"Rita M A Borik, Ashraf H F Abdelwahab, Abdullah A Alamri, Hany M Mohamed, Mohamed S Mostafa, Mohamed R El-Aassar, Khatib Sayeed Ismail, Al-Anood M Al-Dies, Ahmed A Elhenawy, Ahmed M El-Agrody","doi":"10.2174/0118715206403354250808100701","DOIUrl":"https://doi.org/10.2174/0118715206403354250808100701","url":null,"abstract":"<p><strong>Introduction: </strong>Benzochromenes are heterocyclic compounds of growing interest in medicinal chemistry due to their diverse biological activities, including antioxidant, anticancer, and antimicrobial properties.</p><p><strong>Methods: </strong>A one-pot, three-component synthesis was employed to prepare benzochromene derivatives (4a-f) using 2-naphthol or its derivatives, active methylene compounds, and 2-methoxybenzaldehyde in ethanol with piperidine as a catalyst. The compounds were evaluated for their anticancer activity against MCF-7, HepG-2, and HCT-116 cell lines, as well as for their antimicrobial activity through molecular docking studies targeting cancerrelated and microbial proteins.</p><p><strong>Results: </strong>All synthesized compounds were obtained in moderate to good yields. Compounds 4c, 4e, and 4f demonstrated superior biological activity compared to standard drugs Doxorubicin and Augmentin. Docking studies revealed strong binding affinities to key targets, including the TGF-βI receptor and the choline-binding domain.</p><p><strong>Discussion: </strong>The hydroxyl group at position 9 in compounds 4c and 4f likely contributed to enhanced antimicrobial activity, while the bromo group in 4e correlated with significant anticancer effects. These findings suggest meaningful structure-activity relationships and validate the design strategy.</p><p><strong>Conclusion: </strong>The synthesized benzochromene derivatives exhibit promising anticancer and antimicrobial activities. Supported by molecular docking, these findings lay the groundwork for further pharmacological and in vivo evaluations of this scaffold.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144939485","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Gaussian-based 3D-QSAR and Pharmacophore Mapping Studies of Indole Derivatives as Aromatase Inhibitors.","authors":"Neha Bhatia, Suresh Thareja","doi":"10.2174/0118715206390949250805064957","DOIUrl":"https://doi.org/10.2174/0118715206390949250805064957","url":null,"abstract":"<p><strong>Introduction: </strong>Aromatase inhibition is one of the most effective strategies for the treatment of ER+ breast cancer, which accounts for about 70% of breast cancer cases. Indole-based aromatase inhibitors have altered the dynamics of the search for anti-breast cancer drugs with efficacy in nanomolar concentrations. In the present study, we have integrated pharmacophore mapping with Gaussian-based 3D-QSAR analysis to map the essential pharmacophoric features of indole-based aromatase inhibitors, aiming to optimize lead molecules.</p><p><strong>Methods: </strong>Pharmacophore mapping and Gaussian-based 3D-QSAR were integrated to identify the steric and electrostatic features essential for aromatase inhibitory activity.</p><p><strong>Results: </strong>A Gaussian-based 3D-QSAR model with an r² value of 0.7621 and stability of 0.817 was generated to determine the nature of substitutions essential for optimal biological activity. Pharmacophore mapping results indicated that H-bond Donor (D), a Hydrophobic (H) feature, and three aromatic rings are essential for potent inhibitory activity.</p><p><strong>Discussion: </strong>In order to identify important structural characteristics of indole-based aromatase inhibitors, the current study successfully integrated pharmacophore mapping investigations with 3D-QSAR. The developed molecule S1 demonstrated activity comparable to letrozole, with a predicted pIC50 value of 9.332 nM.</p><p><strong>Conclusion: </strong>The designed compound S1 demonstrated a predicted IC50 value of 9.332 nM, comparable to the most active compound 15 and the standard reference Letrozole. The developed models may be utilized by medicinal chemists for the optimization of new indole-based aromatase inhibitors for the effective treatment of ER+ breast cancer.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Timosaponin A-III Induces ROS-mediated Apoptosis and Triggers Protective Autophagy via the AMPK/mTOR Pathway in Prostate Cancer.","authors":"Jianjian Wu, Juntao Li, Qiang Guo, Chutian Xiao, Yifei Zhang, Dejuan Wang, Qiong Wu, Jianguang Qiu","doi":"10.2174/0118715206389520250805135535","DOIUrl":"https://doi.org/10.2174/0118715206389520250805135535","url":null,"abstract":"<p><p>Prostate cancer, timosaponin A‑III, apoptosis, autophagy, reactive oxygen species, AMPK/mTOR.</p><p><strong>Introduction: </strong>Timosaponin A-III (TAIII) is an effective anti-tumor ingredient extracted from the rhizomes of Anemarrhena asphodeloides. However, the effect of TAIII on prostate cancer cells (PCa) and its underlying mechanisms is rarely investigated. The current study aimed to investigate the anti-tumor effect and potential mechanisms of TAIII in PCa cells.</p><p><strong>Methods: </strong>The effect of TAIII on the cell proliferation of PCa was evaluated by CCK-8 assay, colony formation assay, and EDU assay. Cell apoptosis and reactive oxygen species (ROS) production were evaluated by flow cytometry. The puncta of LC3 were detected by immunofluorescence analysis. The protein levels of apoptosis, autophagy, and AMPK/mTOR pathway were assessed by western blot. Finally, a PC3 xenograft nude mouse model was constructed to determine the effect of TAIII combined with chloroquine (CQ) in vivo.</p><p><strong>Results: </strong>Our data showed that TAIII inhibited the proliferation of PCa cells and induced ROS-dependent apoptosis. TAIII treatment dramatically promoted the formation of LC3-positive puncta, and increased the expression of LC3B-II and P62 protein. Moreover, the combination of TAIII with CQ significantly enhanced the pro-apoptosis effect of TAIII in PCa cells and the PC3 xenograft model. In addition, the activation of the AMPK/mTOR pathway and the induction of autophagy induced by TAIII were reversed by Compound C. Suppressing AMPK with Compound C enhanced the apoptosis induced by TAIII in PCa cells.</p><p><strong>Discussion: </strong>This study establishes TAIII as a potent anti-prostate-cancer agent that kills tumor cells via ROSdriven apoptosis while simultaneously triggering cytoprotective autophagy through the AMPK-mTOR axis. However, TAIII's clinical potential awaits pharmacokinetic, bioavailability, and toxicity evaluation.</p><p><strong>Conclusion: </strong>TAIII induced ROS-mediated cell apoptosis and promoted cytoprotective autophagy via the AMPK/mTOR pathway in PCa. These findings may provide a new strategy for combining TAIII with CQ together for PCa treatment.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144871032","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular Pathways and Biomarkers in Endometrial Carcinoma: Paving the Way for Precision Medicine.","authors":"Krishana Kumar Sharma, Swati Tamta, Mohit Pandey, Ritu Gupta, Gajendra Kumar","doi":"10.2174/0118715206390892250803033306","DOIUrl":"https://doi.org/10.2174/0118715206390892250803033306","url":null,"abstract":"<p><p>Endometrial carcinoma (EC) is one of the most prevalent gynecological malignancies, with an increasing incidence globally. This review explores the role of molecular markers in revolutionizing the diagnosis, prognosis, and management of EC. This article provides an overview of endometrial carcinoma, emphasizing its subtypes and the molecular mechanisms driving disease progression. Current biomarkers, while clinically significant, often present limitations in sensitivity, specificity, and predictive value, necessitating the discovery of novel markers. Recent advances in genetic and epigenetic profiling have identified key mutations, such as PTEN, TP53, and POLE, along with DNA methylation patterns and microRNAs, as crucial contributors to EC pathophysiology. Furthermore, transcriptomic and proteomic studies reveal the potential of RNA-based markers (e.g., lncRNAs, mRNAs) and proteomic signatures in improving early diagnosis and prognostic predictions. Immunohistochemical markers and insights into tumor microenvironment dynamics pave the way for targeted therapeutic strategies. In the context of endometrial carcinoma (EC), clinical trials play a pivotal role in validating targeted therapies based on molecular subtypes and biomarkers, such as HER2 amplification, POLE mutations, and mismatch repair deficiency (MMRd). This review underscores the integration of biomarkers into precision oncology, enabling personalized treatment regimens. However, challenges such as barriers to clinical translation and the need for advanced technologies highlight the importance of continued research in marker discovery for EC.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144833785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting SHP2 Reverses BRAF Inhibitor Tolerance in Anaplastic Thyroid Carcinoma","authors":"Tao Tang, Jie Zhou, Li-Xin Zhang, Gang Yang, Wei-Nan Li, Jian-Jiao Zhu, Yong-Fu Xiong, Jing-Dong Li","doi":"10.2174/1871520623666230214093122","DOIUrl":"10.2174/1871520623666230214093122","url":null,"abstract":"<p><strong>Background: </strong>To explore the possibility of a combination of dabrafenib and SHP2 inhibitor in the treatment\u0000of anaplastic thyroid carcinoma and to provide a new therapeutic strategy for the treatment of anaplastic thyroid cancer.</p><p><strong>Methods: </strong>Firstly, a drug resistance model was established, and the expression levels of related RTK were detected by\u0000qPCR. Western blot was used to detect the protein expression levels of Akt and MAPK signaling pathways in the control group, single-drug group and two-drug combination group. The gene silencing of SHP2 was achieved by transfection of siRNA and verified by Western blot. CCK8 kit and clone formation assay were used to detect cell proliferation\u0000activity. In vivo model of mutant thyroid cancer cells was established by subcutaneous injection of mice and then divided into four groups. Tumor diameter was measured every two days. Immunohistochemistry was used to evaluate the\u0000expression of p-ERK, p-AKT and Ki67 in mouse tumors.</p><p><strong>Results: </strong>In this study, dabrafenib-resistant ATC cells were first constructed, and the response of RTKs in drug-resistant cells was upregulated to activate Akt and MER/ERK pathways. The activation of Akt and MEK/ERK pathways in the combination group was significantly inhibited, and the proliferation ability of tumor cells was significantly\u0000reduced compared with Dabrafenib, SHP099 group and DMSO group. To verify that SHP099 was not off-target, we also silenced SHP2 expression by transfection with siRNA and obtained the same results. Finally, by building a mouse drug resistance model, we confirmed that dabrafenib and SHP099 can also play a powerful anti-cancer effect in vivo.</p><p><strong>Conclusion: </strong>The SHP2 inhibitor SHP099 can effectively reverse the drug resistance of dabrafenib through inhibiting\u0000the reactivated RAS signaling pathway in anaplastic thyroid cancer. The combination of dabrafenib with SHP2 inhibitor has shown significant tumor suppressive effects for dabrafenib-resistant cells and it may be a new therapeutic strategy with longer lasting therapeutic benefits.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10767562","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serotonin Metabolism Shapes the Tumor Immune Microenvironment and Serves as a Therapeutic Target in Lung Cancer.","authors":"Miersalijiang Yasen, Naikun Sun, Jiude Jia, Weixiang Hong, Leiting Zhuang, Jinwang Huang, Xiaohui Chen, Wenhui Shen","doi":"10.2174/0118715206408134250801050919","DOIUrl":"https://doi.org/10.2174/0118715206408134250801050919","url":null,"abstract":"<p><strong>Introduction: </strong>Lung cancer progression involves complex interactions between metabolic pathways and the immune microenvironment. The role of serotonin, a tryptophan-derived metabolite, in immune responses to lung tumors remains unclear.</p><p><strong>Methods: </strong>An orthotopic lung cancer model was established by intravenously injecting KP (KrasG12D/p53-/-) cells into C57BL/6 mice. Metabolomic and flux analyses were conducted on tumor versus normal lung tissues. Serotonin was administered to tumor-bearing mice, followed by immunofluorescence and flow cytometry to assess immune responses. Human lung cancer datasets were analyzed to validate clinical relevance.</p><p><strong>Results: </strong>Tumor tissues exhibited a significant decrease in serotonin levels. Although tryptophan, serotonin, and kynurenine levels were decreased overall, flux analysis revealed a metabolic shift favoring kynurenine synthesis, with a ~10-fold increase in the kynurenine-to-serotonin ratio. Serotonin supplementation significantly prolonged survival and enhanced dendritic cell and CD8⁺ T cell infiltration and activation in tumors. Analysis of public datasets showed that serotonin expression positively correlated with CD8⁺ T cell activation signatures and patient prognosis.</p><p><strong>Discussion: </strong>By revealing serotonin as a potential biomarker and therapeutic target, this study paves new avenues for improving lung cancer treatment strategies through modulation of the immune microenvironment. Moreover, the precise receptor-mediated mechanisms underlying serotonin's immunomodulatory effects remain to be clarified, and translational validation in human tissues is warranted to strengthen clinical relevance.</p><p><strong>Conclusion: </strong>Serotonin deficiency in the tumor microenvironment of the lung suppresses antitumor immunity. Its restoration reverses immune dysfunction and limits tumor progression. These findings identify serotonin as a potential metabolic regulator and immunotherapeutic target in lung cancer.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144833786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Hematological Variations and Effect of Cadmium Induced Toxicity on Mammary Tumors Development in Albino Mice. A Comparative Model Study on the Effect of Heavy Metals in Human Breast Cancer.","authors":"Saba Munir, Yasir Nawaz, Fouzia Tanvir, Khalid Mehmood Anjum","doi":"10.2174/0118715206382637250731031214","DOIUrl":"https://doi.org/10.2174/0118715206382637250731031214","url":null,"abstract":"<p><strong>Introduction: </strong>Breast cancer develops in breast tissues, in ducts and lobules. It affects both genders, though it is uncommon in men. Hematological variations are important considerations and deficiencies in metals can negatively impact human health. Cadmium is highly toxic and plays role in breast cancer progression. This study was designed for hematological variations and cadmium induced toxicity in mice and humans causing breast cancer.</p><p><strong>Methods: </strong>Mice, obtained from local supplier, housed at university laboratory for 11 weeks, exposed to cadmium. Following dissection, blood and organs were harvested for examination. Histological analysis of liver and mammary gland tissues was conducted.</p><p><strong>Results: </strong>Affected mice had higher Hb, RBC, HCT, MCV, and MCH, while humans showed lower Hb, HCT, and MCV but similar RBC and MCH. Other blood values also show changes. Histopathology revealed changes in mammary glands (higher cadmium led to increased fat deposition, degeneration of alveolar epithelial cells, and a reduction in alveolar milk lumen size, indicating compromised glandular function) and Liver damage (vacuolation, lipid accumulation, fibrosis, and collagen deposition, was noticeable with prolonged cadmium). These changes causes liver fibrosis and impaired mammary gland function.</p><p><strong>Discussion: </strong>The cadmium exposure induces distinct hematological alterations and severe tissues damage, reflecting species-specific responses. The observed liver fibrosis and mammary gland dysfunction emphasize cadmium's potential to compromise critical organ functions over time.</p><p><strong>Conclusion: </strong>Significant effects of cadmium exposure in mice were observed. Histological damage was seen in mammary glands and liver. Further research on protective measures and dose-response relationships for cadmium exposure is needed.</p>","PeriodicalId":7934,"journal":{"name":"Anti-cancer agents in medicinal chemistry","volume":" ","pages":""},"PeriodicalIF":3.0,"publicationDate":"2025-08-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144833787","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}