{"title":"Ciprofloxacin-encapsulated solid lipid nanoparticles: a comprehensive biochemical analysis of cytotoxic effects, proliferation inhibition, and apoptotic induction in KG1-a leukemia cells.","authors":"Salma Hussein Kadhim, Gholamreza Dehghan, Majid Mahdavi","doi":"10.1007/s12032-025-02619-2","DOIUrl":"https://doi.org/10.1007/s12032-025-02619-2","url":null,"abstract":"<p><p>As a fundamental approach to the treatment of acute myeloid leukemia (AML), chemotherapeutic agents face significant clinical challenges, including poor solubility and low bioavailability. In this context, solid lipid nanoparticles (SLNs) have emerged as a promising drug delivery system in oncologic therapies, owing to their advantageous characteristics, such as enhanced physical stability and controlled drug-release profiles. This study focuses on the synthesis of ciprofloxacin (CP)-loaded SLNs, aiming to enhance the anticancer efficacy of CP, an antibiotic recognized for its potential anticancer properties, while simultaneously reducing its associated side effects. Characterization of blank SLN and CP-SLN was conducted using dynamic light scattering (DLS), atomic force microscopy (AFM), UV-Vis spectrophotometry, and Fourier transform infrared spectroscopy (FTIR). In vitro release was carried out using dialysis bag method in isotonic phosphate buffer (pH = 7.4). The anticancer and pro-apoptotic effects of the CP-SLN formulation were assessed through cell viability assays, Hoechst staining, and Annexin V/PI flow cytometry. Additionally, expression levels of Bax, Bcl2, and p53 were analyzed via Real-Time PCR. The synthesized CP-SLN formulation exhibited optimal characteristics, including a particle size of 340-360 nm, a polydispersity index (PDI) of 0.4, and an entrapment efficiency of 90%. The in vitro drug release showed an initial burst release in the time points 4-10 h. Both CP and the CP-SLN formulations demonstrated significant anti-proliferative and pro-apoptotic effects on KG1-a cells, as indicated by the upregulation of the Bax/Bcl2 ratio and p53, resulting in G0/G1 cell cycle arrest and apoptosis induction. The results suggest that encapsulating CP in SLN enhances its anticancer and pro-apoptotic effects in KG1-a stem-like leukemia cells. Thus, CP-SLN may serve as a promising formulation for leukemia treatment and could improve the efficacy of other therapeutic agents.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"75"},"PeriodicalIF":2.8,"publicationDate":"2025-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143408452","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}
Medical OncologyPub Date : 2025-02-11DOI: 10.1007/s12032-025-02618-3
Tülin Burhanoğlu, Zehra Seda Halbutoğulları, Gulseren Turhal, Asuman Demiroglu-Zergeroglu
{"title":"Evaluation of the anticancer effects of hydroxycinnamic acid isomers on breast cancer stem cells.","authors":"Tülin Burhanoğlu, Zehra Seda Halbutoğulları, Gulseren Turhal, Asuman Demiroglu-Zergeroglu","doi":"10.1007/s12032-025-02618-3","DOIUrl":"10.1007/s12032-025-02618-3","url":null,"abstract":"<p><p>Research on breast cancer stem cells (BCSCs) is crucial for improving our understanding of their roles in tumor resistance, metastasis, and relapse. This study investigated the anti-cancer effects of two isomers of hydroxycinnamic acids (HCA): para-coumaric acid (PCA) and ortho-coumaric acid (OCA) on breast cancer stem cells (BCSCs). The isolated and characterized stem cells contained CD44 + /CD24 surface markers, exhibited high levels of aldehyde dehydrogenase activity, and were able to form mammospheres. The evaluation of HCAs on stem cell proliferation, cell cycle, and apoptosis was conducted by comparing them with MCF-7, the luminal breast cancer cell line. The viability and immunoblot analyses demonstrated that HCA applications resulted in a dose-dependent decrease in the number of viable cells and inhibited phosphorylation of Extracellular regulated kinases 1/2 (ERK1/2). These findings were supported by the detection of suppressed colony formation and delayed wound-healing in HCA-exposed cells. E-cadherin expression increased in OCA-treated cells. Additionally, the arrest of G1/S phase progression and the downregulation of Cyclin D1 expression exhibited that OCA and PCA-induced cytostatic effects in BSCS cells. After treatment, the increased Annexin-V/7-AAD staining, along with elevated expression of caspase-3/7 and a decreased Bcl-2/Bax ratio, indicated apoptosis mediated by the activation of Janus kinase (JNK) and p38 Mitogen-activated kinase (p38 MAPK). In conclusion, both OCA and PCA exhibit anti-carcinogenic potential on BCSCs; However, OCA has a stronger effect and is becoming a promising candidate for further research.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"73"},"PeriodicalIF":2.8,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391223","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}
Medical OncologyPub Date : 2025-02-11DOI: 10.1007/s12032-025-02617-4
Ozgur Tanriverdi
{"title":"Ethical and academic dilemmas in authorship of clinical research publications: a medical oncologist's perspective.","authors":"Ozgur Tanriverdi","doi":"10.1007/s12032-025-02617-4","DOIUrl":"10.1007/s12032-025-02617-4","url":null,"abstract":"<p><p>Authorship in clinical research carries significant academic, financial, and social implications. However, determining rightful authorship often introduces ethical and professional dilemmas, particularly in large, multidisciplinary studies, such as those common in oncology. This article explores the ethical complexities surrounding authorship in clinical research from the viewpoint of a medical oncologist. It addresses issues, such as academic jealousy, the inclusion of industry-affiliated researchers, honorary authorship, and the role of patient recruitment in authorship qualification. By examining current guidelines, ethical considerations, and practical cases, this paper aims to offer insights into fostering fair and transparent authorship practices in the field of clinical oncology.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"74"},"PeriodicalIF":2.8,"publicationDate":"2025-02-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143391128","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}
Medical OncologyPub Date : 2025-02-10DOI: 10.1007/s12032-025-02622-7
Caiyuan Yu, Jinhui Sun, Xinyi Lai, Zhiming Tan, Yang Wang, Haiyan Du, Zhaobin Pan, Tingyu Chen, Ziping Yang, Shicai Ye, Juanhua Quan, Yu Zhou
{"title":"Gefitinib induces apoptosis in Caco-2 cells via ER stress-mediated mitochondrial pathways and the IRE1α/JNK/p38 MAPK signaling axis.","authors":"Caiyuan Yu, Jinhui Sun, Xinyi Lai, Zhiming Tan, Yang Wang, Haiyan Du, Zhaobin Pan, Tingyu Chen, Ziping Yang, Shicai Ye, Juanhua Quan, Yu Zhou","doi":"10.1007/s12032-025-02622-7","DOIUrl":"https://doi.org/10.1007/s12032-025-02622-7","url":null,"abstract":"<p><p>Gefitinib, a selective EGFR-tyrosine kinase inhibitor, exhibits potent cytotoxic effects on colorectal cancer cells, though its precise mechanisms are not fully understood. In this study, we demonstrated that gefitinib induces a dose-dependent cytotoxic response in Caco-2 cells, characterized by disrupted microtubule networks, impaired migration, and reduced viability. Gefitinib triggered apoptosis, as indicated by increased levels of cleaved caspase-3, PARP, and elevated late apoptosis rates. Mechanistically, gefitinib-induced endoplasmic reticulum (ER) stress, marked by the upregulation of IRE1α, CHOP, and ATF4. ER stress inhibition by 4-PBA significantly reduced apoptosis and restored mitochondrial membrane potential (MMP). Additionally, gefitinib-induced apoptosis was mediated through the mitochondrial pathway, reflected by the modulation of Bcl-2 family proteins, including the upregulation of Bax and Bim. Inhibition of the IRE1α-mediated JNK/p38 MAPK pathway further mitigated gefitinib-induced apoptosis and restored MMP. These findings highlight the critical role of ER stress and the IRE1α-JNK/p38 MAPK axis in gefitinib-induced mitochondrial apoptosis, offering potential therapeutic targets for colorectal cancer.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"71"},"PeriodicalIF":2.8,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382853","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}
Medical OncologyPub Date : 2025-02-10DOI: 10.1007/s12032-025-02609-4
Dinesh Kumar Sharma
{"title":"Recent advancements in nanoparticles for cancer treatment.","authors":"Dinesh Kumar Sharma","doi":"10.1007/s12032-025-02609-4","DOIUrl":"https://doi.org/10.1007/s12032-025-02609-4","url":null,"abstract":"<p><p>Nanotechnology is a significant factor that has assisted researchers in overcoming medications' permeability and retention effects. This article discusses how different nanoparticles, such as metallic nanoparticles, carbon nanotubes (CNTs), and extracellular vesicles (EVs), are transforming cancer treatments and diagnosis. While CNTs provide photothermal qualities that enable synergistic effects when paired with chemotherapy, EVs provide biocompatibility and immune evasion, enabling effective drug transport. Because of their special optical and magnetic characteristics, metallic nanoparticles are essential for imaging and targeted medication administration. When compared to traditional treatments, these nanoparticles improve bioavailability, decrease systemic toxicity, and increase therapeutic efficacy. Despite increased investigations, the number of licensed nano-drugs has remained relatively high. More investigation is required into targeted drug delivery using nanocarriers to minimize the shielding impact of the protein corona, increase permeability and retention effects, and reduce toxicity to improve clinical translation. This study focuses on novel approaches and state-of-the-art cancer therapies using nanoparticles that target different cancer cells. It also emphasized the advantages of nanoparticle-based cancer therapies over conventional ones, their difficulties, and future promises.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"72"},"PeriodicalIF":2.8,"publicationDate":"2025-02-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143382854","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}
Medical OncologyPub Date : 2025-02-08DOI: 10.1007/s12032-025-02620-9
Leonardo Duranti, Luca Tavecchio, Luigi Rolli, Clarissa Uslenghi, Piergiorgio Solli
{"title":"Chylothorax in thoracic oncology: diagnostic challenges and management strategies.","authors":"Leonardo Duranti, Luca Tavecchio, Luigi Rolli, Clarissa Uslenghi, Piergiorgio Solli","doi":"10.1007/s12032-025-02620-9","DOIUrl":"https://doi.org/10.1007/s12032-025-02620-9","url":null,"abstract":"<p><p>Chylothorax is a distinctive form of pleural effusion characterized by the accumulation of chyle within the pleural space. We conducted an analysis of published evidence concerning oncological chylothorax, encompassing complications following thoracic surgery or spontaneous occurrences directly linked to thoracic malignancies. Diagnosis can be established based on clinical features of the pleural effusion and through analysis of pleural fluid. The presence of chylomicrons, measured by lipoprotein electrophoresis, triglyceride levels, and cholesterol content are indicative factors. In cases of spontaneous chylothorax, the identification of pleural effusion on CT scans showing suspicious oncological masses, such as lymphomas, prompts pleural drainage for confirmation of chylothorax. Conversely, post-surgical chylothorax diagnoses are immediate due to the pre-existing pleural drainage. In our last 10 years of experience, we have had only 18 cases of chylothorax: 28% underwent successful redo-surgery and 72% were conservatively treated. All the patients recovered well, and none experienced life-threatening situations. Conservative approaches involve hypo/alipidic diets, total parenteral nutrition, and pharmacological interventions. In persistent and challenging cases of chylothorax where drainage output is excessive, redo-surgery is recommended.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"70"},"PeriodicalIF":2.8,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374421","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}
Medical OncologyPub Date : 2025-02-08DOI: 10.1007/s12032-025-02615-6
Ndapewoshali F Shafombabi, Michael Knott, Petrina Kapewangolo, Javad Sharifi-Rad, Daniela Calina
{"title":"Ingenol mebutate in cancer therapy: mechanisms, clinical applications and future directions.","authors":"Ndapewoshali F Shafombabi, Michael Knott, Petrina Kapewangolo, Javad Sharifi-Rad, Daniela Calina","doi":"10.1007/s12032-025-02615-6","DOIUrl":"https://doi.org/10.1007/s12032-025-02615-6","url":null,"abstract":"<p><p>Ingenol mebutate (IM), a diterpene ester derived from Euphorbia species, has demonstrated promising anticancer properties through direct cytotoxicity and immune modulation. Despite initial clinical success, its therapeutic use has been curtailed due to safety concerns, including potential links to increased skin cancer risk. This review evaluates the mechanisms of action, preclinical and clinical efficacy, safety, and limitations of IM as an anticancer agent, identifying areas for further development. A comprehensive literature review was performed using Google Scholar to identify English-language articles published from 2010 to 2023. Keywords included \"Ingenol mebutate,\" \"PEP005,\" and \"cancer therapy.\" Articles focusing on IM's pharmacological properties, therapeutic mechanisms, clinical studies, and safety profile were included. IM exerts anticancer effects through dual mechanisms: mitochondrial dysfunction leading to necrosis and immune-mediated cytotoxicity via protein kinase C activation. Preclinical studies show efficacy against pancreatic, colorectal, and epithelial cancers and clinical studies have reported success in treating actinic keratosis and nonmelanoma skin cancers. Challenges include intense local skin reactions and safety concerns, particularly its potential association with increased skin malignancy risk. IM represents a promising therapeutic agent due to its rapid and potent anticancer effects. However, optimizing its safety profile and exploring advanced delivery methods are critical to expanding its clinical applications. Further studies are required to establish its long-term efficacy and potential for broader use in oncology.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"69"},"PeriodicalIF":2.8,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143374422","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":"Retraction Note: The function of Cav-1 in MDA-MB-231 breast cancer cell migration and invasion induced by ectopic ATP5B.","authors":"Xinjie Dong, Yilei Li, Wei Li, Wenzhe Kang, Rong Tang, Wenyi Wu, Ziyi Xing, Lijuan Zhou","doi":"10.1007/s12032-025-02623-6","DOIUrl":"10.1007/s12032-025-02623-6","url":null,"abstract":"","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"68"},"PeriodicalIF":2.8,"publicationDate":"2025-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11805774/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143370778","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Medical OncologyPub Date : 2025-02-06DOI: 10.1007/s12032-025-02611-w
Arun Radhakrishnan, Nikhitha K Shanmukhan, Linda Christabel Samuel
{"title":"Pharmacogenomics influence on MDR1-associated cancer resistance and innovative drug delivery approaches: advancing precision oncology.","authors":"Arun Radhakrishnan, Nikhitha K Shanmukhan, Linda Christabel Samuel","doi":"10.1007/s12032-025-02611-w","DOIUrl":"https://doi.org/10.1007/s12032-025-02611-w","url":null,"abstract":"<p><p>Currently, there is a growing concern surrounding the treatment of cancer, a formidable disease. Pharmacogenomics and personalized medicine have emerged as significant areas of interest in cancer management. The efficacy of many cancer drugs is hindered by resistance mechanisms, particularly P-glycoprotein (P-gp) efflux, leading to reduced therapeutic outcomes. Efforts have intensified to inhibit P-gp efflux, thereby enhancing the effectiveness of resistant drugs. P-gp, a member of the ATP-binding cassette (ABC) superfamily, specifically the multidrug resistance (MDR)/transporter associated with antigen processing (TAP) sub-family B, member 1, utilizes energy derived from ATP hydrolysis to drive efflux. This review focuses on genetic polymorphisms associated with P-gp efflux and explores various novel pharmaceutical strategies to address this challenge. These strategies encompass SEDDS/SNEDDS, liposomes, immunoliposomes, solid lipid nanoparticles, lipid core nanocapsules, microemulsions, dendrimers, hydrogels, polymer-drug conjugates, and polymeric nanoparticles. The article aims to elucidate the interplay between pharmacogenomics, P-gp-mediated drug resistance in cancer, and formulation strategies to improve cancer therapy by tailoring formulations to genetically susceptible patients.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"67"},"PeriodicalIF":2.8,"publicationDate":"2025-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143256122","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}
Medical OncologyPub Date : 2025-02-05DOI: 10.1007/s12032-024-02581-5
Mrityunjay Tyagi
{"title":"DNA repair in cancers: why is there an alternative?","authors":"Mrityunjay Tyagi","doi":"10.1007/s12032-024-02581-5","DOIUrl":"https://doi.org/10.1007/s12032-024-02581-5","url":null,"abstract":"","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"42 3","pages":"66"},"PeriodicalIF":2.8,"publicationDate":"2025-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143189335","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}