Journal of the Egyptian National Cancer Institute最新文献

{"title":"Ferroptosis in cancer: molecular mechanisms, tumour microenvironment, therapeutic resistance, and clinical translation.","authors":"Ghisaram Dewasi, Sakshi Jain","doi":"10.1186/s43046-026-00419-x","DOIUrl":"10.1186/s43046-026-00419-x","url":null,"abstract":"<p><p>Ferroptosis is a distinct form of regulated cell death driven by iron-dependent lipid peroxidation and oxidative membrane damage, and it differs fundamentally from apoptosis, necroptosis, and pyroptosis in its molecular mechanisms and execution pathways. Increasing evidence indicates that ferroptosis plays a pivotal role in cancer biology by regulating tumour initiation, progression, metastasis, therapeutic resistance, and interactions within the tumour microenvironment (TME). Dysregulation of iron metabolism, lipid peroxidation, amino acid metabolism, and antioxidant defence systems, including the System Xc⁻-GSH-GPX4, FSP1-CoQ₁₀, GCH1-BH4, and DHODH pathways, collectively determines cellular susceptibility to ferroptosis. Recent studies have further highlighted the contribution of organelle crosstalk, immune cell regulation, and stromal interactions in shaping ferroptotic responses and tumour evolution. In this review, we comprehensively summarise the molecular mechanisms underlying ferroptosis, its regulatory signalling networks, and the major milestones that have advanced the field. We further discuss the multifaceted role of ferroptosis across diverse malignancies, its influence on epithelial-mesenchymal transition, tumour invasion, metastasis, and immune modulation, and its emerging significance in overcoming resistance to chemotherapy, radiotherapy, targeted therapy, and immunotherapy. In addition, we critically evaluate recent progress in ferroptosis-based therapeutic strategies, including nanomedicine, combination therapies, and translational advances, while highlighting current clinical challenges such as tumour heterogeneity, limited pharmacodynamic biomarkers, and safety concerns. Collectively, ferroptosis represents a promising therapeutic vulnerability that bridges fundamental cancer biology with precision oncology. Continued development of biomarker-guided patient stratification, targeted drug delivery systems, and rational combination strategies is expected to accelerate the clinical translation of ferroptosis-based therapies and improve outcomes for patients with refractory and treatment-resistant cancers.</p>","PeriodicalId":17301,"journal":{"name":"Journal of the Egyptian National Cancer Institute","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13676557/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149216398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association of XRCC6 -61 C > G and XRCC7 6721G > T polymorphisms with susceptibility to pediatric acute lymphoblastic leukemia.","authors":"Mani Ramzi, Soodabeh Zare, Nasrin Noshadi, Ghasem Nikfar, Zahed Karimi, Mahdiyar Iravani Saadi","doi":"10.1186/s43046-026-00402-6","DOIUrl":"10.1186/s43046-026-00402-6","url":null,"abstract":"<p><strong>Background: </strong>Acute lymphoblastic leukemia (ALL) is the most frequent malignancy in children. The XRCC6 and XRCC7 genes play a key role in the nonhomologous end-joining (NHEJ) repair process and may influence susceptibility to ALL. The aim of this study is to evaluate the polymorphisms XRCC6 -61 C > G (rs2267437) and XRCC7 6721G > T (rs7003908) in children with ALL.</p><p><strong>Materials and methods: </strong>Genomic DNA was extracted from the buffy coat from whole blood samples of patients. Genotyping of XRCC6 -61 C > G and XRCC7 6721G > T polymorphisms was performed by PCR followed by restriction fragment length polymorphism (PCR-RFLP) using specific restriction enzymes (BanI and Pvu II).</p><p><strong>Results: </strong>In this investigation significant associations were discovered between XRCC6 -61 C > G genotypes CC (P = 0.006) and CG (P = 0.01) with ALL patients. It is important to note that while the CC genotype association remained significant after Bonferroni correction (P < 0.01), the CG genotype association was nominal (P between 0.01 and 0.05) and should be interpreted with caution. XRCC7 6721G > T genotypes GT (P = 0.02) and TT (P = 0.05) were significantly associated with ALL in males and females, respectively. In ALL patients with B-Cell subtype, XRCC6 -61 C > G genotypes CC (P = 0.04), GC (P = 0.05), and C allele (P = 0.05) showed significant associations. XRCC7 6721G > T genotypes GT (P = 0.003) and TT (P = 0.05) were also significantly associated in B-Cell ALL. Significant associations were observed for XRCC6 -61 C > G genotype CC (P = 0.04) and C allele (P = 0.03) in ALL patients with favorable cytogenetic abnormalities.</p><p><strong>Conclusions: </strong>In conclusion, our findings suggest that the XRCC6 -61 C > G and XRCC7 6721G > T polymorphisms may be associated with susceptibility to pediatric ALL, with potential lineage-specific and cytogenetic context-dependent effects. However, given the exploratory nature of our subgroup analyses and the statistical limitations, these results should be interpreted cautiously. Large-scale, multi-center studies with functional validation are needed to confirm these associations and elucidate the underlying mechanisms.</p>","PeriodicalId":17301,"journal":{"name":"Journal of the Egyptian National Cancer Institute","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13675453/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cancer nanomedicine and RNA/Lipid nanoparticle platforms in oncology: developmental evolution, translational barriers, and precision-therapy opportunities.","authors":"Bhasker Sambar, Anil Kumar Dudam","doi":"10.1186/s43046-026-00418-y","DOIUrl":"10.1186/s43046-026-00418-y","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Nanomedicine has become an important translational platform in oncology by enabling altered pharmacokinetics, controlled exposure, reduced systemic toxicity, intracellular delivery of nucleic acids, and improved handling of complex therapeutic payloads. Early cancer nanomedicines, including pegylated liposomal cytotoxics and albumin-bound drug products, demonstrated that nanoscale formulation design could improve the clinical utility of established anticancer agents. More recently, lipid nanoparticles, RNA therapeutics, individualized neoantigen vaccines, gene-regulatory approaches, and immune-modulating delivery systems have expanded the role of nanoparticles from passive drug carriers to programmable oncology platforms. This narrative review examines the developmental evolution of cancer-focused pharmaceutical nanoparticles, with emphasis on liposomes, lipid nanoparticles (LNPs), albumin-bound systems, polymeric particles, polymeric micelles, nanocrystals, nanoemulsions, solid lipid nanoparticles, inorganic particles, extracellular vesicles, and hybrid delivery technologies. Each platform class is treated systematically, covering representative approved products, formulation characteristics, route of administration, clinical evidence, and the specific development risks that limit it. There view connects platform design with oncology-specific barriers, including tumor heterogeneity, variable enhanced permeability and retention (EPR) effects, dense extracellular matrix, abnormal tumor vasculature, mononuclear phagocyte clearance, protein-corona formation, endosomal escape, immune activation, and the difficulty of translating animal tumor models into clinical benefit. These barriers are organized as a sequential delivery cascade, and the behavior of each platform class is compared step by step rather than described as a set of universal phenomena. Nanoparticle candidates that accumulated well in preclinical tumors but failed in clinical trials are examined alongside approved products, because the contrast between the two is where most of the transferable lessons sit. A product-development perspective is used to discuss critical quality attributes (CQAs), manufacturing scalability, potency testing, sterility strategy, stability, release methods, regulatory expectations, commercial feasibility, and clinical differentiation. A development-to-translation framework is proposed for comparing cancer nanomedicine platforms across formulation maturity, analytical maturity, manufacturing maturity, biological rationale, clinical evidence, regulatory readiness, and commercial feasibility; regulatory and commercial maturity are scored separately, the criteria behind each level are defined explicitly, and the resulting rankings are presented as a heuristic aid to discussion rather than a validated quantitative metric. Future progress in oncology nanomedicine will depend not only on novel materials or targeting claims, but also on disciplined product desig","PeriodicalId":17301,"journal":{"name":"Journal of the Egyptian National Cancer Institute","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13675451/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149207178","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prediction of treatment response and survival in patients with advanced hepatocellular carcinoma receiving sorafenib: pretreatment prognostic scores.","authors":"Ammar Hatem, Mohamed Mahmoud Nabeel, Samar K Darweesh, Rania Zayed, Ashraf Omar Abdelaziz, Hend Ibrahim Shousha, Ahmed Hosni Abdelmaksoud, Eman Medhat, Tamer Mahmoud Elbaz, Mennatallah Ali Rashwan, Ahmed Ramadan, Rania Lithy","doi":"10.1186/s43046-026-00417-z","DOIUrl":"10.1186/s43046-026-00417-z","url":null,"abstract":"<p><strong>Introduction: </strong>Sorafenib is currently among the recommended first-line medications for patients with advanced hepatocellular carcinoma (HCC); however, response to sorafenib remains unpredictable despite efforts to define prognosis. This study aims to predict treatment response and survival in patients with sorafenib-treated HCC using neutrophil-to-lymphocyte ratio (NLR), albumin-bilirubin (ALBI) grade, CRAFITY score, and Glasgow prognostic score (GPS).</p><p><strong>Methods: </strong>This prospective study recruited 75 Egyptian patients with Sorafenib-treated HCC. Pretreatment laboratory parameters and imaging studies were obtained. The neutrophil-to-lymphocyte ratio, ALBI grade, CRAFITY score, and GPS were calculated for each patient. All the patients were followed for treatment response, overall survival, and sorafenib tolerance.</p><p><strong>Results: </strong>Most of the participants were males, with a median age of 62 years. HCV was the most common underlying cause. Most of the patients had a low pretreatment NLR (77.33%), grade 2 ALBI (65.33%), 41.89% had a high CRAFITY score, and 48.6% had GPS 1. Patients were divided into two groups: group 1: sorafenib-naïve (n = 44) and group 2: patients with previous interventional therapy (n = 31). Pretreatment AST, ALT, mild ascites, portal invasion, and BCLC stage C were significantly higher among sorafenib-naïve patients. Median OS and time to progression for the entire cohort were 4 months and 9 months, respectively. No significant differences were observed in terms of OS between various NLR, ALBI grades, CRAFITY scores, and GPS. Multivariate analysis showed a high risk of mortality among sorafenib-intolerant patients (p = 0.01, HR: 2.33, 95% CI: 1.23-4.42).</p><p><strong>Conclusion: </strong>Overall survival and time to progression are not affected by different pretreatment values of NLR, ALBI grade, CRAFITY score, and Glasgow prognostic score in sorafenib-treated HCC.</p>","PeriodicalId":17301,"journal":{"name":"Journal of the Egyptian National Cancer Institute","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13653014/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149147309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Next-generation CAR-T cell therapy against cancer: precision engineering, programmable immunity, and emerging clinical frontiers.","authors":"Faizan-E- Mustaffa, Muhammad Shahbaz Aslam, Muhammad Junaid","doi":"10.1186/s43046-026-00415-1","DOIUrl":"10.1186/s43046-026-00415-1","url":null,"abstract":"<p><p>While chimeric antigen receptor T-cell (CAR-T) therapy has revolutionized the treatment of hematological malignancies, there are significant hurdles to overcome, such as antigen escape, T-cell exhaustion, limited persistence in the body, severe toxicities, manufacturing complexity, high costs, and low effectiveness in the treatment of solid tumors. There are many reviews describing novel CAR-T technologies, the evidence strength, clinical maturity and unmet translational risks of each are largely included in those reviews. This review highlights the ways in which next-generation engineering increases the safety, efficacy and programmability of CAR-T. The primary and authoritative clinical, regulatory and preclinical evidence on recent advances from 2022 to 2026 was carefully evaluated, including the quality and quality control of the evidence for each strategy. New innovations are Armored CARs, dual-target and logic-gated/synNotch systems, universal and switchable platforms, CRISPR/Cas9 and base/prime editing, allogeneic CAR-Ts, non-viral manufacturing, and lipid-nanoparticles in vivo CAR-T generation. Additionally, the engineering and combination approaches for the treatment of solid tumors with checkpoint inhibitors, radiotherapy, oncolytic viruses, nanotechnology, and artificial intelligence are discussed. An evidence-to-maturity framework separates the clinically proven methods from the emerging technologies and highlights some of the critical translation hurdles related to safety, immunogenicity, durability, manufacturing and scale. Precision Immunotherapy is becoming more and more possible with the next generation CAR-T engineering, however the validation and translational optimization of these cells is dominant to their eventual clinical use.</p>","PeriodicalId":17301,"journal":{"name":"Journal of the Egyptian National Cancer Institute","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13624245/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149081434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Male breast cancer in Arab populations: a systematic review of molecular, genetic, and clinicopathologic characteristics.","authors":"Shaden Abunasser, Raghad Al-Taweel, Shahrazad Elnatsheh, Areej Baraka, Muna Al-Ismail, Waad Rashid Aldosari, Baraah A Alquran, Atiyeh M Abdallah, Amal Al-Haidose","doi":"10.1186/s43046-026-00408-0","DOIUrl":"10.1186/s43046-026-00408-0","url":null,"abstract":"<p><strong>Background: </strong>Male breast cancer (MBC) accounts for less than 1% of all breast cancer cases, yet its incidence is increasing worldwide. Research on MBC remains limited, particularly in Arab populations, where molecular and genetic characteristics are poorly characterized. Improved understanding of MBC biology is essential to support region-specific, biology-driven management strategies.</p><p><strong>Methods: </strong>This systematic review was registered in PROSPERO (CRD42024607019) and conducted according to PRISMA guidelines. PubMed, Embase, and Scopus were searched from inception to 28 December 2025. Eligible studies reported MBC cases from Arab countries and included data on molecular subtypes, receptor status, genetic alterations, and/or clinicopathologic characteristics. Data were extracted independently by four reviewers. Risk of bias was assessed using the Joanna Briggs Institute (JBI) critical appraisal tool, and findings were synthesized narratively with harmonization of tumor grade and stage where applicable.</p><p><strong>Results: </strong>From 9,337 records, 54 studies comprising 1,534 MBC patients met the inclusion criteria. Invasive ductal carcinoma was the predominant histological subtype (92.6%). Among patients with reported intrinsic subtypes (n = 335), luminal A (45.7%) and luminal B (40.9%) accounted for over 86% of cases, whereas HER2-positive (4.8%) and triple-negative (8.4%) tumors were uncommon and triple-positive disease was rare (0.3%). Receptor status was reported for 1,031 patients, with high ER (71.5%) and PR (71.6%) positivity and low HER2 positivity (12.6%), alongside substantial heterogeneity in testing and reporting. Genetic data were available for 59 patients, most frequently identifying pathogenic truncating BRCA2 variants, although BRCA-negative cases were also reported. Surgery was the most reported treatment modality (n = 856), predominantly mastectomy-based, while endocrine therapy was frequently used and HER2-targeted therapy was infrequently reported.</p><p><strong>Conclusion: </strong>MBC in Arab populations is predominantly hormone receptor-driven, characterized by luminal subtypes, high ER/PR positivity, and low HER2 expression. Genetic evidence, though limited, implicates BRCA2 as the most frequently reported susceptibility gene. These findings highlight the need for standardized molecular reporting and broader access to receptor profiling and genetic testing to support personalized, region-specific MBC management.</p>","PeriodicalId":17301,"journal":{"name":"Journal of the Egyptian National Cancer Institute","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13594001/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149017266","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent advances in hormone-based biopharmaceuticals for cancer therapy.","authors":"Syahmi Nuqman Sarifulnazwan, Nur Alia Fatihah Mohd Tajuddin, Siti Nur Nadhirah Mohd Nasaruddin, Nur Malihah Imtiyaz Muhammad Mukmin, Engku Shifaa Nur Sahira Engku Abdul Malik, Muhammad Taher, Deny Susanti, Junaidi Khotib, Md Faiyazuddin, Riyanto Teguh Widodo, Muhammad Salahuddin Haris, Hendra Budiman","doi":"10.1186/s43046-026-00411-5","DOIUrl":"10.1186/s43046-026-00411-5","url":null,"abstract":"<p><p>Hormone-dependent cancers, particularly estrogen receptor-positive breast cancer and androgen receptor-driven prostate cancer, contribute substantially to global cancer-related morbidity and mortality. Endocrine therapy has long been the mainstay of treatment for these tumors because of its specific mechanism and good safety profile. The long-term success of common hormone-based treatments is often undermined by resistance, both intrinsic and acquired, disease recurrence, and the activation of compensatory pathways that tumor cells have adapted to. To overcome these challenges, it has been necessary to develop high-quality hormone-based biopharmaceuticals that target the molecular level, enhance pharmacokinetics, and apply precision medicine strategies. The goal of this literature review is to provide an update on progress in hormone-based biopharmaceuticals for cancer management, with a particular focus on preventing endocrine resistance in hormone-dependent cancers. Among the treatments mentioned in the review, most are oral selective estrogen receptor degraders (SERDs) for ER-positive breast cancer, oral gonadotropin-releasing hormone antagonists for prostate cancer, genomically guided combination therapy that integrates inhibitors of the CDK4/6 and PI3K/AKT/mTOR signaling pathways, and next-generation androgen receptor (AR) degraders based on proteolysis-targeting chimera (PROTAC) technology. There is new evidence that these biopharmaceutical methods may be able to treat patients better over longer periods. For those who are less responsive, these approaches are even more effective when paired with proper biopharmaceutical methods, as in the case of hormone therapy. While targeted protein degradation and biomarker-driven combination therapies are repositioning drug development away from receptor blockade, the latter remains the mainstay of treatment. However, these developments do not eliminate concerns related to long-term safety, cost-effectiveness, appropriate patient selection, and resistance to novel agents. The path for hormone-based biopharmaceuticals in personalized cancer therapy requires continuous translational research and clinical validation to determine the best place.</p>","PeriodicalId":17301,"journal":{"name":"Journal of the Egyptian National Cancer Institute","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13594064/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149017229","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigallocatechin-3-Gallate, the green tea polyphenol suppresses expression of CD31 and VEGFR2 and enhances the chemotherapeutic potential of irinotecan in AOM/DSS model of colorectal cancer in mice.","authors":"Sabana Sargam Rahman, Sukanya Baruah, Nabila Akhtara, Jaydeep Kumar Nath, Manuj Kumar Bharali","doi":"10.1186/s43046-026-00412-4","DOIUrl":"10.1186/s43046-026-00412-4","url":null,"abstract":"<p><strong>Background: </strong>Conventional chemotherapeutic treatment of colorectal cancer causes adverse effects such as severe diarrhoea, mucositis and hepatotoxicity. This study aimed to investigate the anti-carcinogenic potential of epigallocatechin-3-gallate and its effects on major angiogenic markers, alone and in combination with irinotecan in colorectal cancer model.</p><p><strong>Methods: </strong>Colorectal cancer was induced in mice by injecting azoxymethane and oral administration of dextran sulfate sodium in drinking water as described previously. After 16th week of experimentation, animals were sacrificed, morphometrical assessment was conducted and tissues were processed for histopathological, immunohistochemical and gene expression analysis by qRT-PCR.</p><p><strong>Results: </strong>Results showed reduction in tumour count, alleviation of colorectal cancer symptoms, improvement in histopathological alterations and goblet cell count with combination therapy. Suppression of key oncogenic and angiogenic markers and reduction in liver injury with combination treatment.</p><p><strong>Conclusion: </strong>Combined treatment of epigallocatechin-3-gallate with irinotecan enhanced the anti-tumour potential of irinotecan, and inhibited cancer progression and expression of tumour-associated angiogenesis markers. Moreover, treatment associated liver injury was also reduced by epigallocatechin-3-gallate supplementation.</p>","PeriodicalId":17301,"journal":{"name":"Journal of the Egyptian National Cancer Institute","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13586132/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: Identification of potential biomarkers for oral squamous cell carcinoma through multi-cohort bioinformatic analysis.","authors":"Duanreiliu Kamei, Simran Kaur, Anjali Priya, Akshay Bansal, Aarti Yadav, Ashwini Kumar Ray, Yamini Agrawal","doi":"10.1186/s43046-026-00413-3","DOIUrl":"10.1186/s43046-026-00413-3","url":null,"abstract":"","PeriodicalId":17301,"journal":{"name":"Journal of the Egyptian National Cancer Institute","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13582666/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982965","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative efficacy and safety of first, second, and third-generation EGFR tyrosine kinase inhibitors in treatment-naïve EGFR-mutant advanced non-small cell lung cancer: a systematic review and network meta-analysis of randomized controlled trials.","authors":"Sumit Mahato, Shiv Mudgal, Harminder Singh, Seshadri Reddy Varikasuvu, Hansraj Kumar, Jameema Thankachan, Subodh Kumar","doi":"10.1186/s43046-026-00414-2","DOIUrl":"10.1186/s43046-026-00414-2","url":null,"abstract":"<p><strong>Background: </strong>The optimal first-line epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor (TKI) for EGFR-mutant advanced non-small cell lung cancer (NSCLC) remains uncertain due to the availability of multiple generations of TKIs and limited head-to-head comparisons.</p><p><strong>Methods: </strong>A systematic review and network meta-analysis (NMA) of randomized controlled trials (RCTs) was conducted comparing first, second, and third-generation EGFR-TKIs in treatment-naïve EGFR-mutant NSCLC. Databases including PubMed, Embase, Scopus, and the Cochrane Central Register of Controlled Trials were searched. Outcomes included overall survival (OS), progression-free survival (PFS), and grade ≥ 3 adverse events (AEs). Hazard ratios (HRs) and odds ratios (ORs) were pooled using a frequentist random-effects NMA. Treatments were ranked using P-scores.</p><p><strong>Results: </strong>Nine RCTs were included for PFS and eight for OS and AEs. For OS, dacomitinib (HR 0.75, 95% CI 0.59-0.95) and osimertinib (HR 0.80, 95% CI 0.67-0.96) showed significant benefit versus first-generation TKIs. For PFS, all evaluated second- and third-generation TKIs significantly improved PFS, with furmonertinib (HR 0.44, 95% CI 0.34-0.57) having the highest P-score. In safety analysis, no EGFR-TKI showed a statistically significant difference in grade ≥ 3 adverse events compared with first-generation TKIs. Although befotertinib and dacomitinib had numerically higher odds, all confidence intervals were wide and crossed the null value.</p><p><strong>Conclusions: </strong>While several EGFR-TKIs improved efficacy over first-generation agents, no single treatment was clearly superior across all efficacy and safety outcomes. Osimertinib showed consistent efficacy, while its safety advantage became evident in the sensitivity analysis excluding FLAURA China.</p>","PeriodicalId":17301,"journal":{"name":"Journal of the Egyptian National Cancer Institute","volume":"38 1","pages":""},"PeriodicalIF":2.2,"publicationDate":"2026-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13574751/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148969538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}