Medical Oncology最新文献

{"title":"DNMT1 is associated with QDPR downregulation and chemotherapy response in lung adenocarcinoma.","authors":"Lyubo Wang, Guicai Liang, Lei Zhu, Zurui Liu, Yuxian Dong, Kun Wang, Hong Yao, Chunlei Ge, Lincan Duan","doi":"10.1007/s12032-026-03360-0","DOIUrl":"https://doi.org/10.1007/s12032-026-03360-0","url":null,"abstract":"<p><p>In lung adenocarcinoma (LUAD), DNA methylation-mediated gene silencing may contribute to tumor initiation, progression, and heterogeneity in treatment response. However, the key methyltransferases involved and their therapeutic potential have not been systematically characterized. This study aimed to address three major questions: which methylation-associated gene silencing events occur in LUAD, which upstream methyltransferase predominantly drives these events, and whether targeted inhibition of this enzyme can mitigate drug-resistant phenotypes and enhance chemosensitivity. Differential expression analysis was initially performed using the GSE75037 dataset to screen candidate genes. Expression quantitative trait locus (eQTL) and protein quantitative trait locus (pQTL) data were then integrated, and key candidate genes were prioritized according to the concordance in the directions of genetic effects. Subsequently, mediation Mendelian randomization analysis was conducted to determine whether the effect of locus-specific methylation on LUAD was mediated by QDPR expression, thereby providing genetic causal evidence that methylation contributes to transcriptional repression. In addition, the associations between DNA methylation-related enzymes and QDPR expression were analyzed in the GSE33532, GSE43458, and GSE75037 datasets, followed by cross-dataset validation to identify potential key upstream regulators. Finally, cell-based experiments were performed to verify the functional effects of DNMT1 inhibition. Changes in QDPR expression were assessed by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting, and the potential chemosensitizing effect of DNMT1 inhibition in combination with platinum-based chemotherapy was further evaluated in patient-derived organoids. This study provided genetic causal evidence that locus-specific methylation influences LUAD risk, with part of this effect mediated by QDPR expression. Analyses across multiple independent datasets consistently suggested that DNMT1 may act as a key upstream epigenetic regulator contributing to the reduced expression of QDPR. Functional experiments demonstrated that DNMT1 inhibition increased QDPR expression and suppressed the proliferation and migration of LUAD cells. Drug sensitivity assays using patient-derived organoids further showed that DNMT1 inhibition exerted a significant chemosensitizing effect in the platinum low-sensitivity group. This study suggests that DNMT1 may contribute to the reduced expression of QDPR and related malignant phenotypes through epigenetic regulation. Functional and drug sensitivity experiments further support the potential of DNMT1 as a therapeutic target for improving the response to platinum-based chemotherapy in a subset of patients with LUAD. These findings provide a potential therapeutic target and offer mechanistic insights into treatment response heterogeneity and chemoresistance in LUAD.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 10","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148874658","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":"Chrysin treatment is associated with altered microrna expression and reduced levels of HPV16 E6 protein in caski cervical cancer cells.","authors":"Mahdis Gholami Fashkhami, Hadi Habibollahi, Seyedeh Tooba Shafighi","doi":"10.1007/s12032-026-03381-9","DOIUrl":"https://doi.org/10.1007/s12032-026-03381-9","url":null,"abstract":"<p><p>Persistent infection with high-risk human papillomavirus type 16 (HPV16) is a major cause of cervical cancer and is associated with viral oncoproteins that disrupt tumor suppressor pathways and influence cellular microRNA (miRNA) expression. Given increasing interest in phytochemicals as potential anticancer agents, this study evaluated the effects of chrysin, a natural flavonoid, on cell viability, selected cancer-related miRNAs, and HPV16 E6 protein levels in HPV16-positive CaSki cervical cancer cells. CaSki cells and normal human dermal fibroblasts (HDF) were treated with chrysin (31.5-500 µg/ml) for 24 and 48 h. Cell viability was assessed by MTT assay. Expression of miR-34a, miR-218, miR-20a, miR-195, and miR-23b was quantified by qRT-PCR (2^-ΔΔCt method), and E6 protein levels were analyzed by Western blot. Chrysin selectively reduced CaSki cell viability with minimal toxicity toward HDF cells, resulting in a high selectivity index. Treatment was associated with increased expression of miR-34a (10.05-fold, P < 0.0001) and miR-218 (5.64-fold, P < 0.01), a moderate increase in miR-20a (1.7-fold, P < 0.05), decreased miR-195 expression (0.18-fold, P < 0.01), and no significant change in miR-23b. A significant reduction in E6 protein levels was also observed (0.64 ± 0.01 vs. control, P < 0.001). These findings indicate that chrysin treatment is associated with selective cytotoxicity and concurrent modulation of HPV16 E6 protein levels and several cancer-related miRNAs in CaSki cells. Further studies in additional cellular models and mechanistic systems are required to clarify the underlying pathways.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 10","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857515","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":"Risk-adapted first-line therapy selection in advanced EGFR-mutant NSCLC: a practical clinical algorithm integrating tumor biology and patient factors.","authors":"Ashish Sharma, Joecelyn Kirani Tan, Harendra Kumar, Hareesha Rishab Bharadwaj","doi":"10.1007/s12032-026-03338-y","DOIUrl":"10.1007/s12032-026-03338-y","url":null,"abstract":"<p><p>Advanced EGFR-mutant non-small cell lung cancer (NSCLC), specifically tumors harboring classical activating mutations (exon 19 deletions and L858R substitutions, which are the exclusive focus of this review), is no longer a single-treatment landscape. The MARIPOSA and FLAURA2 phase 3 trials have established that combination regimens of amivantamab plus lazertinib and osimertinib plus platinum-pemetrexed, respectively, extend both progression-free and overall survival compared with osimertinib monotherapy. Each carries substantially greater toxicity, treatment complexity, and cost. No validated, prospective framework exists to guide first-line selection between combination and single-agent strategies. Decision-making is currently anchored to trial eligibility criteria and institutional norms rather than individualized risk stratification. This review synthesizes evidence from landmark trials, molecular biomarker analyses, and real-world cohort studies to propose a practical risk-adapted algorithm integrating tumor biology, molecular co-alterations, patient performance status, comorbidities, logistical feasibility, and treatment preference. Patients with biologically high-risk features, including liver metastases, baseline central nervous system (CNS) involvement, circulating tumor DNA (ctDNA) elevation, or heavy disease burden, may derive the greatest absolute benefit from combination therapy. TP53 co-mutation warrants consideration but should be interpreted as a prognostic marker rather than a definitive treatment-selection criterion given conflicting predictive data across trials. The subcutaneous (SC) formulation of amivantamab, demonstrated in PALOMA-3 to reduce infusion-related reactions and administration time relative to the intravenous formulation, may improve the tolerability and logistical feasibility of MARIPOSA-based therapy, though prospective comparative evidence across formulations remains limited. Prospective biomarker-driven trials are needed to validate treatment selection; until that evidence matures, individualized shared decision-making guided by the proposed algorithm is the most defensible clinical approach.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 10","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13526081/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857507","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}

{"title":"Vasopressin boosts the antiproliferative effect of dynasore and wortmannin in triple-negative breast cancer cells.","authors":"Samar Sami AlKafaas, Thoria Diab, Samah A Loutfy, Mohamed Hessien","doi":"10.1007/s12032-026-03368-6","DOIUrl":"https://doi.org/10.1007/s12032-026-03368-6","url":null,"abstract":"<p><p>Arginine vasopressin hormone (AVP) is ectopically expressed in breast cancer. Also, in intestinal epithelial and mesangial cells, for example, it acts as a growth-promoting factor when it binds to the GPCR receptor and triggers multiple downstream mitogenic signalling pathways leading to cell proliferation. As Dynamin 2 GTPase (Dyn2) is an integral protein involved in membrane receptor endocytosis, it is unclear how far AVP and Dynasore (DYN), a selective Dyn2 GTPase inhibitor, can modulate the proliferation of invasive breast cancer cells. To explore this, triple-negative breast cancer cells (MDA MB-231), which express V1A, were exposed to 100 nM AVP for 24 h, either alone or in combination with DYN. The cytotoxic effect, apoptosis, and autophagy-mediated cell death were assessed and compared to untreated cells and cells in which the PI3K/AKT pathway was inhibited by wortmannin (Wort). Also, cell cycle progression, migration, and the expression of the drug-resistance gene were investigated. We found that AVP alone developed apoptosis in about 20% of cells, and in the presence of DYN, apoptosis increased to 28%. This was associated with overexpression of Bax and Caspase-3, cell cycle arrest in G0/G1 phase, and regression of cell migration and invasion. In parallel, wortmannin alone or in combination with DYN induced apoptosis in 29% and 35% of cells, respectively. The autophagy markers (the microtubule-associated protein (LC3II) and Beclin1 mRNA) increased in AVP and AVP+DYN-treated cells but decreased in Wort and Wort+DYN-treated cells. Mechanistically, dual treatments (AVP+DYN or Wort+DYN) decreased the AKT activation and downregulated the multidrug resistance gene (MDR1). These findings suggest that AVP demonstrates apoptosis- and autophagy-related cell death and exerts a synergistic antiproliferative effect with DYN against invasive breast cancer cells.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 10","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857533","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":"KS79356, a novel kynureninase inhibitor, suppresses triple-negative breast cancer progression by attenuating the TNF-α/NFκB-CD44-Akt signaling axis.","authors":"Maha Alamodi Alghamdi, Hemali Deshpande, Ashish Kumar, Prasanna Rajagopalan","doi":"10.1007/s12032-026-03377-5","DOIUrl":"10.1007/s12032-026-03377-5","url":null,"abstract":"<p><p>Kynureninase (KYNU), a hydrolase in tryptophan metabolism, has been implicated in cancer progression. However, the therapeutic relevance of targeting KYNU-mediated inflammatory signaling in triple-negative breast cancer (TNBC) remains poorly defined High-throughput virtual screening (HTVS) of the ChemBridge library, combined with protein-ligand interaction profiling, molecular dynamics simulations (GROMACS), and binding free energy analysis (GMX_MMPBSA), was employed to identify KYNU inhibitors. In vitro assays were performed in SUM159, MDA-MB-231, and HBL-100 cell lines. KS79356 was identified as the lead compound, displaying strong binding affinity (- 7.8 kcal/mol), stable interactions (RMSD ≈ 0.075 nm), and favorable binding free energy (ΔG = - 23.93 kcal/mol). KS79356 effectively inhibited KYNU activity (IC₅₀ = 63.7 nM) and selectively suppressed proliferation of SUM159 (GI₅₀ = 233 nM) and MDA-MB-231 (GI₅₀ = 450.8 nM) cells. Mechanistically, KS79356 downregulated TNF-α-induced activation of the NFκB-CD44-Akt signaling axis, leading to reduced proliferation, invasion, and trans-endothelial migration, while inducing both early and late apoptosis in TNBC cells. By targeting KYNU and attenuating the TNF-α/NFκB/CD44-Akt signaling axis, KS79356 demonstrates strong antitumor activity in TNBC. These findings highlight the novelty of KYNU as a therapeutic target and support the development of KS79356 as a potential treatment strategy for TNBC progression and metastasis.Clinical trial registrationNot applicable.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 10","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857544","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 the PI3K/AKT/mTOR pathway in gastrointestinal cancers: a comprehensive review of mechanisms, preclinical evidence, and clinical challenges.","authors":"Faride Kaikavoosnejad, Hamed Haddad Kashani, Khadijeh Dizaji Asl, Zeinab Mazloumi, Ali Keyhani, Seyyede Sepide Ashraf Moosavi, Milad Verdi, Ali Rafat","doi":"10.1007/s12032-026-03374-8","DOIUrl":"https://doi.org/10.1007/s12032-026-03374-8","url":null,"abstract":"<p><p>Gastrointestinal (GI) cancers encompass malignant conditions of the GI tract and accessory digestive organs, including the esophagus, gastric cancer (GC), biliary system, hepatocellular carcinoma (HCC), pancreatic cancer (PC), and colorectal cancer (CRC). Globally, CRC ranks as the third most commonly diagnosed cancer, with gastric, hepatic, and esophageal cancers following in fifth, sixth, and seventh places, respectively. PC contributes notably to cancer mortality, ranking 12th in incidence and 7th in mortality. Despite major advances in diagnosis and treatment, GI cancers remain among the most aggressive malignancies and continue to drive substantial global morbidity and mortality. In 2020, GI cancers accounted for more than 4.8 million new cases and 3.4 million deaths. Although early-stage GI tumors can be surgically resected with curative intent, the overall 5-year relapse rate remains high. Neoadjuvant or adjuvant chemotherapy and radiotherapy provide only modest long-term survival improvements when applicable. In recent decades, prognosis for advanced GI cancers has improved due to tailored therapies that combine cytotoxic and targeted agents and integrate systemic treatments with more effective surgical and locoregional approaches. Nevertheless, GI malignancies remain a leading cause of cancer death, underscoring the need for novel therapeutic options. A central molecular driver is the PI3K/AKT/mTOR signaling axis, which governs chemotherapy resistance, metastasis, survival, metabolism, and growth, and modulates the tumor microenvironment via angiogenesis and inflammatory infiltration. Dysregulation of this axis is common across GI cancers, guiding exploration of pathway-targeted therapies, alone or in combination. Although several agents show promise, toxicities such as neuropsychiatric effects, diarrhea, hepatotoxicity, and hyperglycemia limit clinical utility. Therefore, refined personalization and combination strategies targeting PI3K/AKT/mTOR are critical to improving efficacy and reducing resistance in GI malignancies.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 10","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857561","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":"Neuro-immune crosstalk in lung cancer brain metastasis: mechanisms, therapeutic targets, and translational opportunities.","authors":"Zhanhai Wei, Jingyi Zhou, Wendi Mo, Haijun Zhang","doi":"10.1007/s12032-026-03366-8","DOIUrl":"https://doi.org/10.1007/s12032-026-03366-8","url":null,"abstract":"<p><p>Brain metastasis remains one of the most devastating complications of lung cancer, contributing to poor prognosis and limited therapeutic efficacy. Increasing evidence suggests that the development and progression of lung cancer brain metastasis are shaped by dynamic and reciprocal interactions among tumor cells, neural components, and immune elements within the brain microenvironment. Neurotrophic factors, neurotransmitters, and glial cells participate in blood-brain barrier remodeling, immune modulation, and metabolic adaptation, while tumor cells exploit these neuro-immune interactions to facilitate colonization, survival, and therapeutic resistance. In this review, we organize current knowledge within a stage-specific and spatiotemporal framework encompassing early blood-brain barrier disruption and colonization, intermediate microenvironmental remodeling with immunosuppression formation, and late-stage stabilization characterized by sustained neuro-tumor interaction. Importantly, rather than summarizing neural or immune pathways in isolation, we integrate adaptive immune dynamics, glial reprogramming, and neurotransmitter-dependent signaling into a unified neuro-immune-tumor network model and explicitly prioritize context-dependent hub molecules according to graded levels of supporting evidence. Within this staged framework, we delineate regulatory axes that may define context-dependent therapeutic windows. Rather than providing an exhaustive catalog of mechanisms, we emphasize pathways with emerging translational relevance, including BDNF-TrkB signaling, adrenergic pathways, and glial reprogramming. This integrative perspective aims to clarify the organizational principles of neuro-immune-tumor networks in lung cancer brain metastasis and to inform future studies exploring combinatorial neural and immune modulation strategies, biomarker development, and rational clinical trial design, while acknowledging that direct LCBM validation remains limited for some pathways.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 10","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857482","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":"Narciclasine reduces proliferation and migration of neuroblastoma cells and decreases FAK/PI3K pathway activation.","authors":"Ceren Oy, Sema Serter Kocoglu, Seda Isıklar, Duygu Gok Yurtseven","doi":"10.1007/s12032-026-03359-7","DOIUrl":"https://doi.org/10.1007/s12032-026-03359-7","url":null,"abstract":"<p><p>Neuroblastoma is a highly aggressive childhood malignancy originating from neural crest-derived cells. Narciclasine, an Amaryllidaceae-derived alkaloid isolated from plants such as Lycoris radiata, has been reported to exhibit various pharmacological activities; however, its effects in neuroblastoma remain poorly understood. In this study, we investigated the effects of narciclasine on SH-SY5Y neuroblastoma cells, focusing on proliferation, migration, apoptosis, DNA damage, and FAK/PI3K-associated signaling. Cell viability was evaluated using the CCK-8 assay; proliferation by Ki67 immunofluorescence staining; migration and colony formation by wound-healing and colony formation assays; apoptosis by TUNEL and cleaved caspase-3 immunofluorescence staining; DNA damage by COMET assay; and FAK/PI3K-related protein expression by immunohistochemistry and Western blot analysis. Treatment with 50 and 100 nM narciclasine significantly reduced SH-SY5Y cell viability while exhibiting comparatively lower cytotoxic effects in HUVEC cells under the tested conditions; therefore, these concentrations were selected for subsequent experiments. Narciclasine treatment also reduced cell proliferation, migration, and colony formation, while increasing apoptosis and DNA damage. Immunofluorescence analyses demonstrated decreased Ki67 expression and increased cleaved caspase-3 immunoreactivity in narciclasine-treated groups. In addition, immunohistochemical and Western blot analyses revealed reduced expression levels of FAK and PI3K following narciclasine treatment. Collectively, these findings suggest that narciclasine exerts anti-neuroblastoma effects associated with reduced proliferative and migratory activity, increased apoptotic response, and modulation of FAK/PI3K-associated signaling in SH-SY5Y cells. Further studies are needed to clarify the precise molecular basis and therapeutic relevance of these effects.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 10","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857555","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":"FAK regulates leptin-induced angiogenesis and vasculogenic mimicry in breast cancer.","authors":"Ana K Herrera-Vargas, Ricardo Jaime-Cruz, Alejandra Rodríguez-Leviz, Miguel A Mendoza-Catalán, Monserrat Olea-Flores, Laura Villavicencio-Guzmán, Marcela Salazar-García, Carlos C Patiño-Morales, Napoleón Navarro-Tito","doi":"10.1007/s12032-026-03370-y","DOIUrl":"10.1007/s12032-026-03370-y","url":null,"abstract":"<p><p>Leptin, an adipokine primarily secreted by adipose tissue, has been implicated in tumor progression by regulating angiogenesis. Leptin also plays a key role in tumor vascularization by promoting vasculogenic mimicry (VM). During tumor progression, leptin activates several signaling pathways, including the focal adhesion kinase (FAK) pathway. This study aimed to determine whether leptin promotes and regulates angiogenesis and VM through the FAK pathway. We used the chick chorioallantoic membrane (CAM) as a model to evaluate blood vessel formation and to induce tumors to assess angiogenic expression. Matrigel-based cell cultures were used to analyze the formation of tubular structures characteristic of VM. The expression of specific markers was then evaluated for each process. These models were employed with or without the inhibitor PF-573,228. Our results showed that leptin enhances the sprouting, branching, and vasodilation of blood vessels via FAK signaling by increasing the expression of vascular endothelial growth factor (VEGF) and N-cadherin in tumors derived from MCF-7 and MDA-MB-231 cells. Furthermore, leptin stimulation promoted tubular-type VM in MCF-7 cells and matrix-type VM in MDA-MB-231 cells; the former was dependent on FAK signaling. Lastly, leptin increased the levels of several proteins associated with angiogenesis and VM, including TIE-1, MMP-9, VE-cadherin, ANG-2, VEGF, and VEGFR1. In conclusion, leptin promotes tumor vascularization in breast cancer through angiogenesis and VM, in a manner dependent on FAK signaling.</p>","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 10","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13525964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148857495","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}

{"title":"Correction to: DLBCL-microenvironment interactions: cytokine profiling and ECM mediated ibrutinib resistance in a 3D bone-based model.","authors":"Jessica Ceccato, Maria Piazza, Giulia Gualtiero, Samuela Carraro, Francesco Cinetto, Carlo Biz, Sabrina Manni, Marco Pizzi, Sabrina Pianalto, Simone Zoletto, Valeria Carabotta, Nicolo' Danesin, Pietro Ruggieri, Angelo Paolo Dei Tos, Francesco Piazza, Livio Trentin, Fabrizio Vianello","doi":"10.1007/s12032-026-03356-w","DOIUrl":"10.1007/s12032-026-03356-w","url":null,"abstract":"","PeriodicalId":18433,"journal":{"name":"Medical Oncology","volume":"43 10","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13518517/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148829733","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}