Oncology Research最新文献

{"title":"Advances in the Research and Development of Breast Cancer Organoids.","authors":"Ling Li, Shuai Zhao, Xiaoxiao Wang, Jiahui Du, Zhen Jin, Song-Bai Liu, Xiaohua Li","doi":"10.32604/or.2026.083636","DOIUrl":"10.32604/or.2026.083636","url":null,"abstract":"<p><p>Breast cancer ranks first in global cancer incidence. Due to its high heterogeneity, cancer cells often develop drug resistance during metastasis, leading to therapeutic challenges and poor prognosis. Consequently, breast cancer organoid models have emerged, which can effectively recapitulate the tumor microenvironment and serve as important tools for investigating the mechanisms underlying breast cancer initiation and progression. Breast cancer organoids exhibit interactions between cells and the extracellular matrix (ECM) while retaining the heterogeneity of the original tumor cells. Owing to these advantages, such models have been widely applied in studies of tumor pathogenesis, disease modeling, drug screening, therapeutic response prediction, and microenvironment reconstruction. Although breast cancer organoids still have certain limitations in terms of construction, long-term culture, and fully recapitulating the tumor microenvironment, they represent an emerging technology that promotes the development of high-throughput drug screening and precision personalized therapy. At the same time, the integrated culture of breast cancer organoid models with immune cells or endothelial cells and microfluidic chips was also explored. This approach enhances the complexity of the <i>in vitro</i> tumor microenvironment, making it closer to the human microenvironment, thereby improving the authenticity and reliability of preclinical research data. Compared with traditionally statically cultured breast cancer organoids, it possesses more dynamic regulatory characteristics and is more accurate in simulating the tumor microenvironment. The aim of the study is to discuss the applications of breast cancer organoids and to incorporate new technologies into traditional breast cancer organoid models, making the research outcomes more clinically relevant.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 9","pages":"5"},"PeriodicalIF":4.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13494472/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148796362","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":"Ovarian Cancer Stem Cells: Mechanisms of Progression and Therapeutic Strategies.","authors":"Jie Wu, Zhewei Zhang, Kit Ying Chan, Tat San Lau, Chi Chiu Wang","doi":"10.32604/or.2026.083359","DOIUrl":"10.32604/or.2026.083359","url":null,"abstract":"<p><p>Ovarian cancer is the most lethal gynecological malignancy, with most patients diagnosed at an advanced stage and eventually relapsed after post-platinum-taxane chemotherapy. High intratumoral heterogeneity, extensive peritoneal dissemination, and acquired chemoresistance continue to restrict the clinical benefits of current therapeutic strategies. Increasing evidence indicates that ovarian cancer stem cells (OCSCs), a rare but highly plastic subpopulation characterized by self-renewal, multilineage differentiation, quiescence, tumor-initiating capacity, and intrinsic stress tolerance, play pivotal roles in tumor initiation, metastasis, recurrence, and therapeutic resistance. In this review, we systematically summarize current knowledge regarding the identification and functional characterization of OCSCs and discuss their clinical relevance to disease progression and poor prognosis. We then delineate the multifaceted mechanisms by which OCSCs drive ovarian cancer progression, with particular emphasis on dysregulated stemness-associated signaling networks, adaptive cellular plasticity, metabolic and stress-response programs, and dynamic interactions with the tumor microenvironment. Furthermore, we review emerging therapeutic strategies aimed at eradicating OCSCs and discuss key barriers that hinder their clinical translation. A deeper understanding of OCSC biology may facilitate the development of precise, combination-based strategies to overcome recurrence, reverse therapeutic resistance, and improve long-term outcomes in ovarian cancer patients.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 9","pages":"4"},"PeriodicalIF":4.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13494496/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148796182","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":"MicroRNA320e Augments the Synthetic Lethality of Olaparib by Regulating the PI3K-AKT-mTOR Pathway.","authors":"Wei Zheng, Qianlong Meng, Yunhan Deng, Ruizhen Liu, Siyu Bai, Longyu Jia, Jing Wang, Huimin Bai","doi":"10.32604/or.2026.081656","DOIUrl":"10.32604/or.2026.081656","url":null,"abstract":"<p><strong>Objectives: </strong>Given the increasing drug resistance in ovarian cancer (OC), the use of poly ADP-ribose polymerase inhibitors (PARPi) for treating homologous recombination repair defects (HRD) has encountered new challenges. MicroRNA320e (miR-320e) exerts a negative regulatory role in the progression of multiple cancers. This study aimed to investigate the association between miR-320e and drug resistance in ovarian cancer.</p><p><strong>Methods: </strong>The Cell Counting Kit-8 (CCK-8) assay, migration and invasion assays, and colony formation assay were employed to evaluate the proliferation, migration, and invasion abilities of cells. Western blot (WB) analysis was used to verify the expression levels of proteins related to the relevant signaling pathways in cells. The xenograft subcutaneous tumor model was established to investigate the effect of miR-320e on <i>in vivo</i> tumor growth. Immunohistochemistry (IHC) and fluorescence <i>in situ</i> hybridization (FISH) assays were performed to detect the expression levels of related proteins and miR-320e in tumor tissues from patients and animals, respectively.</p><p><strong>Results: </strong>miR-320e was overexpressed in both A2780 and SKOV3 cells. The results showed that transfection with miR-320e significantly reduced cell proliferation, invasion, and migration, while enhancing autophagy and apoptosis. Additionally, the PI3K-AKT-mTOR signaling pathway was significantly inhibited in the treatment groups. In nude mouse models, overexpression of miR-320e also significantly suppressed tumor growth. These findings indicate that overexpression of miR-320e enhances the sensitivity of OC cells to olaparib therapy.</p><p><strong>Conclusion: </strong>In conclusion, miR-320e overexpression significantly inhibits the malignancy of ovarian cancer and increases the sensitivity of ovarian cancer cells to olaparib.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 9","pages":"27"},"PeriodicalIF":4.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13494476/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795969","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":"Regulation of the Wnt/β-Catenin Signaling Pathway by Non-Coding RNAs in Esophageal Squamous Cell Carcinoma: Mechanisms, Translational Relevance, and Therapeutic Implications.","authors":"Chao Han, Ming Hou, Ruifeng Yang, Xiaoping Wei, Cheng Wang","doi":"10.32604/or.2026.081222","DOIUrl":"10.32604/or.2026.081222","url":null,"abstract":"<p><p>Esophageal Squamous Cell Carcinoma (ESCC) is a highly aggressive malignancy characterized by a poor long-term prognosis. Aberrant activation of the canonical Wnt/β-catenin pathway serves as a central oncogenic driver in ESCC, with large-scale genomic analyses revealing that most patients harbor alterations in pathway-associated genes. This signaling axis orchestrates a wide array of malignant phenotypes, including tumor proliferation, invasion, epithelial-mesenchymal transition (EMT), cancer stemness, and therapeutic resistance. Therefore, this review aims to provide a comprehensive synthesis of the multifaceted crosstalk between various ncRNA classes and the Wnt/β-catenin axis, highlighting their roles in ESCC progression and their potential as mechanism-based clinical tools. Emerging evidence identifies non-coding RNAs (ncRNAs)-including microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs)-as key regulators of this pathway in ESCC. In this article, we systematically summarize the molecular mechanisms by which 36 unique ncRNA species (20 miRNAs, 10 lncRNAs, and 6 circRNAs) modulate Wnt signaling. Oncogenic ncRNAs promote malignant progression by suppressing negative regulators within complex competing endogenous RNA (ceRNA) networks, whereas tumor-suppressive ncRNAs inhibit pathway activation by targeting Wnt ligands, receptors, or downstream effectors. Furthermore, we discuss the translational relevance of ncRNA-based biomarkers for risk stratification and prognosis in clinical cohorts. Finally, we evaluate pharmacological strategies for ncRNA-based therapeutics while highlighting critical challenges related to delivery efficiency, specificity, molecular stability, off-target effects, tumor heterogeneity, and clinical validation. Ultimately, a clearer understanding of the ncRNA-Wnt regulatory network is essential for developing personalized, mechanism-based diagnostic and therapeutic strategies.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 9","pages":"8"},"PeriodicalIF":4.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13494495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148796269","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":"Targeting the Neuro-Immune Axis in Next-Generation Oncology: Discovery and Validation of β₂-Adrenergic Blockade to Reverse Ecosystem-Wide Resistance.","authors":"Heng Xu, Jiaan Lu, Zizhang Wang, Jiayu Xu, Shihui Peng, Haiqing Chen, Qiang Cao, Qing Sun, Shangke Huang","doi":"10.32604/or.2026.083919","DOIUrl":"10.32604/or.2026.083919","url":null,"abstract":"<p><p>Despite the potential of current cancer immunotherapies, tumor cells frequently evade immune surveillance by forming an immunosuppressive microenvironment, leading to treatment resistance. Current inquiry positions the sympathetic nervous system (SNS) at the forefront of tumor immunology as a critical driver of this immune evasion. This review delineates the cellular pharmacology of SNS-mediated immune regulation across the tumor ecosystem. Operating predominantly through the cyclic adenosine monophosphate-protein kinase A (cAMP-PKA) signaling axis, the SNS engages in bidirectional regulation with immune cells of the tumor microenvironment (TME). Norepinephrine and epinephrine interact with β₂-adrenergic receptors (β₂-ARs), triggering G-protein dissociation, adenylyl cyclase stimulation, and cAMP generation. This pharmacological cascade promotes the polarization of macrophages to the M2 phenotype, hinders dendritic cell maturation, impairs natural killer (NK) cell function, fosters the differentiation of regulatory T cells (Tregs), and suppresses the effector activity of CD8⁺ T cells. Consequently, we evaluate the translational prospects of repurposing β-blockers as potent anti-cancer immunomodulators. Preclinical evidence demonstrates that pharmacological blockade of β₂-AR signaling can reverse these immunosuppressive effects, augmenting intratumoral CD8⁺ T-cell infiltration and enhancing the efficacy of immune checkpoint inhibitors (ICIs). Ultimately, engineering multimodal combination regimens-guided by multi-omics biomarker stratification-offers a novel trajectory to overcome resistance, restore therapeutic sensitivity, and advance precision cancer immunotherapy.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 9","pages":"6"},"PeriodicalIF":4.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13494482/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148796403","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":"The Role of Mitochondrial ROS in Neoplastic Transformations, Progression and Therapeutic Targeting.","authors":"Bharath Kumar Velmurugan, Shu Hui Lin, Chih-Yang Huang, Ming-Ju Hsieh, Rathinasamy Baskaran","doi":"10.32604/or.2026.083159","DOIUrl":"10.32604/or.2026.083159","url":null,"abstract":"<p><p>Mitochondria are central regulators of cellular metabolism and survival and play a pivotal role in cancer development and progression through the production of reactive oxygen species (ROS), control of calcium homeostasis, regulation of autophagy, and modulation of cell death pathways. Mitochondria-derived ROS (mtROS) act as signaling mediators that influence tumor initiation, proliferation, metabolic reprogramming, metastasis, and therapeutic resistance by altering redox homeostasis, damaging mitochondrial DNA, and reshaping the tumor microenvironment. In addition to meeting the bioenergetic and biosynthetic requirements of rapidly proliferating cancer cells, mitochondrial metabolism modulates immune responses and supports cancer cell adaptation to hypoxia and nutrient deprivation. Accumulating evidence also highlights the dual role of mtROS, which can promote tumor progression at moderate levels yet trigger oxidative stress-induced cell death when excessively increased, making mitochondrial redox signaling an attractive therapeutic target. This review summarizes the major sources and regulation of mtROS, their involvement in cancer-associated signaling pathways, mitochondrial calcium dynamics, metabolic adaptations, and resistance to anticancer therapies, and discusses current and emerging mitochondrial-targeted strategies aimed at exploiting mtROS signaling to improve cancer treatment outcomes.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 9","pages":"12"},"PeriodicalIF":4.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13494497/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148796415","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":"Efficacy and Safety of Durvalumab plus Tremelimumab for Unresectable Hepatocellular Carcinoma: A Real-World Multicenter Observational Study.","authors":"Krittiya Korphaisarn, Kosin Wirasorn, Suebpong Tanasanvimon, Kijjakom Thanasombunsukh, Kunlatida Maneenil, Jirawat Thanestada, Nattaya Teeyapun, Jarin Chindaprasirt, Chirawadee Sathitruangsak, Teerada Siripoon, Phannin Tiraswasdichai, Chanchai Charonpongsuntorn, Passakorn Wanchaijiraboon, Wannisa Laosuangkoon, Patrapim Sunpaweravong, Ekapop Sirachainan, Charuwan Akewanlop","doi":"10.32604/or.2026.083206","DOIUrl":"10.32604/or.2026.083206","url":null,"abstract":"<p><p><b>Introduction:</b> Durvalumab plus tremelimumab (Durva/Treme) improved survival in the HIMALAYA trial for unresectable hepatocellular carcinoma (HCC), but real-world evidence remains limited. This study aimed to evaluate clinical outcomes of Durva/Treme in routine practice. <b>Methods:</b> This retrospective multicenter study included patients with unresectable or advanced HCC who received Durva/Treme through the Expanded Access Program in Thailand between August 2023 and November 2025. Treatment outcomes and adverse events (AEs) were analyzed and descriptively compared with the HIMALAYA trial. <b>Results:</b> Fifty patients were included; median age was 62 years and 80% were male. Etiologies included hepatitis B (44%), hepatitis C (30%), and nonviral liver disease (26%). Most patients had Child-Pugh A (92%), while 24% had macrovascular invasion, including five with Vp4 portal vein involvement. The objective response rate (ORR) and disease control rate (DCR) were 12% and 60%, respectively. Among 43 patients meeting HIMALAYA eligibility criteria, ORR and DCR were 12% and 56%, respectively. With a median follow-up of 28.9 months, median progression-free survival (mPFS) and overall survival (mOS) were 4.6 and 10.5 months in the overall cohort, and 6.9 and 14.0 months in the HIMALAYA-eligible subgroup. Any-grade AEs occurred in 76% of patients, with grade ≥ 3 AEs in 24%. Hepatitis was the most common toxicity (48% overall; 14% grade ≥ 3). <b>Conclusions:</b> Durva/Treme demonstrated clinically meaningful activity with manageable toxicity in unresectable HCC. Outcomes among HIMALAYA-eligible patients were broadly consistent with the pivotal trial, supporting the feasibility of this regimen in routine clinical practice.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 9","pages":"16"},"PeriodicalIF":4.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13494501/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148796027","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":"On-Treatment Grade 3-4 Neutropenia and Clinical Outcomes with Trifluridine/Tipiracil in Refractory Metastatic Colorectal Cancer: ReTrITA Real-World Evidence.","authors":"Carlo Signorelli, Michele Basso, Annunziato Anghelone, Maria Alessandra Calegari, Alessandro Passardi, Chiara Gallio, Alessandro Bittoni, Jessica Lucchetti, Lorenzo Angotti, Emanuela Di Giacomo, Ina Valeria Zurlo, Cristina Morelli, Emanuela Dell'Aquila, Adele Artemi, Donatello Gemma, Domenico Cristiano Corsi, Alessandra Emiliani, Marta Ribelli, Federica Mazzuca, Giulia Arrivi, Federica Zoratto, Maria Grazia Morandi, Fiorenza Santamaria, Manuela Dettori, Antonella Cosimati, Rosa Saltarelli, Alessandro Minelli, Emanuela Lucci-Cordisco, Mario Giovanni Chilelli","doi":"10.32604/or.2026.080964","DOIUrl":"10.32604/or.2026.080964","url":null,"abstract":"<p><p><b>Background</b>: Trifluridine/tipiracil (T) is a standard treatment for refractory metastatic colorectal cancer (mCRC). In randomized trials, treatment-emergent neutropenia has been associated with improved outcomes, suggesting a potential link with drug activity. However, evidence from routine clinical practice remains limited. This sub-analysis of the multicenter ReTrITA study evaluated the association between severe neutropenia and clinical outcomes in a real-world setting. <b>Methods</b>: Patients with refractory mCRC treated with T within the ReTrITA cohort were included. Patients were stratified according to the occurrence of grade 3-4 neutropenia. Overall survival (OS) and progression-free survival (PFS) were estimated using the Kaplan-Meier method and compared with the log-rank test. Hazard ratios (HRs) and 95% confidence intervals (CIs) were calculated using Cox models. <b>Results</b>: Among 843 patients, 271 (32.1%) developed grade 3-4 neutropenia. The occurrence of severe neutropenia was significantly associated with improved survival outcomes. Median OS was 10.9 months versus 7.6 months, HR 0.64; 95% CI, 0.55-0.75; <i>p</i> < 0.0001), and median PFS was 4.3 months versus 3.3 months (HR 0.63; 95% CI, 0.55-0.73; <i>p</i> < 0.0001) in patients with versus without neutropenia, respectively. <b>Conclusions</b>: In this large real-world cohort, grade 3-4 neutropenia during T treatment was associated with significantly improved OS and PFS, supporting its role as a potential on-treatment prognostic marker. Prospective studies are warranted to confirm these findings.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 9","pages":"15"},"PeriodicalIF":4.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13494493/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148796158","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":"Combinatorial Effects of Plasma-Treated Solution and Plasma-Treated Hydrogel with Cisplatin in Vulvar Cancer Cells.","authors":"Estelle C I D Schad, Janet P Raja Xavier, Hortense Decool, Marcel Arnholdt, Franziska Keßler, Jan Schöttke, Sara Y Brucker, Ernst Oberlechner, Johanna Laupp, Martin Weiss","doi":"10.32604/or.2026.081755","DOIUrl":"10.32604/or.2026.081755","url":null,"abstract":"<p><p><b>Background:</b> Vulvar squamous cell carcinoma (VSCC) is a rare, but increasingly prevalent malignancy with limited therapeutic options in the advanced disease state. Cisplatin-based chemoradiation remains the standard of care but is constrained by cumulative toxicity. Precancerous lesions, including high-grade squamous intraepithelial lesions (HSIL) and differentiated vulvar intraepithelial neoplasia (dVIN), similarly require effective yet tolerable treatments. Low-thermal Argon plasma devitalization (ltAPD), a source of reactive oxygen and nitrogen species (RONS), has emerged as a promising approach for redox-based tumor modulation. This study aimed to evaluate the anti-tumor efficacy of two plasma modalities, plasma-treated solution (PTS) and plasma-treated hydrogel (PTH) in combination with cisplatin in VSCC cells. <b>Methods:</b> PTS and PTH were applied as monotherapies and in sequential combination with cisplatin (plasma-first vs. cisplatin-first). RONS kinetics, cell viability, and treatment interactions were assessed following plasma monotherapy and sequential combination with cisplatin. Apoptosis and redox balance were evaluated by caspase-3/7 activity and GSH/GSSG ratios, respectively. <b>Results:</b> PTS induced a rapid oxidative burst, whereas PTH enabled delayed and sustained RONS release. Both modalities reduced cell viability in a time-dependent manner, with rapid cytotoxic effects observed for PTS. Plasma pre-treatment enhanced cisplatin efficacy, with higher synergy scores in the plasma-first sequence. Increased caspase-3/7 activity and decreased GSH/GSSG ratios, observed in the combination treatment of plasma and cisplatin, indicated enhanced oxidative stress and apoptotic priming. <b>Conclusions:</b> PTS and PTH exhibit intrinsic anti-tumor activity and sensitize VSCC cells to cisplatin through redox modulation. These findings support the integration of plasma-based strategies into combinatorial therapeutic approaches for VSCC and its precancerous lesions.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 9","pages":"1"},"PeriodicalIF":4.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13494491/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795655","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":"Concordant Shared Transcriptomic Signatures and Candidate Regulatory Features in Chronic Lymphocytic Leukemia and Multiple Myeloma.","authors":"Abtin Tondar, David Hervás Marín, Laura Calvet Liñán, Asim Kumar Bepari","doi":"10.32604/or.2026.082424","DOIUrl":"10.32604/or.2026.082424","url":null,"abstract":"<p><p><b>Background:</b> Chronic lymphocytic leukemia (CLL) and multiple myeloma (MM) are B-cell malignancies with distinct cellular origins and microenvironmental dependencies. We aimed to identify concordant transcriptomic signatures and candidate transcriptional regulatory features between CLL CD19-positive B cells and MM-associated bone marrow-derived mesenchymal stromal cells (MSCs). <b>Methods:</b> Public Gene Expression Omnibus bulk RNA sequencing datasets were analyzed separately within each context using DESeq2. Differentially expressed genes (DEGs) were defined using adjusted <i>p</i>-value < 0.05 and absolute log₂ fold change > 1. Cross-disease analyses assessed overlap, directionality, log₂ fold-change concordance, expressed-gene background-adjusted enrichment, coexpression structure, and transcription factor annotation. <b>Results:</b> We found a focused concordant gene-level signature shared across contexts. We identified 5965 DEGs in CLL and 1021 DEGs in MM; 323 were shared, and 262 were concordantly regulated, including 52 upregulated and 210 downregulated genes in both contexts. These genes showed strong log₂ fold change concordance between CLL and MM. No Gene Ontology or Kyoto Encyclopedia of Genes and Genomes terms remained significant after expressed-gene background correction, supporting stronger gene-level than pathway-level evidence. Exploratory coexpression analysis identified PSMA3-AS1, SNORD58A, 100124516, MSS51, and 652966 as the top degree-ranked hubs and seven shared differentially expressed transcription factor candidates: MAFB, MYB, CCDC17, MYSM1, ZMAT1, ZNF491, and ZNF789. Expression-matched permutation analysis did not support global transcription factor enrichment. <b>Conclusion:</b> These findings support a cross-contextual concordant transcriptomic signature shared by CLL CD19-positive B cells and MM-associated MSCs, warranting validation in harmonized cohorts and experiments.</p>","PeriodicalId":19537,"journal":{"name":"Oncology Research","volume":"34 9","pages":"21"},"PeriodicalIF":4.6,"publicationDate":"2026-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13494498/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148795975","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}