Cancer Cell International最新文献

{"title":"Medicinal plants: nutritional, immunological and therapeutic role in treating cancer-related malnutrition: a comprehensive review.","authors":"Mohamed T El-Saadony, Samar Sami Alkafaas, Ahmed M Saad, Dina Mostafa Mohammed, Sameh A Korma, Heba M Salem, Taia A Abd El-Mageed, Mohamed I Elsalahaty, Sara Samy Elkafas, Walid F A Mosa, Ahmed Ezzat Ahmed, Essam H Ibrahim, Fawze Alnadari, Betty T Mathew, Alaa S Abdelhamid, Sahar F Allaban, Samah A Loutfy, Soumya Ghosh, Hanya Y Assal, Marawan K El-Tarabily, Synan F AbuQamar, Khaled A El-Tarabily","doi":"10.1186/s12935-025-03720-2","DOIUrl":"10.1186/s12935-025-03720-2","url":null,"abstract":"<p><p>Cancer is the second leading cause of death globally, following microbial infection, with an estimated 16 million deaths projected by 2040. However, natural resources can potentially treat up to 60% of cancer cases. Various cancers, including those affecting the breast, prostate, stomach, colon, lung, liver, kidney, bone, skin, and blood, have strong dietary connections regarding their occurrence and prevention. Cancer and its treatments, particularly chemotherapy, are closely associated with malnutrition in humans. The adverse effects of medical therapies and the disease itself often prevent patients with cancer from meeting their nutritional needs through regular food intake. The etiology of malnutrition in patients with cancer is complex and multifactorial, influenced by the type and location of cancer, disease stage, side effects of treatment, economic status, functional capacity, symptoms impacting nutrition, fasting requirements, inadequate dietary therapy, and awareness of the clinical staff regarding the role of dietary habits in diagnosis, treatment, and quality of life. Although there have been advances in drug-targeted therapies, they remain unelucidated, and therefore, this review aims to elucidate the relationship between cancer, chemical treatments, and malnutrition. In addition, it highlights the significant role of medicinal plants in treating various cancers and mitigating the adverse side effects of chemotherapy, offering a comprehensive understanding of their nutritional, immunological, and therapeutic benefits.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"266"},"PeriodicalIF":5.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269176/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A LINC00472-encoded polypeptide impedes migration and proliferation through modulation of the HDAC2/SP1 axis in non-small cell lung cancer cells.","authors":"Lei Xu, Haoyong Kuang, Haodong Peng, Sen Wu, Yu Bai, Xiangbo Jia, Wenjian Yao","doi":"10.1186/s12935-025-03901-z","DOIUrl":"10.1186/s12935-025-03901-z","url":null,"abstract":"<p><strong>Objective: </strong>While long non-coding RNAs (lncRNAs) are increasingly recognized as sources of functional micropeptides, their roles in non-small cell lung cancer (NSCLC) remain poorly characterized. This study investigates the therapeutic potential and molecular mechanism of LINC00472-encoded polypeptide in NSCLC.</p><p><strong>Methods: </strong>Through integration of ribosome profiling, transcriptomics, and co-expression analysis, we systematically identified lncRNA-encoded polypeptides in NSCLC. Translational competence was validated via ribosome affinity purification (TRAP), Western blot, and immunofluorescence (IF). Functional assays (CCK-8, EdU, wound healing, transwell) and xenograft models assessed anti-tumor effects. HDAC2/SP1 interaction dynamics were analyzed by co-IP and luciferase reporter systems.</p><p><strong>Results: </strong>Multi-omics screening identified LINC00472 as a bifunctional transcript encoding a 15-aa polypeptide (LINC00472-ORF). LINC00472-ORF exhibited potent tumor-suppressive activity, reducing NSCLC proliferation and motility in vitro, while suppressing xenograft growth in vivo. Mechanistically, LINC00472-ORF disrupted HDAC2/SP1 interaction, inducing SP1 hyperacetylation, cytoplasmic retention, and transcriptional inactivation of downstream oncogenic genes.</p><p><strong>Conclusion: </strong>We unveil LINC00472-ORF as a dual-function therapeutic agent that targets the HDAC2/SP1 axis to inhibit NSCLC progression.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"263"},"PeriodicalIF":5.3,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12269243/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144648659","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stromal PLAU mediates tumor progression and informs a novel therapeutic target in triple-negative breast cancer.","authors":"Jun Zou, Jingyao Zhang, Yu Li, Baowen Yuan, Yuanyi Wang, Yalong Qi, Qian Wang, Wan Qin, Xianglin Yuan, Binghe Xu","doi":"10.1186/s12935-025-03867-y","DOIUrl":"10.1186/s12935-025-03867-y","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is an aggressive subtype characterized by limited treatment options and poor prognosis. Recent evidence highlights the crucial role of cancer-associated fibroblasts (CAFs) in TNBC progression, yet their molecular characteristics remain incompletely understood. In this study, we performed a comprehensive analysis combining bioinformatics approaches with experimental validation to investigate CAF-related genes in TNBC. Using weighted gene co-expression network analysis (WGCNA) of TNBC samples from TCGA and METABRIC datasets, we identified 185 CAF-related genes significantly associated with extracellular matrix organization and TGF-β signaling pathways. Through rigorous statistical modeling, we developed a 3-gene prognostic signature (CERCAM, JAM3, PLAU) that effectively stratified TNBC patients into high- and low-risk groups with distinct survival outcomes. Importantly, we validated the functional role of PLAU, one of the signature genes, through in vitro and in vivo experiments. Results showed that CAF-derived PLAU played key role in the malignant behaviors of TNBC. Our findings provide new insights into CAF-mediated TNBC progression and suggest potential stromal targets for therapeutic intervention.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"259"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255126/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616324","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A multi-analyte liquid biopsy approach for nonseminomatous testicular germ cell tumors: combining cfDNA and N-glycan analysis in blood and seminal plasma.","authors":"Jure Krasic, Dinko Soic, Lucija Skara Abramovic, Ivona Kolosnjaj, Miroslav Tomic, Alen Vrtaric, Sasa Kralik Oguic, Nina Gelo, Ana Katusic Bojanac, Davor Jezek, Dinko Mitrecic, Monika Ulamec, Tomislav Kulis, Olga Gornik, Nino Sincic","doi":"10.1186/s12935-025-03887-8","DOIUrl":"10.1186/s12935-025-03887-8","url":null,"abstract":"<p><strong>Background: </strong>Nonseminomatous testicular germ cell tumors (NSE) present significant diagnostic challenges, especially for the early detection of serum tumor marker (STM) negative cases. Current diagnostic tools are limited, highlighting the need for innovative approaches. This study investigates a novel multi-analyte approach combining circulating cell-free DNA (cfDNA) and N-glycan profiling in both blood and seminal plasma to improve NSE diagnostics.</p><p><strong>Methods: </strong>The study included 41 NSE patients and 114 healthy controls. Diagnostic potential of cfDNA parameters (quality and fragmentation), cfDNA methylation (RASSF1A, PRSS21, and LINE-1) and N-glycan alterations in blood plasma and seminal plasma samples was investigated using logistic regression models. Pre- and post-radical orchidectomy longitudinal samples from NSE patients were analyzed to assess surgical treatment response and disease monitoring utility.</p><p><strong>Results: </strong>Blood plasma analysis of combined cfDNA and N-glycan profiling demonstrated high diagnostic precision, with an AUC of 0.96, identifying 85% of STM-negative patients and all pure-form teratomas. Post-operative blood plasma analysis showed that LINE-1 cfDNA methylation levels returned to those of healthy controls. Seminal plasma analysis revealed an increased cfDNA fragmentation index (CFI) and cfDNA methylation changes in LINE-1 and PRSS21, with an AUC of 0.83 and identifying 85% of STM-negative patients.</p><p><strong>Conclusion: </strong>The proposed multi-analyte approach significantly improves early diagnostics of NSE, particularly for STM-negative cases and teratomas. LINE-1 cfDNA methylation is a promising biomarker for NSE detection and treatment monitoring. These findings could transform diagnostic strategies and patient management in testicular germ cell tumors, with potential applications in reducing overtreatment and improving outcomes .</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"257"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616319","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"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 platelets in tumor immune evasion and metastasis: mechanisms and therapeutic implications.","authors":"Jiaqi Gan, Xinjun Zhang, Jie Guo","doi":"10.1186/s12935-025-03877-w","DOIUrl":"10.1186/s12935-025-03877-w","url":null,"abstract":"<p><p>Only circulating tumor cells (CTCs) that successfully evade immune surveillance upon entering the bloodstream can lead to clonal expansion and metastasis. Cancer progression is accompanied by pathophysiological processes such as platelet activation and thrombosis. Platelets secrete a variety of growth factors to stimulate cancer cell proliferation, regulate tumor angiogenesis, and subsequently mediate surface changes in cancer cells to promote invasion and progression. As part of a dangerous alliance, CTCs and platelets induce mutual activation. Activated platelets aggregate and encapsulate tumor cells, forming microtumor thrombi containing fibrin clots that act as protective barriers. These platelets interact with immune cells, including NK cells, macrophages, neutrophils, and T cells, to facilitate cancer metastasis and progression through various mechanisms. The formation of a favorable tumor microenvironment (TME) and pre-metastatic niche aids cancer cells in evading immune surveillance. Multiple signaling pathways and immune checkpoints are also involved in this process. Given the significant role of platelets in tumor immune evasion, anti-cancer strategies targeting platelets and their potential use as \"bionic drug delivery systems\" for anti-tumor drugs hold broad prospects in emerging tumor therapies.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"258"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255057/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616325","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Specificity protein 1 initiates epithelial-mesenchymal transition of circulating tumor cells to inhibit metastasis in prostate cancer.","authors":"Mei Yang, Lin Jie Li, Guo Ping Qiu, Hui Liu, Fei Gao","doi":"10.1186/s12935-025-03888-7","DOIUrl":"10.1186/s12935-025-03888-7","url":null,"abstract":"<p><p>Circulating tumor cells (CTCs), as seeds for metastasis, hold great promise for cancer diagnosis, prognosis, and treatment. Based on the expression of biomarkers, CTCs can be categorized as epithelial (E), mesenchymal (M), or hybrid (M/E) phenotypes. At present, the role of CTC phenotypes in metastatic prostate cancer (PCa) is not clear. In the current study, CTCs were isolated from 102 PCa patients using the Canpatrol™ technology. Fluorescence in situ hybridization (FISH) was used to categorize CTCs. The EMT regulators were analyzed by bioinformatics software. Specificity protein 1 (SP1) was overexpressed in PC3 cells by lentiviral transfection. Transwell assay was used to assess cell invasion in vitro. A mouse model of metastasis was used to evaluate the seeding capability of SP1-overexpressing PC3 cells administered via tail vein injection. It was found that the cell counts of total CTCs (T-CTCs), E-CTCs, and hybrid-CTCs were significantly higher in metastatic PCa than local PCa. T-CTC count (> 14) was identified as an independent risk factor for metastasis, predicting metastatic PCa with a sensitivity of 90.48% and a specificity of 96.67%. SP1 was identified as a valuable EMT regulator by bioinformatics. SP1 overexpression in PC3 cells induced EMT and enhanced cell invasion in vitro, however, it inhibited lung metastasis in vivo. In conclusion, the T-CTC count predicted metastatic PCa. Polarization of PCa CTCs toward the M phenotype reduced their metastasis-initiating capability. SP1 overexpression induced EMT and repressed metastatic colonization of PCa CTCs. Thus, the induction of EMT in CTCs by SP1 augmentation may hold promise as a novel treatment for PCa by staving off metastasis.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"255"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MicroRNA-1303 in cancer pathogenesis and therapy: clinical implications for biomarker development and targeted treatment strategies.","authors":"Lingzi Zheng, Ling Hu, Bita Badehnoosh","doi":"10.1186/s12935-025-03895-8","DOIUrl":"10.1186/s12935-025-03895-8","url":null,"abstract":"<p><p>Cancer remains one of the most formidable global health challenges due to its complex pathogenesis, late-stage diagnosis, and limited therapeutic options for many subtypes. Despite advancements in reducing cancer-related mortality through lifestyle modifications and early interventions, it continues to rank among the top ten causes of death worldwide. A growing body of evidence highlights the critical role of non-coding RNAs, particularly microRNAs (miRNAs), in cancer biology. MiRNAs are short, non-coding RNA molecules approximately 19-25 nucleotides in length that regulate gene expression at the post-transcriptional level. Among these, miRNA-1303 has garnered increasing attention due to its aberrant expression across a variety of malignancies and its involvement in diverse cellular processes, including cell proliferation, apoptosis, migration, invasion, and chemoresistance. In this review, we provide a comprehensive overview of miRNA-1303, emphasizing its dysregulation in different cancer types such as colorectal, breast, prostate, and lung cancers. We explore the molecular mechanisms and signaling pathways modulated by miRNA-1303, including its interaction with oncogenes, tumor suppressors, and key cellular networks like PI3K/AKT, Wnt/β-catenin, and MAPK pathways. We also discuss its functional role in tumor development and progression, supported by both in vitro and in vivo studies. Furthermore, we evaluate the potential of miRNA-1303 as a clinically relevant biomarker for early cancer detection, prognosis prediction, and treatment monitoring. Its expression patterns have been correlated with tumor stage, metastasis, and patient survival, suggesting promising utility in clinical decision-making. In addition, we explore the emerging therapeutic strategies targeting miRNA-1303, including miRNA mimics, inhibitors, and delivery systems designed to modulate its expression in cancer cells. By synthesizing current findings, this review underscores the clinical significance of miRNA-1303 in oncology and proposes future directions for its application in personalized medicine.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"256"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12247361/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparison of local effects and systemic T-cell responses in patients with breast cancer treated by radiofrequency ablation versus microwave ablation.","authors":"Muxin Yu, Bangjie Wang, Ying Qu, Wen Sun, Mengdi Liang, Xinrui Mao, Yunshan Jiang, Jiaming Wang, Xinyu Tang, Hong Pan, Yi Zhao, Hui Xie, Qiang Ding, Shui Wang, Wenbin Zhou","doi":"10.1186/s12935-025-03896-7","DOIUrl":"10.1186/s12935-025-03896-7","url":null,"abstract":"<p><strong>Background: </strong>Radiofrequency ablation (RFA) and microwave ablation (MWA) have been investigated as treatments for early-stage breast cancer. However, it is unclear which minimally invasive thermal therapy demonstrates superior local efficacy. Also, the cytolytic functions of peripheral T cells after thermal ablation in solid tumors have not been reported.</p><p><strong>Materials and methods: </strong>In this study, 60 patients with breast cancer were enrolled from two clinical trials conducted between March 2020 and December 2021. The local effect of thermal ablation evaluated through pathological examinations or radiological imaging was the primary outcome. The secondary outcome involved systemic T-cell responses. Peripheral blood samples were collected before and after treatments. The ablation-induced immune responses were analyzed using flow cytometry, enzyme-linked-immunosorbent assay (ELISA), quantitative real-time PCR (qRT-PCR) and single-cell RNA sequencing.</p><p><strong>Results: </strong>Both RFA and MWA showed favorable local effects in the treatment of breast cancer. Compared to surgery, RFA increased peripheral CD8 + T-cell proportions but did not enhance their cytolytic functions. Conversely, MWA induced stronger cytolytic functions of peripheral T cells and upregulated memory CD4 + T cells. The distinct immune responses induced by MWA and RFA were associated with variations in antigen presentation pathways, types of antigen-presenting cells (APCs), and cytokine secretion profiles. Single-cell RNA sequencing further revealed that dendritic cells were the APCs activated by MWA, exhibiting upregulated fatty acid metabolism.</p><p><strong>Conclusion: </strong>Both thermal ablation therapies are technically feasible for early-stage breast cancer. However, MWA appears superior in enhancing the cytolytic functions of peripheral T cells compared to RFA. This study provides the first mechanistic insight into the different immune responses induced by MWA and RFA, although future clinical trials are necessary to validate these findings.</p><p><strong>Trial registration: </strong>ChiCTR2000029665. Registered February 09, 2020 ( https://www.chictr.org.cn/showproj.html?proj=48315 ) and ChiCTR2000029155. Registered January 16, 2020 ( https://www.chictr.org.cn/showproj.html?proj=48314 ).</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"261"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12254964/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616321","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chimeric Antigen Receptor (CAR)-NK92 cells effective against glioblastoma, breast- and pancreatic cancer in vitro and in a murine xenograft model of ovarian cancer.","authors":"Abdelhadi Boulifa, Alexander Sebastian Franzén, Martin J Raftery, Clarissa Radecke, Gabriele Pecher","doi":"10.1186/s12935-025-03865-0","DOIUrl":"10.1186/s12935-025-03865-0","url":null,"abstract":"<p><strong>Background: </strong>Aggressive tumors such as glioblastoma, breast, ovarian and pancreatic cancer have low survival rates and new therapies are urgently needed. One potential target is CD44v6, a splice variant of CD44 that is associated with poor prognosis. Recently, NK cells expressing CAR molecules have shown promise in combining specific targeting of solid tumors with a low risk of side effects. The aim of the current study is to explore the efficacy of the CD44v6-CAR construct expressed in the NK cell line NK92 against solid tumors both in vitro and in vivo.</p><p><strong>Methods: </strong>Flow cytometry was used to evaluate the expression of CD44v6 on glioblastoma, breast, ovarian and pancreatic cancer cell lines. In order to investigate the efficacy of CD44v6-CAR-NK92 against these solid tumors in 2D and 3D models, cytotoxicity was measured using a luminescent cell viability assay. Additionally, we assessed the levels of IFN-γ in cell culture supernatants using an ELISA method. Finally, we evaluated our therapeutic in vivo using a xenografted murine model of ovarian cancer through bioluminescent imaging.</p><p><strong>Results: </strong>CD44v6-CAR-NK92 cells exhibit specific cytotoxicity against glioblastoma, breast, ovarian and pancreatic cancer after 24 h compared to the control, both in 2D and 3D models. Furthermore, the activity of CD44v6-CAR-NK92 was validated by quantifying specific cytokine release in response to target cells. Finally, we could show that CD44v6-CAR-NK92 was effective in reducing tumor burden in a xenografted murine model of ovarian cancer.</p><p><strong>Conclusion: </strong>Our results demonstrate that CD44v6-CAR-NK92 cells could be an attractive therapeutic agent for the treatment of solid tumors.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"260"},"PeriodicalIF":5.3,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12255008/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144616320","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"One step further in targeting acute leukemia by combining antibody-based immunotherapies and small molecule inhibitors.","authors":"Armin Dozandeh-Jouybari, Erfan Rohaninia, Sara Faaliat, Nazanin Joudaki, Sara Ghandi, Maryam Talebi Moghaddam, Saeid Taghiloo, Tohid Kazemi","doi":"10.1186/s12935-025-03869-w","DOIUrl":"10.1186/s12935-025-03869-w","url":null,"abstract":"<p><strong>Background: </strong>Acute leukemia is a bone marrow-related disease characterized by fast progression and the production of immature blood cells rather than normal ones that are classified as either acute lymphoblastic leukemia (ALL) or acute myeloid leukemia (AML). Chemotherapy as a conventional treatment has many side effects, thus new medications that target intracellular molecules and cell surface markers on leukemic cells have been developed in the last decades.</p><p><strong>Main body: </strong>This review focuses on antibody-based targeted treatments, which so far, have been shown to improve the treatment outcomes, including the immune checkpoint inhibitors (ICIs), monoclonal antibodies, and bispecific T-cell engagers (BiTE). Other classes are small molecule inhibitors (as a new generation of chemotherapeutic drugs in targeted therapies) that are discussed herein include SMIs of intracellular target molecules, including tyrosine kinases, serine/threonine kinases, BCL-2, and smoothened (SMO). These inhibitors have been very effective in dealing with certain genetic changes besides blocking the important cell molecules in acute leukemia responsible for the failure of the immune system. A focus is made on assessing the use of antibody-mediated therapies in combination with SMIs for treating acute leukemia.</p><p><strong>Short conclusion: </strong>Given the distinct mechanisms and objectives of these two therapeutic modalities that have the potential to synergistically enhance one another, along with the findings from clinical trial investigations, it appears that combination therapy may yield superior efficacy compared to monotherapy, representing a progressive advancement in the treatment of acute leukemia.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"254"},"PeriodicalIF":5.3,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12235782/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144583080","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}