Cancer Cell International最新文献

{"title":"Progress of PD-1/PD-L1 immune checkpoint inhibitors in the treatment of triple-negative breast cancer.","authors":"Hongshu Li, Ying Chang, Tiefeng Jin, Meihua Zhang","doi":"10.1186/s12935-025-03769-z","DOIUrl":"https://doi.org/10.1186/s12935-025-03769-z","url":null,"abstract":"<p><p>Triple-negative breast cancer (TNBC) is a highly heterogeneous cancer with substantial recurrence potential. Currently, surgery and chemotherapy are the main treatments for this disease. However, chemotherapy is often limited by several factors, including low bioavailability, significant systemic toxicity, inadequate targeting, and multidrug resistance. Immune checkpoint inhibitors (ICIs), including those targeting programmed death protein-1 (PD-1) and its ligand (PD-L1), have been proven effective in the treatment of various tumours. In particular, in the treatment of TNBC with PD-1/PD-L1 inhibitors, both monotherapy and combination chemotherapy, as well as targeted drugs and other therapeutic strategies, have broad therapeutic prospects. In addition, these inhibitors can participate in the tumour immune microenvironment (TIME) through blocking PD-1/PD-L1 binding, which can improve immune efficacy. This article provides an overview of the use of PD-1/PD-L1 inhibitors in the treatment of TNBC and the progress of multiple therapeutic studies. To increase the survival of TNBC patients, relevant biomarkers for predicting the efficacy of PD-1/PD-L1 inhibitor therapy have been explored to identify new strategies for the treatment of TNBC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"139"},"PeriodicalIF":5.3,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11987362/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143965983","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":"Lysosomes: guardians and healers within cells- multifaceted perspective and outlook from injury repair to disease treatment.","authors":"Jianlei Bi, Yincong Sun, Meihua Guo, Xiaoxin Sun, Jie Sun, Rujiao Jiang, Ning Wang, Gena Huang","doi":"10.1186/s12935-025-03771-5","DOIUrl":"https://doi.org/10.1186/s12935-025-03771-5","url":null,"abstract":"<p><p>Lysosomes, as crucial organelles within cells, carry out diverse biological functions such as waste degradation, regulation of the cellular environment, and precise control of cell signaling. This paper reviews the core functions and structural characteristics of lysosomes, and delves into the current research status of lysosomes damage repair mechanisms. Subsequently, we explore in depth the close association between lysosomes and various diseases, including but not limited to age-related chronic diseases, neuro-degenerative diseases, tumors, inflammation, and immune imbalance. Additionally, we also provide a detailed discussion of the application of lysosome-targeted substances in the field of regenerative medicine, especially the enormous potential demonstrated in key areas such as stem cell regulation and therapy, and myocardial cell repair. Though the integration of multidisciplinary research efforts, we believe that lysosomes damage repair mechanisms will demonstrate even greater application value in disease treatment and regenerative medicine.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"136"},"PeriodicalIF":5.3,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11984033/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974838","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":"Cuproplasia and cuproptosis in hepatocellular carcinoma: mechanisms, relationship and potential role in tumor microenvironment and treatment.","authors":"Ruoyu Zhang, Yunfei Tan, Ke Xu, Ning Huang, Jian Wang, Mei Liu, Liming Wang","doi":"10.1186/s12935-025-03683-4","DOIUrl":"https://doi.org/10.1186/s12935-025-03683-4","url":null,"abstract":"<p><strong>Background: </strong>Hepatocellular carcinoma (HCC) is the main phenotype of liver cancer with a poor prognosis. Copper is vital in liver function, and HCC cells rely on it for growth and metastasis, leading to cuproplasia. Excessive copper can induce cell death, termed cuproptosis. Tumor microenvironment (TME) is pivotal in HCC, especially in immunotherapy, and copper is closely related to the TME pathogenesis. However, how these two mechanisms contribute to the TME is intriguing.</p><p><strong>Main body: </strong>We conducted the latest progress literature on cuproplasia and cuproptosis in HCC, and summarized their specific roles in TME and treatment strategies. The mechanisms of cuproplasia and cuproptosis and their relationship and role in TME have been deeply summarized. Cuproplasia fosters TME formation, angiogenesis, and metastasis, whereas cuproptosis may alleviate mitochondrial dysfunction and hypoxic conditions in the TME. Inhibiting cuproplasia and enhancing cuproptosis in HCC are essential for achieving therapeutic efficacy in HCC.</p><p><strong>Conclusion: </strong>An in-depth analysis of cuproplasia and cuproptosis mechanisms within the TME of HCC unveils their opposing nature and their impact on copper regulation. Grasping the equilibrium between these two factors is crucial for a deeper understanding of HCC mechanisms to shed light on novel directions in treating HCC.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"137"},"PeriodicalIF":5.3,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11983883/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143974873","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":"Single-cell transcriptome sequencing reveals the mechanism of Realgar improvement on erythropoiesis in mice with myelodysplastic syndrome.","authors":"Hao Xu, Kexin Hu, Yanlu Wang, Shuyang Cai, Fan Wu, Jizhang Bao, Qi Hu, Yu Guan, Yuchen Tao, Jiahui Lu","doi":"10.1186/s12935-025-03768-0","DOIUrl":"10.1186/s12935-025-03768-0","url":null,"abstract":"<p><p>Myelodysplastic syndrome (MDS) is a malignant hematologic disorder with limited curative options, primarily reliant on hematopoietic stem cell transplantation. Anemia, a prevalent symptom of MDS, has few effective treatment strategies. Realgar, though known for its therapeutic effects on MDS, remains poorly understood in terms of its mechanism of action. In this study, both in vivo and in vitro experiments were conducted using Realgar and its primary active component, As₂S₂, to examine their impact on mouse erythroblasts at the single-cell level. Realgar treatment significantly altered the transcriptional profiles and cellular composition of bone marrow in mice, both in vivo and in vitro. Differentially expressed genes in erythroblasts regulated by Realgar were identified, unveiling potential regulatory functions and signaling pathways, such as heme biosynthesis, hemoglobin production, oxygen binding, IL-17 signaling, and MAPK pathways. These findings suggest that Realgar enhances the differentiation of erythroblasts in mouse bone marrow and improves overall blood cell counts. This work offers preliminary insights into Realgar's mechanisms, expands the understanding of this mineral medicine, and may inform strategies to optimize its therapeutic potential in hematologic diseases.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"135"},"PeriodicalIF":5.3,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11978147/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810517","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":"CD44 on cancer stem cell is a potential immunological and prognostic pan-cancer biomarker.","authors":"Ya-Juan Zhu, Si-Ying Li, Shan-Shan Yang, Yang Du, Zhuo-Yuan Zhang, Ji-Yan Liu","doi":"10.1186/s12935-025-03748-4","DOIUrl":"10.1186/s12935-025-03748-4","url":null,"abstract":"<p><strong>Background: </strong>CD44, a widely recognized cancer stem cell marker, displayed a vital participation in the cancer immune invasion and may related with the response to the immunotherapy. However, the role of CD44 in cancer immunology is not well defined. Therefore, we intended to explore its prognostic value and potential immunological functions across 33 human cancer types.</p><p><strong>Methods: </strong>Based on the data of patients from The Cancer Genome Atlas (TCGA), Sangerbox was used to analyze the correlations between CD44 expression and tumor-infiltrated immune cells, immune checkpoints, neoantigens, microsatellite instability (MSI), and tumor mutational burden (TMB) in human cancers. A mouse model xenografted with shRNA-CD44 MC38 was established.</p><p><strong>Results: </strong>The elevated CD44 was associated with tumor stage and prognosis in several different cancers. GSEA results showed that upregulated CD44 involved in cancer stem cell associated process, antigen processing and presentation, and immune cells proliferation and activation. CD44 plays an essential role in the tumor immune regulation and immune checkpoints inhibitor response. The correlation of CD44 gene expression and infiltration levels of immune cells varied across different cancer types. Notably, the upregulation of CD44 expression is positively correlated with regulatory CD4 T cells, macrophages M1 and M2 in several analyzed cancers. Furthermore, we verified the effect of CD44 on tumor growth and immune microenvironment in mouse xenografted with shRNA-CD44 MC38. Moreover, DNA methylation existed in CD44 expression and associated with dysfunctional T-cell phenotypes via different mechanisms, thus resulting in tissue-dependent prognoses.</p><p><strong>Conclusion: </strong>CD44 is both a cancer stem cell marker and a potential prognostic and immunological biomarker in various malignant tumors. Moreover, CD44 could be a novel target for immune-based therapy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"134"},"PeriodicalIF":5.3,"publicationDate":"2025-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11978154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143810514","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":"CXCL2: a key player in the tumor microenvironment and inflammatory diseases.","authors":"Yuanhao Lv, Caizheng Chen, Miaomiao Han, Chenfei Tian, Fuyang Song, Sijia Feng, Miaoming Xu, Ziyin Zhao, Hongyan Zhou, Wei Su, Jiateng Zhong","doi":"10.1186/s12935-025-03765-3","DOIUrl":"10.1186/s12935-025-03765-3","url":null,"abstract":"<p><p>CXCL2 (C-X-C Motif Chemokine Ligand 2), a constituent of the C-X-C chemokine subfamily, serves as a powerful chemotactic factor for neutrophils, facilitating leukocyte recruitment and movement while initiating an inflammatory response. Recent investigations have demonstrated the pivotal involvement of CXCL2 in carcinogenesis. Within the tumor microenvironment, CXCL2 modulates cellular activity primarily via its interaction with the CXCR2 receptor. The activation of signaling pathways, including ERK/MAPK, NF-κB/MAPK, PI3K/AKT, and JAK/STAT3, highlights CXCL2's inclination to promote tumorigenesis. Furthermore, the role of CXCL2 encompasses inflammatory conditions like lung inflammation, atherosclerosis, and obesity. This article examines the structural characteristics, biological roles, and molecular foundation of CXCL2 in carcinogenesis and inflammatory disorders.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"133"},"PeriodicalIF":5.3,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11978139/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802547","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":"Brachyury promotes proliferation and migration of colorectal cancer cells by targeting MMP14.","authors":"Ming Chen, Huiheng Qu, Xiao Liang, Ying Huang, Zhengjie Yang, Pei Lu, Keqin Shi, Peng Chen, Yanjing Zhang, Hui Zhou, Jiazeng Xia, Jun Shen","doi":"10.1186/s12935-025-03726-w","DOIUrl":"10.1186/s12935-025-03726-w","url":null,"abstract":"<p><strong>Background: </strong>The incidence and mortality rates of colorectal cancer (CRC) are rising, and it is the second most common cause of cancer-related deaths worldwide. Although the transcription factor, Brachyury is intricately linked with various clinical malignancies, the mechanisms by which it influences CRC cell proliferation and migration are inadequately understood.</p><p><strong>Methods: </strong>Tissue microarray was used to evaluate Brachyury expression in CRC and adjacent normal tissues. The effects of Brachyury on HCT116 and SW480 CRC cells were also examined in vitro, including using Cell Counting Kit-8, colony formation, and transwell assays, and in vivo through subcutaneous tumorigenesis assays in a nude mouse xenograft model. Chromatin immunoprecipitation was used to evaluate Brachyury binding to the MMP14 promoter and its impact on MMP14 expression. Rescue experiments were used to elucidate MMP14's role in mediating Brachyury's effect on CRC cell behavior.</p><p><strong>Results: </strong>Brachyury expression was significantly higher in CRC tissues than in adjacent normal tissues, and it promotes CRC oncogenesis in vitro and in vivo. Rescue experiments established MMP14 as a direct, downstream Brachyury target, affirming that MMP14 enhanced Brachyury-driven CRC cell proliferation.</p><p><strong>Conclusion: </strong>Our findings highlight targeting the Brachyury-MMP14 axis as a potential novel approach for CRC clinical therapy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"132"},"PeriodicalIF":5.3,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11977941/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143802545","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":"Long noncoding RNAs in acute myeloid leukemia: biomarkers, prognostic indicators, and treatment potential.","authors":"Maryam Farajzadeh, Mehrdad Fathi, Pooya Jalali, Armin Mahmoudsalehi Kheshti, Shahla Khodayari, Mohammad Hojjat-Farsangi, Farhad Jadidi","doi":"10.1186/s12935-025-03763-5","DOIUrl":"10.1186/s12935-025-03763-5","url":null,"abstract":"<p><p>Long noncoding RNAs (lncRNAs) have been recognized as significant modulators of gene expression and are essential for various biological functions, even though they don't appear to have the ability to encode proteins. Originally considered dark matter, lncRNAs have been recognized as being dysregulated and contributing to the onset, progression, and resistance to treatment of acute myeloid leukemia (AML). AML is a prevalent type of leukemia characterized by the disruption of myeloid cell differentiation, leading to an increased number of immature myeloid progenitor cells. Currently, the need for novel biomarkers and treatment targets to enhance therapeutic alternatives has led to a focus on lncRNAs as possible indicators for prognostic, therapeutic, and diagnostic systems in various human cancers, including AML. Recent research has recognized a limited set of lncRNAs as possible prognostic biomarkers or diagnoses in AML. This review evaluates the key research that highlights the significance of lncRNAs in AML and discusses their roles and impacts on the disease. Furthermore, we intend to underscore the importance of lncRNAs as new and trustworthy markers for the diagnosis, prediction, drug resistance, and targets for treatment in AML.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"131"},"PeriodicalIF":5.3,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11972515/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787966","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":"Ginger extract inhibits c-MET activation and suppresses osteosarcoma in vitro and in vivo.","authors":"Ruoping Yanzhang, Mingyang Yan, Zhaojie Yang, Huijun Zhang, Yin Yu, Xiangping Li, Ruifang Shen, Xiao Chu, Siyuan Han, Ziliang Zhang, Junyan Teng, Hao Li, Tao Li, Guoguo Jin, Zhiping Guo","doi":"10.1186/s12935-025-03759-1","DOIUrl":"10.1186/s12935-025-03759-1","url":null,"abstract":"<p><strong>Background: </strong>Osteosarcoma (OS) as an invasive and lethal malignancy showing a low 5-year survival rate requires novel therapeutic targets and their suppressors to improve prevention and treatment strategies.</p><p><strong>Methods: </strong>Our research served to clarify the therapeutic potential of ginger extract and its underlying antineoplastic mechanisms in OS. In vitro studies were used to detect the anti-proliferation ability of ginger extract towards OS cells. Patient-derived xenograft (PDX) was performed to confirm whether ginger extract suppressed tumor growth. Cancer Heat Shock Protein (HSP) database was utilized to identify the potential target of ginger extract, which was subsequently validated through a computational docking model screening method, molecular dynamics simulations and pull-down assay. Analysis of the Gene Expression Omnibus (GEO) database revealed the c-MET expression among OS samples as well as the potential mechanism. Immunohistochemistry (IHC) staining corroborated the c-MET expression level among OS tissues relative to the controls. Functional studies involving c-MET knockdown among OS cell lines were produced to elucidate the functional role of c-MET in OS cellular processes.</p><p><strong>Results: </strong>In vitro studies demonstrated that ginger extract administration impeded OS cell progress while inducing apoptosis and inhibiting migration. Moreover, in vivo tests unveiled that ginger extract prominently inhibited patient-derived xenograft (PDX) tumor development. Cancer HSP database analysis recognized c-MET as an underlying target of ginger extract, which was subsequently validated through a computational docking model screening, molecular dynamics simulations and pull-down assay. Analysis of the Gene Expression Omnibus (GEO) database combined with immunohistochemistry (IHC) staining corroborated the c-MET overexpression among OS tissues in contrast with the controls. Next, our study confirmed the significant suppression of cell progress and anchorage-independent growth, while concomitantly inducing apoptosis after c-MET knockdown, underscoring its prospect for a therapeutic target.</p><p><strong>Conclusion: </strong>Collectively, our findings show that c-MET is a prospective therapeutic target for OS. Ginger extract, a natural c-MET inhibitor, exhibits potent antineoplastic effects by suppressing OS growth both in vitro and in vivo, highlighting its prospect for a new therapeutic agent of this aggressive malignancy.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"130"},"PeriodicalIF":5.3,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11971884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787962","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":"Heme oxygenase 1 confers gilteritinib resistance in FLT3-ITD acute myeloid leukemia in a STAT6-dependent manner.","authors":"Tianzhuo Zhang, Danna Wei, Yun Zhan, Zhengmei Long, Tingting Lu, Peng Zhao, Rui Gao, Qian Kang, Luxin Zhang, Min Liu, Xueying Yang, Jishi Wang","doi":"10.1186/s12935-025-03757-3","DOIUrl":"10.1186/s12935-025-03757-3","url":null,"abstract":"<p><strong>Background: </strong>Acute myeloid leukemia (AML) is the most common type of acute leukemia in adults. We previously discovered that heme oxygenase 1 (HO1) is crucial for chemoresistance in AML, but the detailed molecular mechanism of that remains unclear.</p><p><strong>Methods: </strong>RNA sequencing was conducted to assess transcriptomic changes in three pairs of AML cells after regulating the expression of HO1. The molecular mechanism by which HO1 induces gilteritinib resistance in FLT3-ITD (FMS-like tyrosine kinase 3 (FLT3) internal tandem duplication (ITD)) AML was evaluated by quantitative real-time PCR (qRT-PCR), CCK-8, flow cytometry, and western blotting. FLT3-ITD AML mouse models were established to investigate the effects of HO1 expression on gilteritinib resistance in vivo.</p><p><strong>Results: </strong>In these three pairs of AML cells, we discovered that HO1-mediated drug resistance is connected to the interleukin-4-mediated signaling pathway (specifically STAT6) only in MV4-11 cells with the FLT3-ITD mutation. Further findings revealed that HO1 overexpression confers gilteritinib resistance in FLT3-ITD AML cell lines and primary individual specimens. While suppression of HO1 sensitized FLT3-ITD AML cell lines and primary individual specimens to gilteritinib. Mechanistically, western blotting and flow cytometry confirmed that HO1-mediated gilteritinib resistance is related to STAT6 phosphorylation in FLT3-ITD AML cell lines and primary individual specimens. Moreover, tumor-bearing mice were employed to determine that HO1 overexpression conferred gilteritinib resistance in vivo.</p><p><strong>Conclusions: </strong>Collectively, these studies illustrate that HO1 may act as a successful treatment target for gilteritinib-resistant FLT3-ITD AML patients.</p>","PeriodicalId":9385,"journal":{"name":"Cancer Cell International","volume":"25 1","pages":"129"},"PeriodicalIF":5.3,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11969713/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143787964","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}