Molecular and Cellular Biochemistry最新文献

{"title":"CAR19-T/NK cell and circular aptamer-drug conjugate (ApDC) combination treatment increases immunotherapy efficacy.","authors":"Ling-Qi Kong, Su-Yun Chen, Xu Cui, Ya-Hui Hu, Lian Wang, Jia-Yao Zhu, Lan-Xuan Guan, Bing-Kun Wang, Li-Ting Yang, Kai-Ming Chen, Chao-Ming Zhou","doi":"10.1007/s11010-025-05347-3","DOIUrl":"https://doi.org/10.1007/s11010-025-05347-3","url":null,"abstract":"<p><p>Chimeric antigen receptor (CAR)-based cell therapies have transformed the treatment of haematological malignancies, especially acute lymphoblastic leukaemia (ALL). However, drug resistance limits long-term efficacy. This study aimed to develop a novel combination therapy using aptamer‒drug conjugates and CAR19-T/natural killer (NK) cells to eliminate tumour cells completely and improve the efficacy of CAR-based cell therapies. A novel circular aptamer‒drug conjugate (C-ApDC) targeting protein tyrosine kinase-7 (PTK7) was designed and synthesized, and CD19 CAR-T and CAR-NK cells were constructed. The stability of C-ApDC was analysed by agarose gel electrophoresis, its binding specificity was evaluated by flow cytometry, and its cytotoxicity was measured by a CCK-8 assay. The synergistic effect between C-ApDC and CAR19-T/NK cells was comprehensively assessed through flow cytometry cytotoxicity analysis. To further validate the feasibility of combination therapy, we synthesized a novel C-ApDC-nanobody conjugate and combined it with CAR19-NK/T cells. The stability of the conjugate was analysed by agarose gel electrophoresis, and the cytotoxic effects of the combination regimen on tumour cells were detected by flow cytometry. C-ApDC exhibited greater stability than linear ApDC and specifically bound to and killed PTK7-expressing Nalm6 cells in vitro. C-ApDC significantly enhanced the cytotoxicity of CAR19-T/NK cells to tumour cells. Similarly, the C-ApDC-nanobody conjugate, when used in combination with CAR19-NK/T cells, exhibited high stability. A combination therapy composed of C-ApDC nanobodies and CAR19-T/NK cells was successfully developed. This innovative approach effectively enhances the cytotoxicity of CAR19-T/NK cells against tumour cells, providing a novel therapeutic strategy for tumour treatment and offering a promising solution to overcome CAR-T resistance.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Natural polysaccharides with the reduction of intestinal barrier damage in cardiovascular diseases.","authors":"Guo-Chen Zhong, Peng Zhou","doi":"10.1007/s11010-025-05352-6","DOIUrl":"https://doi.org/10.1007/s11010-025-05352-6","url":null,"abstract":"<p><p>Natural polysaccharides are a potential therapy for cardiovascular diseases (CVDs) resulting from intestinal barrier injury. More studies on the protective effects of natural polysaccharides on intestinal barrier injury are being conducted, although the underlying mechanisms remain unknown. Thus, the objective of this paper is to discuss current research on natural polysaccharides to reduce the risk of CVDs by preventing intestinal barrier injury. In addition, the protective benefits of natural polysaccharides against CVDs are explored. Finally, the preliminary structure-activity relationship of natural polysaccharides was discussed, which provided the theoretical basis for the modification of lead compound. These natural polysaccharides can enhance the intestinal barrier function of the intestine, hence preventing the incidence and development of CVDs.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-07-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626627","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ATF-4 deficiency increases ER stress and induces osteoarthritis formation in mice.","authors":"Peng-Yu Xie, Shan-Shan Li, Xu Liang, Hang Ma, Ying-Chao Yang, Tian-Fang Li","doi":"10.1007/s11010-025-05349-1","DOIUrl":"https://doi.org/10.1007/s11010-025-05349-1","url":null,"abstract":"<p><p>Although osteoarthritis (OA) is a leading cause of morbidity, no disease-modifying osteoarthritis drugs (DMOADs) are currently available. An in-depth understanding of OA pathogenesis may help the development of novel and effective treatments. Activating transcription factor 4 (ATF-4) plays a critical role in skeletal biology as it is closely involved in ER stress, autophagy, cell senescence, etc. Our study showed that meniscal injury in Atf-4 deficient (Atf-4^-/-) mice resulted in complete destruction of mouse knee joints. In addition, these mice developed spontaneous OA-like lesions with aging. In vitro study demonstrated that the ER stress was increased and proliferation was decreased in articular chondrocytes from Atf-4^-/- mice compared to wild-type (WT) chondrocytes, which enhanced apoptosis of Atf-4^-/- chondrocytes. Re-introduction of ATF-4 into the joint cavity of Atf-4^-/- mice significantly alleviated joint damage. Taken together, our study demonstrates that ATF-4 is a critical molecule for normal functionality of articular chondrocytes and its modification may facilitate the identification of novel therapeutic targets.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanism of hydrogen-rich water alleviating radiation-induced cognitive impairment through PI3K/AKT/Caspase-9 pathway mediating anti-oxidation.","authors":"Mengya Liu, Yong Wang, Yuhao Wang, Huan Liu, Jianhua Li, Jianguo Li, Xiujun Qin","doi":"10.1007/s11010-025-05350-8","DOIUrl":"https://doi.org/10.1007/s11010-025-05350-8","url":null,"abstract":"&lt;p&gt;&lt;p&gt;Explore the mechanism by which the antioxidant effect of hydrogen-rich water alleviates radiation-induced cognitive impairment based on the PI3K/AKT/Caspase-9 signaling pathway. Male SD rats were randomly divided into control group (Control group), simple irradiation (IR) group, high-dose hydrogen-rich water intervention (IR + HHRW) group, and low-dose hydrogen-rich water intervention (IR + LHRW) group. The irradiation dose was 20 Gy, and the whole brain was irradiated. The control group and IR group were given pure water (20 mL·kg&lt;sup&gt;-1&lt;/sup&gt;), and the IR + HHRW group and IR + LHRW group were given hydrogen-rich water (20 mL·kg&lt;sup&gt;-1&lt;/sup&gt;, 10 mL·kg&lt;sup&gt;-1&lt;/sup&gt;) for 30 days. Within 30 days after irradiation, the irradiated rats all had hair loss on the head, and the IR group showed the most obvious hair loss, and the IR + HHRW group had the mildest degree of hair loss. In the second week after irradiation, the irradiated rats showed a decrease in food intake and weight loss. During this period, the food intake and body weight loss of the rats in the IR + HHRW group were lower than those in the IR and IR + LHRW groups. At the third week after irradiation, the food intake and body weight of the rats in each group began to gradually recover, and the rats in the IR + HHRW group fastest recovered. Hematological tests showed that after irradiation, the BRC and HGB of the rats in the IR group decreased, and the levels of RBC and HGB in the IR + HHRW group tended to increase compared with the IR group. The results of the novel object recognition (NOR) experiment showed that compared with the IR group, the rats in the IR + HHRW group had a significantly higher preference index for new objects. The results of the Morris water maze test showed that compared with the IR group, the escape latency of the rats in the IR + LHRW group and the IR + HHRW group was shortened, among which, on the 5th day, the IR + HHRW group had a significant difference; on the 6th day, compared with the Control group, the time for the rats in the IR group to reach the platform for the first time was significantly longer, and the time for the rats in the IR + HHRW group to reach the original platform for the first time was significantly shorter than that of the IR group, and the times of crossing the platform and the time of staying in the quadrant of the original platform were both prolonged (p &lt; 0.05). HE staining and TUNEL staining showed that the number of apoptotic hippocampal neurons in the IR group was significantly higher than that in the control group, and the number of apoptotic hippocampal neurons in the IR + HHRW group was less than that in the IR group. The detection of oxidative stress indicators in brain tissue showed that compared with the IR group, the levels of ROS, MDA and IL-6 in the IR + HHRW group were significantly lower; SOD and GSH were significantly higher. PCR results: Compared with the IR group, the expression levels of genes PI3K and AKT in the ","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144619085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic reprogramming by air pollution: linking prenatal exposures to birth outcomes.","authors":"Garvita Parikh, Bhoomika Patel","doi":"10.1007/s11010-025-05345-5","DOIUrl":"https://doi.org/10.1007/s11010-025-05345-5","url":null,"abstract":"<p><p>Exposure during pregnancy has a significant impact on foetal programming and can have long-term health effects. The rising levels of air pollution worldwide, in tandem with their substantial impact on human health, highlight the need for a better understanding of the molecular mechanisms by which air pollutants cause harm to developing foetuses and epigenetic modifications are one such important mechanism. The placenta is crucial for foetal programming throughout pregnancy; it controls the environment inside the womb and serves as a gatekeeper for the passage of waste products and nutrients between the mother and the developing foetus. Air pollutants, including heavy metals, can enter the placenta during pregnancy and lead to changes in DNA methylation patterns, histone modification, and non-coding RNA regulation, resulting in alterations in placental function and foetal programming. Further, the prenatal exposure to air pollutants may cause both global and locus-specific changes in epigenetic marks, which may affect gene expression and metabolic pathways required for proper foetal development. This review highlights the effect of prenatal exposure to air pollutants, including heavy metals, on foetal development and disease susceptibility while also examining the state of knowledge about epigenetic changes linked to this exposure, as well as its emphasis on determining windows of vulnerability and how these changes contribute to adverse birth outcomes.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144600979","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"METTL16 promotes progression of clear cell renal cell carcinoma via up-regulating N6-methyladenosine modification of KLK4 mRNA.","authors":"Bo Fan, Yunfeng Niu, Tao Li, Hao Chen, Kunpeng Zeng, Shujun Li, Yongliang Ma","doi":"10.1007/s11010-025-05346-4","DOIUrl":"https://doi.org/10.1007/s11010-025-05346-4","url":null,"abstract":"<p><p>The advancement of clear cell renal cell carcinoma (ccRCC) is a significant problem in clinical practice, and understanding the molecular determinants of malignancy progression is essential for the creation of viable treatment targets. METTL16, a methyltransferase enzyme responsible for RNA modifications, has been linked to a variety of cancers. However, its specific role in ccRCC remain unclear. The function of METTL16 was validated using in vivo and in vitro gain/loss of function experiments. Our functional assays indicated that silencing METTL16 significantly impaired cell proliferation, migration, and invasive capabilities. Mechanistically, MeRIP-PCR and luciferase assays confirmed that METTL16 promoted m6A modification of KLK4 and enhanced its stability through recognition of the m6A reader protein, IGF2BP2. KLK4 overexpression reversed the proliferation and migration defects caused by METTL16 knockdown, possibly through activation of ERK and AKT signaling pathways. In vivo experiments further demonstrated that KLK4 overexpression mitigated tumor growth inhibition caused by METTL16 depletion. These findings suggest that METTL16 promotes ccRCC progression via KLK4-mediated signaling, highlighting a potential therapeutic target.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584358","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The clinical implication of β-arrestins-mediated signaling in memory and cognition.","authors":"Mahdi Maleki Aghdam, Mehdi Mohebalizadeh, Parsa Sameei, Maryam Majidinia","doi":"10.1007/s11010-025-05323-x","DOIUrl":"https://doi.org/10.1007/s11010-025-05323-x","url":null,"abstract":"<p><p>Arrestins, particularly β-arrestins, are multifunctional adapter proteins that regulate G protein-coupled receptors (GPCRs). These proteins are central to the desensitization, internalization, and downstream signaling of GPCRs, which are integrated into various physiological processes. Many studies have explored the extensive roles of β-arrestins in memory formation, consolidation, and psychoneurological disorders. The distribution of arrestins in the brain and their high expression in dopaminergic neurons and cortical pyramidal cells reveals their significant involvement in neural processes. Emerging evidence shows that β-arrestins contribute to memory modulation through receptor internalization and synaptic plasticity mechanisms. Notably, β-arrestins influence long-term potentiation (LTP) and long-term depression (LTD), essential processes in memory consolidation. In psychoneurological disorders, β-arrestins regulate neurotransmitter-receptor interactions, like dopaminergic pathways, which are implicated in mood and cognitive functions. The underlying role of β-arrestins in depression, schizophrenia, and autism spectrum disorder (ASD) highlights their therapeutic potential. β-Arrestin-biased ligands and the modulation of β-arrestin signaling pathways promise approaches for developing treatments with improved efficacy and reduced side effects. This review aims to underscore the diverse roles of β-arrestins in preserving neuronal function and their therapeutic potential in addressing memory-related and psychiatric disorders.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-07-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144567548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prolonged sepsis triggers abnormal mitochondrial dynamics in the limb muscles and diaphragm.","authors":"Chao Xiong, Fasheng Guan, Jianguo Feng, Jing Jia, Jumei Zhang, Rui Tu, Jie Li, Jun Zhou, Jianglin Wang, Li Liu","doi":"10.1007/s11010-025-05338-4","DOIUrl":"https://doi.org/10.1007/s11010-025-05338-4","url":null,"abstract":"<p><p>Mitochondrial dysfunction is considered as a major trigger of sepsis-induced intensive care unit-acquired weakness (ICU-AW), but the precise role of impaired mitochondrial dynamics in sepsis-induced ICU-AW remains unclear. The cecal ligation and puncture (CLP) model was used to induce sepsis in mice. Fluid resuscitation and antibiotic treatment were used to establish a 5-day duration sepsis model, with sham-operated animals serving as controls. The muscle function of the diaphragm (DM) and tibialis anterior (TA) was assessed individually. Transmission electron microscopy (TEM) was used to observe changes in mitochondrial ultrastructure and measure the morphological parameters. Western blot analysis and quantitative real-time polymerase chain reaction were used to examine the expression of mitochondrial fusion and fission proteins and genes in DM and TA muscles. Additionally, inflammation and apoptosis were assessed in these muscles by measuring the level of pro-inflammatory cytokines and apoptotic DNA degradation, respectively. Mice subjected to CLP developed severe sepsis. Limb muscle dysfunction was more severe than that of the DM, as indicated by a greater reductions in compound muscle action potential, strength, fatigue index, and muscle fiber cross-sectional area. TEM analysis revealed sepsis-induced intermyofibrillar mitochondrial fragmentation and accumulation of injury. Both muscles showed reduced levels of Opa1 and Mfn2 mRNA and protein, and increased levels of Fis1 mRNA and protein. Correlation analysis revealed significant associations between muscle strength and Opa1, Mfn2, and Opa1/Drp1 at 5 days post-sepsis. Surviving mice at 5 days showed persistent inflammation, injury, and apoptosis in both muscles, but were more pronounced in the TA muscle. Prolonged sepsis leads to an impairment in mitochondrial dynamics, resulting in skeletal muscle weakness and atrophy, which may be one of the possible mechanisms of sepsis-induced ICU-AW.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144540873","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypoxia-induced histone lactylation promotes pulmonary arterial smooth muscle cells proliferation in pulmonary hypertension.","authors":"Ai Chen, Zhihai Chen, Bangbang Huang, Guili Lian, Li Luo, Liangdi Xie","doi":"10.1007/s11010-025-05342-8","DOIUrl":"https://doi.org/10.1007/s11010-025-05342-8","url":null,"abstract":"<p><p>Pulmonary hypertension (PH) is characterized by pulmonary vascular remodeling and excessive proliferation of pulmonary artery smooth muscle cells (PASMCs). Glycolysis plays a crucial role in PH pathogenesis, but the epigenetic mechanisms linking glycolysis to PASMCs proliferation remain unclear. Histone lactylation, a novel post-translational modification derived from glycolytic lactate, may regulate PASMCs proliferation. Primary rat PASMCs were cultured under hypoxia and treated with sodium L-lactate (NaLa) to assess glycolytic activity and histone lactylation. RNA sequencing, RT-qPCR, and Western blotting identified differentially expressed genes (DEGs), while ChIP-qPCR evaluated histone lactylation enrichment at gene promoters. In vivo, a hypoxia-induced PH rat model was used to examine the effect of glycolysis inhibition using oxamate. Mendelian randomization (MR) analysis assessed the causal relationship between placental growth factor (PGF) and PH. Hypoxia and NaLa treatment significantly increased glycolytic activity, lactate production, and histone lactylation, promoting PASMCs proliferation. Transcriptomic analysis identified 157 DEGs, with five key genes (Gbe1, Pgf, Mt2A, Ythdf2 and Gys1) upregulated in response to histone lactylation. ChIP-qPCR confirmed H3K18la enrichment at their promoters. Glycolysis inhibition with oxamate effectively reduced histone lactylation, PASMCs proliferation, and vascular remodeling in hypoxic PH rats. MR analysis identified PGF as a causal factor contributing to PH risk, suggesting a potential therapeutic target. This study reveals that glycolysis-induced histone lactylation drives PASMCs proliferation and vascular remodeling in PH. Targeting lactate metabolism and histone lactylation may provide a novel therapeutic approach.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528917","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Liquid biopsy in breast cancer: clinical implications of ctDNA and CTCs in diagnosis, treatment and monitoring.","authors":"Muhammad Umer Khan, Arooj Khawar, Muhammad Ikram Ullah, Muhammad Adnan Shan, Luca Falzone, Massimo Libra, Graziana Spoto, Javad Sharifi-Rad, Daniela Calina","doi":"10.1007/s11010-025-05343-7","DOIUrl":"https://doi.org/10.1007/s11010-025-05343-7","url":null,"abstract":"<p><p>One of the leading causes of cancer-related death in women is breast cancer (BC). BC is a heterogeneous tumor. Although tissue biopsy is the gold standard for the diagnosis of BC, often tissue specimens are not informative enough about the tumor heterogeneity. The concept of \"Liquid Biopsy\" has recently emerged as a powerful clinical tool capable of better identifying mutations associated with the presence of primary or metastatic tumors. This article focuses on the clinical applications of circulating tumor cells (CTCs) and circulating tumor DNA (ctDNA) in breast cancer progression, relapse, diagnosis, and treatment response. The most important molecules analyzed in Liquid Biopsy are cfDNA, ctDNA, and CTCs. All these factors may be considered as non-invasive biomarkers for the early diagnosis of BC or to predict the progression and prognosis of patients, including BC recurrence and patients' treatment response. However, the clinical utility of ctDNA analysis and CTCs requires further investigation through better-designed studies to ensure their precision and diagnostic performance. In conclusion, liquid biopsy and ctDNA analysis demonstrate the potential to transform breast cancer management, with applications in screening, monitoring tumor progression, or response to treatment.</p>","PeriodicalId":18724,"journal":{"name":"Molecular and Cellular Biochemistry","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144528918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}