{"title":"An Occult Primary Thymic Mucosa-Associated Lymphoid Tissue Lymphoma With Sjögren's Syndrome Revealed by CXCR4 Targeted 68Ga-Pentixafor PET/CT","authors":"Xuehan Gao, Xingtong Peng, Rongxi Wang, Zhihong Qian, Xiaoyun Zhou, Zhaohui Zhu, Yeye Chen","doi":"10.1111/jcmm.70248","DOIUrl":"10.1111/jcmm.70248","url":null,"abstract":"<p>Mucosa-associated lymphoid tissue (MALT) lymphoma is an extranodal low-grade non-Hodgkin lymphoma that extremely rarely localises to the mediastinum. A 34-year-old female with chronic arthralgia, sicca and rash was found to have a well-demarcated mediastinal cystic mass with equivocal nodular enhancement within the cystic wall on chest CT during a workup for Sjögren's syndrome. Subsequent <sup>68</sup>Ga-Pentixafor-PET/CT revealed focal uptake increase within the cystic capsule. The patient underwent thoracoscopic resection of the mediastinal lesion, and pathology revealed MALT lymphoma in the wall of a thymic cyst. This case highlights that <sup>68</sup>Ga-pentixafor PET/CT could be valuable for the non-invasive detection of occult thymic MALT lymphoma.</p><p><b>Trial Registration:</b> ClinicalTrials.gov. (www.clinicaltrials.gov, NCT06086327)</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11783169/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065829","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Alessandro Broccoli, Marzia Del Re, Romano Danesi, Pier Luigi Zinzani
{"title":"Covalent Bruton tyrosine kinase inhibitors across generations: A focus on zanubrutinib","authors":"Alessandro Broccoli, Marzia Del Re, Romano Danesi, Pier Luigi Zinzani","doi":"10.1111/jcmm.70170","DOIUrl":"10.1111/jcmm.70170","url":null,"abstract":"<p>Bruton tyrosine kinase (BTK), the primary target of BTK inhibitors, is a key enzyme in the proliferation and survival pathway of neoplastic B-cells. BTK inhibitors are approved in many hematologic malignancies: chronic lymphocytic leukaemia, mantle cell lymphoma, marginal zone lymphoma, Waldenström macroglobulinaemia and follicular lymphoma. Second-generation BTK inhibitors display high target selectivity thus resulting in a reduction in off-target and off-tissue effects, better therapeutic index and improved tolerability. This paper summarizes the mechanisms of action of first and second generation BTK inhibitors and elucidates results in any disease setting, with a precise focus on zanubrutinib.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11783154/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065835","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Leonie Hartl, JanWillem Duitman, Hella L. Aberson, Jan Paul Medema, Maarten F. Bijlsma, C. Arnold Spek
{"title":"Identification of C/EBPδ-Modifying Compounds as Potential Anticancer Agents Using a High-Throughput Drug Screen","authors":"Leonie Hartl, JanWillem Duitman, Hella L. Aberson, Jan Paul Medema, Maarten F. Bijlsma, C. Arnold Spek","doi":"10.1111/jcmm.70287","DOIUrl":"10.1111/jcmm.70287","url":null,"abstract":"<p>CCAAT/enhancer-binding protein delta (C/EBPδ) has been shown to promote tumour growth, drug resistance and metastasis formation in some cancers, whereas we have shown that its re-expression limits the features of tumour progression in pancreatic ductal adenocarcinoma (PDAC). The pharmacological targeting—either activation or inhibition—of C/EBPδ may therefore harbour clinical relevance and is desirable for preclinical studies on C/EBPδ in different contexts. Regrettably, to date, only few molecules have been identified that modify C/EBPδ. Here, we present a high-throughput compound screen in conjunction with a novel eGFP reporter to identify further compounds that either increase or decrease C/EBPδ transcriptional activity. Of 1402 small molecule inhibitors, we identified a total of 22 potent inducers and 18 inhibitors of C/EBPδ-mediated eGFP fluorescence. Using pathway enrichment analysis, we found that, generally, inhibition of the cell cycle elicits an increase in C/EBPδ activity whereas PI3K/Akt/mTOR-targeting compounds reduce C/EBPδ activity. We confirmed the potential importance of cell cycle-mediated regulation of C/EBPδ by showing that four of the most potent C/EBPδ activators—R547, PHA793387, AZD5438 and AT7519, all multi-cyclin-dependent kinase (CDK) inhibitors—limited the clonal expansion of PDAC cells. Next to providing a valuable selection of C/EBPδ-modulating compounds for the use in preclinical studies, this report contributes to our understanding of the molecular regulatory mechanisms of C/EBPδ in general and in PDAC in particular.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11783153/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143065862","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Qi Shang, Xin Zhang, Yingyan Pu, Junjian Lin, Peng Ma, Yuchen Pan, Ming Zhao, Dingya Sun, Li Cao
{"title":"LPCAT1, the Enzyme Responsible for Converting LPC to PC, Promotes OPC Differentiation In Vitro","authors":"Qi Shang, Xin Zhang, Yingyan Pu, Junjian Lin, Peng Ma, Yuchen Pan, Ming Zhao, Dingya Sun, Li Cao","doi":"10.1111/jcmm.70387","DOIUrl":"10.1111/jcmm.70387","url":null,"abstract":"<p>Myelin is the key structure for high-speed information transmission and is formed by oligodendrocytes (OLs) which are differentiated from oligodendrocyte precursor cells (OPCs) in the central nervous system. Lipid is the main component of myelin and the role of lipid metabolism-related molecules in myelination attach increasing attention. Lysophosphatidylcholine acyltransferase 1 (LPCAT1) mediates the conversion of lysophosphatidylcholine (LPC) to phosphatidylcholine (PC), and its role in myelination draws our interest as LPC is a classical demyelination inducer and PC is a major component of myelin. In this work, LPCAT1 is found expressed in the oligodendrocyte lineage cells during myelination. In vitro experiments showed that the expression level of LPCAT1 gradually increased along with the differentiation process from OPCs to OLs, and over-expression and interference experiments showed that LPCAT1 promoted OPCs differentiation without affecting their proliferation or apoptosis. Mechanistically, the undertaker of LPCAT1's pro-differentiation role is not PC, but the phosphorylated mTOR which is a key regulator in OPCs differentiation. RNA sequencing analysis showed LPCAT1 promoted the expression of ZBTB20 which is an important transcription factor related to lipid metabolism and regulates mTOR phosphorylation. In vivo, complex myelin tomacula involving multiple axons was formed after conditionally knocking out LPCAT1 in oligodendrocyte lineage cells, but no obvious myelin thickness abnormalities were observed. Our results indicate that LPCAT1 is an important regulator of myelination, and lipid metabolism-related molecules may be new valuable targets for the treatment of diseases with myelin abnormalities.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11775935/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059169","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"AQP3 Influences Unexplained Recurrent Abortion by Regulating Trophoblast Cell Migration and Invasion via the METTL14/IGF2BP1/AQP3/PI3K/AKT Pathway","authors":"Yingqi Nong, Qiyi Zhai, Wenjuan Liu, Jiahui Wei, Zhaoyi Wang, Xiaoyin Lv, Zitao Li, Xiqian Zhang, Fenghua Liu","doi":"10.1111/jcmm.70325","DOIUrl":"10.1111/jcmm.70325","url":null,"abstract":"<p>Reduced trophoblast migration and invasion contribute to unexplained recurrent spontaneous abortion (URSA). Aquaporin 3 (AQP3) plays a crucial role in facilitating trophoblast migration and invasion during early pregnancy through fetal-maternal crosstalk. This study aimed to comprehensively investigate the mechanism involving AQP3 and its modulatory effects on human extravillous trophoblast (HTR-8/SVneo cells) migration and invasion. AQP3 and IGF2BP1 expression was analysed using immunohistochemistry and quantitative real-time polymerase chain reaction. The AQP3-associated molecular mechanisms were explored using western blot, meRIP, RNA stability assays and RNA-protein pull-down experiments. Furthermore, the role of IGF2BP1 in HTR-8/SVneo cells was assessed using transwell assays. AQP3 and IGF2BP1 expression was lower in the chorionic villi samples of the URSA group than in those of the control group. AQP3 was involved in regulating the activation of the PI3K/AKT signalling pathway. Additionally, METTL14 interacted with AQP3 mRNA, thereby influencing its stability. Furthermore, AQP3 mRNA bound to the IGF2BP1 protein, and IGF2BP1 knockdown resulted in reduced AQP3 mRNA stability and impaired trophoblast migration and invasion. METTL14 and IGF2BP1 stabilise AQP3 mRNA expression by mediating m6A, thereby facilitating HTR-8/SVneo cell migration and invasion via the PI3K/AKT signalling pathway. Targeting AQP3 could potentially contribute to strategies aimed at mitigating URSA development.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11775936/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059158","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Temozolomide-Promoted MGMT Transcription Contributes to Chemoresistance by Activating the ERK Signalling Pathway in Malignant Melanoma","authors":"Meiyi Deng, Bingjie Ren, Jing Zhao, Xia Guo, Yuanyuan Yang, Huiling Shi, Xuyu Bian, Mengyao Wu, Caihua Xu, Min Tao, Rongrui Liang, Qiang Li","doi":"10.1111/jcmm.70380","DOIUrl":"10.1111/jcmm.70380","url":null,"abstract":"<p>Tumour cells possess a multitude of chemoresistance mechanisms, which could plausibly contribute to the ineffectiveness of chemotherapy. O<sup>6</sup>-methylguanine-DNA methyltransferase (MGMT) is an important effector protein associated with Temozolomide (TMZ) resistance in various tumours. To some extent, the expression level of MGMT determines the sensitivity of cells to TMZ, but the mechanism of its expression regulation has not been fully elucidated. Cultured malignant melanoma cell lines A375 and Sk-MEL28 were employed. A luciferase assay was used to detect the transcriptional activity of the MGMT promoter. Western blotting was used to compare the expression levels of phosphorylated ERK1/2 (P-ERK1/2) after TMZ treatment. Immunofluorescent staining was used to detect TMZ-induced DNA damage protein levels. The sensitivity of melanoma cells to TMZ was detected by MTT assay and animal experiments. The expression of MGMT mRNA was tested by Quantitative real-time PCR (RT-qPCR). Flow cytometry was used to measure the apoptosis of TMZ-treated cells. TMZ enhanced the transcription of MGMT through activating the ERK pathway. ERK inhibitors U0126 and vemurafenib (vMF) inhibited the TMZ induced transcription of MGMT. The expression of MGMT and p-ERK1/2 was closely related in human MM tissues. vMF increased the sensitivity of melanoma (MM) to TMZ in vitro and in vivo through downregulating MGMT and promoting the TMZ induced DNA damage in MM. TMZ-promoted MGMT transcription contributed to instinctive chemoresistance by activating the ERK signalling pathway in malignant melanoma. Our study indicates that the use of the ERK inhibitor in combination with TMZ could potentially enhance the effectiveness of clinical treatment for malignant melanoma.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11773391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143052712","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"CN7:1h Alleviates Inflammation, Apoptosis and Extracellular Matrix Degradation in Osteoarthritis by Modulating the NF-κB and mTOR Pathways","authors":"Chih-Chien Wang, Jeng-Wei Lu, Ya-Wun Wu, You-Hsiang Chu, Yi-Jung Ho, Feng-Cheng Liu, Yi-Jen Peng","doi":"10.1111/jcmm.70368","DOIUrl":"10.1111/jcmm.70368","url":null,"abstract":"<p>Osteoarthritis (OA) is a degenerative joint disease with a complex aetiology, which includes inflammation, cellular growth dysregulation and extracellular matrix (ECM) degradation. This study investigated the therapeutic potential of a small-molecule compound, 2-amino-4-(3,4,5-trimethoxyphenyl)-4H-benzo[h]chromene-3-carbonitrile (CN7:1h) in modulating these critical biochemical pathways in OA. Cellular models and rat models of OA were used to explore the impact of CN7:1h on the nuclear factor kappa light chain enhancer of activated B cells (NF-κB) and mechanistic target of rapamycin (mTOR) signalling pathways. Parameters such as autophagy, apoptosis and ECM preservation were evaluated. CN7:1h demonstrated a non-cytotoxic profile at a concentration as high as 140 μM as confirmed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay. At a concentration of 5 μM, CN7:1h was shown to inhibit the activation of NF-κB and mTOR pathways. CN7:1h was also shown to promote autophagy and reduce apoptosis in cellular models. In rat models, CN7:1h facilitated cartilage repair and demonstrating the therapeutic efficacy of this compound. In conclusion, CN7:1h is a promising bioactive compound for the modulation of key biochemical pathways with therapeutic benefits in degenerative conditions, such as OA. Its high bioavailability and lack of cytotoxicity make CN7:1h an excellent candidate for further research aimed at clinical applications.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 3","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774621/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143059162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Neonatal Sevoflurane Exposure Exerts Sex-Specific Effects on Cognitive Function via C3- and TLR4-Related M1/M2 Microglial Cell Polarisation in Rats","authors":"Jiangxia Cheng, Yuxin He, Zhuo Wang, Zhengchao Wang, Xiaohong Peng, Liangcheng Zhang","doi":"10.1111/jcmm.70311","DOIUrl":"10.1111/jcmm.70311","url":null,"abstract":"<p>In this study, we aimed to explore the sex-specific effects and mechanisms of sevoflurane exposure on the neural development of pubertal rats on the basis of M1/M2 microglial cell polarisation and related signalling pathways. A total of 48 rat pups (24 males and 24 females) were assigned to the 0- or 2-h sevoflurane exposure group on the seventh day after birth. The Morris water maze (MWM) test was subsequently conducted on the 32nd to 38th days after birth. M1/M2 microglial cell polarisation, C3 and TLR4 expression, and synapse growth were analysed within specific brain zones by immunofluorescence after the MWM test. We found that the negative effects caused by sevoflurane exposure were weaker in female rats than in male rats and had less influence on spatial memory. Sevoflurane exposure has opposite effects on microglial M1 polarisation in the different sexes but can promote M2 polarisation, with more obvious effects seen in female rats. In addition, sevoflurane exposure had bidirectional effects on C3 expression in different zones, while it clearly downregulated C3 expression in female rats. Moreover, sevoflurane decreased TLR4 expression in the hippocampus, whereas female rats exhibited better resistance, especially in the dentate gyrus. Compared with male rats, female rats were more resistant to the synaptic reduction effect of sevoflurane exposure. In conclusion, we found that neonatal sevoflurane exposure could exhibit sex-specific effects via the regulation of C3- and TLR4-related microglial cell polarisation. In addition, subregional regulation in the hippocampus might also contribute to its sex-specific effects.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 2","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11774238/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143052708","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Identification and Validation of a m6A-Related Long Noncoding RNA Prognostic Model in Colorectal Cancer","authors":"Peng Jiang, Mingfei Chu, Yu Liang","doi":"10.1111/jcmm.70376","DOIUrl":"10.1111/jcmm.70376","url":null,"abstract":"<p>Accumulating research indicates that N6-methyladenosine (m6A) modification plays a pivotal role in colorectal cancer (CRC). Hence, investigating the m6A-related long noncoding RNAs (lncRNAs) significantly improves therapeutic strategies and prognostic assessments. This study aimed to develop and validate a prognostic model based on m6A-related lncRNAs to improve the prediction of clinical outcomes and identify potential immunological mechanisms in CRC. We obtained high-throughput CRC data from The Cancer Genome Atlas to identify a prognostic model based on m6A-related lncRNAs. Then, the model was constructed and validated through LASSO analysis and Cox regression using R software. The clinical applicability was enhanced by developing a nomogram. We further conducted experiments to reveal the biological function of LINC00543. The prognostic model based on eight m6A-related lncRNAs exhibited impressive accuracy, achieving an area under the receiver-operating curve value of 0.753, 0.682 and 0.706 for predictions after 1, 3 and 5 years, respectively. The Kaplan–Meier analysis confirmed the consistency of the model across different pathological characteristics, with a high-risk group showing a poorer prognosis. Furthermore, the model was linked to immune function, particularly the type I interferon response, through gene set enrichment analysis and experimental validation. Our study presented a m6A-related lncRNA prognostic model for CRC with potential clinical utility. The model not only provided improved accuracy over traditional staging but also offered insights into the immunological mechanisms of CRC, facilitating personalised medicine approaches.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 2","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11770481/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046845","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Integrative Machine Learning of Glioma and Coronary Artery Disease Reveals Key Tumour Immunological Links","authors":"Youfu He, Ganhua You, Yu Zhou, Liqiong Ai, Wei Liu, Xuantong Meng, Qiang Wu","doi":"10.1111/jcmm.70377","DOIUrl":"10.1111/jcmm.70377","url":null,"abstract":"<p>It is critical to appreciate the role of the tumour-associated microenvironment (TME) in developing strategies for the effective therapy of cancer, as it is an important factor that determines the evolution and treatment response of tumours. This work combines machine learning and single-cell RNA sequencing (scRNA-seq) to explore the glioma tumour microenvironment's TME. With the help of genome-wide association studies (GWAS) and Mendelian randomization (MR), we found genetic variants associated with TME elements that affect cancer and cardiovascular disease outcomes. Using machine learning techniques high dimensional data was analysed to obtain new molecular sub-types and biomarkers that are important for prognosis and treatment response. F3 was identified as a top regulator and revealed potential angiogenic and immunogenic characteristics within the TME that could be harnessed in immunotherapy. These results demonstrate the potential of machine-learning approaches in identifying and dissecting TME heterogeneity and informing treatment in precision oncology. This work proposes improving the immunotherapeutic response through targeted modulation of relevant cellular and molecular interactions.</p>","PeriodicalId":101321,"journal":{"name":"JOURNAL OF CELLULAR AND MOLECULAR MEDICINE","volume":"29 2","pages":""},"PeriodicalIF":5.3,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11770474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143046846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}