Cell Reports MedicinePub Date : 2025-01-21Epub Date: 2025-01-06DOI: 10.1016/j.xcrm.2024.101885
Yulia Chulanova, Dor Breier, Dan Peer
{"title":"Delivery of genetic medicines for muscular dystrophies.","authors":"Yulia Chulanova, Dor Breier, Dan Peer","doi":"10.1016/j.xcrm.2024.101885","DOIUrl":"https://doi.org/10.1016/j.xcrm.2024.101885","url":null,"abstract":"<p><p>Muscular dystrophies are a group of heterogenic disorders characterized by progressive muscle weakness, the most common of them being Duchenne muscular dystrophy (DMD). Muscular dystrophies are caused by mutations in over 50 distinct genes, and many of them are caused by different genetic mechanisms. Currently, none of these diseases have a cure. However, in recent years, significant progress has been made to correct the underlying genetic cause. The clinical development of adeno-associated viral vector-based therapies has simultaneously produced excitement and disappointment in the research community due to the moderate effect, making it clear that new methods of muscle delivery have to be created. Herein, we review the main characteristics of major muscular dystrophies and outline various muscle-targeted delivery methods being explored for genetic medicines.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":"6 1","pages":"101885"},"PeriodicalIF":11.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022353","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Reports MedicinePub Date : 2025-01-21Epub Date: 2024-12-20DOI: 10.1016/j.xcrm.2024.101878
Marjolein M G Kes, Francisco Morales-Rodriguez, Esther A Zaal, Terezinha de Souza, Natalie Proost, Marieke van de Ven, Marry M van den Heuvel-Eibrink, Jeroen W A Jansen, Celia R Berkers, Jarno Drost
{"title":"Metabolic profiling of patient-derived organoids reveals nucleotide synthesis as a metabolic vulnerability in malignant rhabdoid tumors.","authors":"Marjolein M G Kes, Francisco Morales-Rodriguez, Esther A Zaal, Terezinha de Souza, Natalie Proost, Marieke van de Ven, Marry M van den Heuvel-Eibrink, Jeroen W A Jansen, Celia R Berkers, Jarno Drost","doi":"10.1016/j.xcrm.2024.101878","DOIUrl":"10.1016/j.xcrm.2024.101878","url":null,"abstract":"<p><p>Malignant rhabdoid tumor (MRT) is one of the most aggressive childhood cancers for which no effective treatment options are available. Reprogramming of cellular metabolism is an important hallmark of cancer, with various metabolism-based drugs being approved as a cancer treatment. In this study, we use patient-derived tumor organoids (tumoroids) to map the metabolic landscape of several pediatric cancers. Combining gene expression analyses and metabolite profiling using mass spectrometry, we find nucleotide biosynthesis to be a particular vulnerability of MRT. Treatment of MRT tumoroids with de novo nucleotide synthesis inhibitors methotrexate (MTX) and BAY-2402234 lowers nucleotide levels in MRT tumoroids and induces apoptosis. Lastly, we demonstrate in vivo efficacy of MTX in MRT patient-derived xenograft (PDX) mouse models. Our study reveals nucleotide biosynthesis as an MRT-specific metabolic vulnerability, which can ultimately lead to better treatment options for children suffering from this lethal pediatric malignancy.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"101878"},"PeriodicalIF":11.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871538","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Hormone therapy enhances anti-PD1 efficacy in premenopausal estrogen receptor-positive and HER2-negative advanced breast cancer.","authors":"I-Chun Chen, Ching-Hung Lin, Dwan-Ying Chang, Tom Wei-Wu Chen, Ming-Yang Wang, Wei-Li Ma, Yi-Ting Lin, Shu-Min Huang, Chia-Lang Hsu, Yen-Shen Lu","doi":"10.1016/j.xcrm.2024.101879","DOIUrl":"10.1016/j.xcrm.2024.101879","url":null,"abstract":"<p><p>The efficacy of immunotherapy for estrogen receptor-positive/HER2-negative (ER+/HER2-) metastatic breast cancer (MBC) has not been proven. We conduct a phase 1b/2 trial to assess the efficacy of combining pembrolizumab (anti-PD1 antibody), exemestane (nonsteroidal aromatase inhibitor), and leuprolide (gonadotropin-releasing hormone agonist) for 15 patients with premenopausal ER+/HER2- MBC who had failed one to two lines of hormone therapy (HT) without chemotherapy. The primary endpoint of progression-free survival rate at 8 months (i.e., 64.3%) is achieved. Moreover, 5 of the 14 evaluable subjects exhibited partial responses (overall response rate = 35.7%). The combination of anti-PD1 antibody and anti-hormone therapy is associated with an enhanced immunoreactive microenvironment influencing treatment efficacy, as observed in pre- and post-treatment tumor samples through NanoString analysis. Post-treatment tumors are associated with increased immune response and immune cells. The findings indicate that combining HT with anti-PD1 antibody is a promising treatment strategy for patients with premenopausal ER+/HER2- MBC. This study was registered at ClinicalTrials.gov (NCT02990845).</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"101879"},"PeriodicalIF":11.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892314","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"High-alcohol-producing Klebsiella pneumoniae aggravates lung injury by affecting neutrophils and the airway epithelium.","authors":"Jinghua Cui, Ziying Xu, Zihui Yu, Qun Zhang, Shiyu Liu, Bing Du, Lin Gan, Chao Yan, Guanhua Xue, Junxia Feng, Zheng Fan, Tongtong Fu, Yanling Feng, Hanqing Zhao, Zanbo Ding, Xiaoran Li, Rui Zhang, Xiaohu Cui, Ziyan Tian, Kewu Huang, Wenjun Wang, Yu Bai, Haijian Zhou, Ying Sun, Xiaopeng Yang, Meng Wan, Yuehua Ke, Jing Yuan","doi":"10.1016/j.xcrm.2024.101886","DOIUrl":"10.1016/j.xcrm.2024.101886","url":null,"abstract":"<p><p>We have previously reported that high-alcohol-producing Klebsiella pneumoniae (HiAlc Kpn) in the gut can cause endo-alcoholic fatty liver disease. Here, we discover that 91.2% of Kpn isolates from pulmonary disease samples also produce excess ethanol, which may be associated with respiratory disease severity. To further explore the potential mechanism, a murine model is established with high-dose bacteria. Kpn stimulates granular neutrophils (G0), subsequently transforming them into phagocytic neutrophils (G1). HiAlc Kpn also causes dysfunction of pyrimidine metabolism, leading to neutrophil apoptosis. These changes inhibit phagocytosis of neutrophils and possibly suppress inflammasome-dependent innate immunity. In a persistent infective murine model, HiAlc Kpn induces lung fibrosis and production of reactive oxygen species (ROS), possibly affecting epithelial cell apoptosis and lung function. The results suggest that the subtype of neutrophil is a potential biomarker for the severity of lung injury caused by HiAlc Kpn.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"101886"},"PeriodicalIF":11.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142925953","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Phase 1/2 trial of brogidirsen: Dual-targeting antisense oligonucleotides for exon 44 skipping in Duchenne muscular dystrophy.","authors":"Hirofumi Komaki, Eri Takeshita, Katsuhiko Kunitake, Takami Ishizuka, Yuko Shimizu-Motohashi, Akihiko Ishiyama, Masayuki Sasaki, Chihiro Yonee, Shinsuke Maruyama, Eisuke Hida, Yoshitsugu Aoki","doi":"10.1016/j.xcrm.2024.101901","DOIUrl":"10.1016/j.xcrm.2024.101901","url":null,"abstract":"<p><p>Duchenne muscular dystrophy (DMD) is a severe muscle disorder caused by mutations in the DMD gene, leading to dystrophin deficiency. Antisense oligonucleotide (ASO)-mediated exon skipping offers potential by partially restoring dystrophin, though current therapies remain mutation specific with limited efficacy. To overcome those limitations, we developed brogidirsen, a dual-targeting ASO composed of two directly connected 12-mer sequences targeting exon 44 using phosphorodiamidate morpholino oligomers. An open-label, dose-escalation, phase 1/2 trial assessed the safety, pharmacokinetics, and efficacy of brogidirsen in six ambulant patients with DMD amenable to exon 44 skipping. Following dose escalation, extended 24-week treatment with 40 mg/kg and 80 mg/kg yielded dose-dependent increases in dystrophin (16.63% and 24.47% of normal). Functional assessments indicated motor stabilization, and plasma proteomics revealed reductions in peptidyl arginine deiminase 2 (PADI2), titin (TTN), and myomesin 2 (MYOM2), highlighting potential biomarkers. Brogidirsen's efficacy was supported in vitro using urine-derived cells from patients with DMD. These promising results warrant a subsequent trial for DMD. This study was registered at ClinicalTrials.gov (NCT04129294).</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"101901"},"PeriodicalIF":11.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142964133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Reports MedicinePub Date : 2025-01-21Epub Date: 2025-01-10DOI: 10.1016/j.xcrm.2024.101900
Xue Qian Wu, Fan Ying, Katherine Po Sin Chung, Carmen Oi Ning Leung, Rainbow Wing Hei Leung, Karl Kam Hei So, Martina Mang Leng Lei, Wing Ki Chau, Man Tong, Jun Yu, Dai Wei, William Chi Shing Tai, Stephanie Ma, Yin Ying Lu, Terence Kin Wah Lee
{"title":"Intestinal Akkermansia muciniphila complements the efficacy of PD1 therapy in MAFLD-related hepatocellular carcinoma.","authors":"Xue Qian Wu, Fan Ying, Katherine Po Sin Chung, Carmen Oi Ning Leung, Rainbow Wing Hei Leung, Karl Kam Hei So, Martina Mang Leng Lei, Wing Ki Chau, Man Tong, Jun Yu, Dai Wei, William Chi Shing Tai, Stephanie Ma, Yin Ying Lu, Terence Kin Wah Lee","doi":"10.1016/j.xcrm.2024.101900","DOIUrl":"10.1016/j.xcrm.2024.101900","url":null,"abstract":"<p><p>Immune checkpoint inhibitors are not effective for metabolic dysfunction-associated fatty liver disease (MAFLD)-hepatocellular carcinoma (HCC) patients, and identifying the key gut microbiota that contributes to immune resistance in these patients is crucial. Analysis using 16S rRNA sequencing reveals a decrease in Akkermansia muciniphila (Akk) during MAFLD-promoted HCC development. Administration of Akk ameliorates liver steatosis and effectively attenuates the tumor growth in orthotopic MAFLD-HCC mouse models. Akk repairs the intestinal lining, with a decrease in the serum lipopolysaccharide (LPS) and bile acid metabolites, along with decrease in the populations of monocytic myeloid-derived suppressor cells (m-MDSCs) and M2 macrophages. Akk in combination with PD1 treatment exerts maximal growth-suppressive effect in multiple MAFLD-HCC mouse models with increased infiltration and activation of T cells. Clinically, low Akk levels are correlated with PD1 resistance and poor progression-free survival. In conclusion, Akk is involved in the immune resistance of MAFLD-HCC and serves as a predictive biomarker for PD1 response in HCC.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"101900"},"PeriodicalIF":11.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969678","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Reports MedicinePub Date : 2025-01-21Epub Date: 2025-01-13DOI: 10.1016/j.xcrm.2024.101917
Shuhong Sun, Chao Wang, Junyan Hu, Pei Zhao, Xi Wang, William E Balch
{"title":"Spatial covariance reveals isothiocyanate natural products adjust redox stress to restore function in alpha-1-antitrypsin deficiency.","authors":"Shuhong Sun, Chao Wang, Junyan Hu, Pei Zhao, Xi Wang, William E Balch","doi":"10.1016/j.xcrm.2024.101917","DOIUrl":"10.1016/j.xcrm.2024.101917","url":null,"abstract":"<p><p>Alpha-1 antitrypsin (AAT) deficiency (AATD) is a monogenic disease caused by misfolding of AAT variants resulting in gain-of-toxic aggregation in the liver and loss of monomer activity in the lung leading to chronic obstructive pulmonary disease (COPD). Using high-throughput screening, we discovered a bioactive natural product, phenethyl isothiocyanate (PEITC), highly enriched in cruciferous vegetables, including watercress and broccoli, which improves the level of monomer secretion and neutrophil elastase (NE) inhibitory activity of AAT-Z through the endoplasmic reticulum (ER) redox sensor protein disulfide isomerase (PDI) A4 (PDIA4). The intracellular polymer burden of AAT-Z can be managed by combination treatment of PEITC and an autophagy activator. Using Gaussian process (GP)-based spatial covariance (SCV) (GP-SCV) machine learning to map on a residue-by-residue basis at atomic resolution all variants in the worldwide AATD clinical population, we reveal a global rescue of monomer secretion and NE inhibitory activity for most variants triggering disease. We present a proof of concept that GP-SCV mapping of restoration of AAT variant function serves as a standard model to discover natural products such as the anti-oxidant PEITC that could potentially impact the redox/inflammatory environment of the ER to provide a nutraceutical approach to help minimize disease in AATD patients.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"101917"},"PeriodicalIF":11.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The direct and indirect inhibition of proinflammatory adipose tissue macrophages by acarbose in diet-induced obesity.","authors":"Xiaohui Li, Shimeng Zheng, Haozhe Xu, Zihan Zhang, Xiaotong Han, Yunxiong Wei, Hua Jin, Xiaonan Du, Hufeng Xu, Mengyi Li, Zhongtao Zhang, Songlin Wang, Guangyong Sun, Dong Zhang","doi":"10.1016/j.xcrm.2024.101883","DOIUrl":"10.1016/j.xcrm.2024.101883","url":null,"abstract":"<p><p>Inflammation is critical for obesity and obesity-induced insulin resistance (IR). In this study, we reveal the function and mechanism of acarbose on adipose tissue macrophage (ATM)-mediated inflammation in obesity and obesity-induced IR. First, acarbose enhances the abundance of propionic acid-producing Parasutterella, therefore indirectly inhibiting the survival and proinflammatory function of M1-like ATMs via GPR43. Most interestingly, acarbose can directly inhibit M1-like ATM-mediated inflammation through GPR120. Diet-induced obese mice exhibit nitrobenzoxadiazoles (NBD) fluorescence-labeled ATMs, but lean mice that also orally received NBD fluorescence-labeled acarbose do not exhibit NBD fluorescence-labeled ATMs. This direct inhibition of macrophages by acarbose is validated in mouse and human macrophages in vitro. In conclusion, our study reveals that acarbose directly and indirectly inhibits proinflammatory macrophage phenotype, which contributes to the improvement of obesity and obesity-induced IR. The understanding of the immune regulatory effects of acarbose may extend its potential for further therapeutic applications.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"101883"},"PeriodicalIF":11.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142913625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Reports MedicinePub Date : 2025-01-21Epub Date: 2024-12-19DOI: 10.1016/j.xcrm.2024.101876
Yuanyuan Peng, Aidi Lin, Meng Wang, Tian Lin, Linna Liu, Jianhua Wu, Ke Zou, Tingkun Shi, Lixia Feng, Zhen Liang, Tao Li, Dan Liang, Shanshan Yu, Dawei Sun, Jing Luo, Ling Gao, Xinjian Chen, Ching-Yu Cheng, Huazhu Fu, Haoyu Chen
{"title":"Enhancing AI reliability: A foundation model with uncertainty estimation for optical coherence tomography-based retinal disease diagnosis.","authors":"Yuanyuan Peng, Aidi Lin, Meng Wang, Tian Lin, Linna Liu, Jianhua Wu, Ke Zou, Tingkun Shi, Lixia Feng, Zhen Liang, Tao Li, Dan Liang, Shanshan Yu, Dawei Sun, Jing Luo, Ling Gao, Xinjian Chen, Ching-Yu Cheng, Huazhu Fu, Haoyu Chen","doi":"10.1016/j.xcrm.2024.101876","DOIUrl":"10.1016/j.xcrm.2024.101876","url":null,"abstract":"<p><p>Inability to express the confidence level and detect unseen disease classes limits the clinical implementation of artificial intelligence in the real world. We develop a foundation model with uncertainty estimation (FMUE) to detect 16 retinal conditions on optical coherence tomography (OCT). In the internal test set, FMUE achieves a higher F1 score of 95.74% than other state-of-the-art algorithms (92.03%-93.66%) and improves to 97.44% with threshold strategy. The model achieves similar excellent performance on two external test sets from the same and different OCT machines. In human-model comparison, FMUE achieves a higher F1 score of 96.30% than retinal experts (86.95%, p = 0.004), senior doctors (82.71%, p < 0.001), junior doctors (66.55%, p < 0.001), and generative pretrained transformer 4 with vision (GPT-4V) (32.39%, p < 0.001). Besides, FMUE predicts high uncertainty scores for >85% images of non-target-category diseases or with low quality to prompt manual checks and prevent misdiagnosis. Our FMUE provides a trustworthy method for automatic retinal anomaly detection in a clinical open-set environment.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"101876"},"PeriodicalIF":11.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142871536","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Cell Reports MedicinePub Date : 2025-01-21Epub Date: 2025-01-13DOI: 10.1016/j.xcrm.2024.101915
Yichen Liu, Qingyan Sun, Jingwen Guo, Li Yan, Yue Yan, Yiting Gong, Jiayi Lin, Hu Yuan, Jinmei Jin, Bei Wang, Hongzhuan Chen, Lijun Zhang, Weidong Zhang, Xin Luan
{"title":"Dual ferroptosis induction in N2-TANs and TNBC cells via FTH1 targeting: A therapeutic strategy for triple-negative breast cancer.","authors":"Yichen Liu, Qingyan Sun, Jingwen Guo, Li Yan, Yue Yan, Yiting Gong, Jiayi Lin, Hu Yuan, Jinmei Jin, Bei Wang, Hongzhuan Chen, Lijun Zhang, Weidong Zhang, Xin Luan","doi":"10.1016/j.xcrm.2024.101915","DOIUrl":"10.1016/j.xcrm.2024.101915","url":null,"abstract":"<p><p>Tumor-associated neutrophils (TANs) play a critical role in the progression and prognosis of triple-negative breast cancer (TNBC), with N2-type TANs known for their pro-tumor characteristics. This study introduces CT-1, a derivative of cryptotanshinone that effectively suppresses TNBC growth while selectively reducing the proportion of N2-type TANs within tumor tissue. Notably, CT-1 induces simultaneous ferroptosis in both N2-type TANs and TNBC cells, a dual mechanism that enhances its therapeutic efficacy. The study identifies ferritin heavy chain 1 (FTH1), a key protein in iron metabolism, as the direct target of CT-1. By targeting FTH1, CT-1 facilitates the interaction between NCOA4 and ferritin, triggering ferritinophagy-mediated ferroptosis. These findings position CT-1 as a promising therapeutic agent, offering a strategy to combat TNBC by inducing ferroptosis in both N2-type TANs and cancer cells. This approach underscores the potential of FTH1 as a therapeutic target for treating TNBC.</p>","PeriodicalId":9822,"journal":{"name":"Cell Reports Medicine","volume":" ","pages":"101915"},"PeriodicalIF":11.7,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982868","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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