Journal of Clinical Investigation最新文献_第10页

Lysyl hydroxylase 2 glucosylates collagen VI to drive lung cancer progression. 赖基羟化酶2葡萄糖化胶原VI驱动肺癌进展。

IF 13.3 1区医学

Journal of Clinical Investigation Pub Date : 2025-04-01 DOI: 10.1172/JCI189197

Shike Wang, Houfu Guo, Reo Fukushima, Masahiko Terajima, Min Liu, Guan-Yu Xiao, Lenka Koudelková, Chao Wu, Xin Liu, Jiang Yu, Emma Burris, Jun Xu, Alvise Schiavinato, William K Russell, Mitsuo Yamauchi, Xiaochao Tan, Jonathan M Kurie

{"title":"Lysyl hydroxylase 2 glucosylates collagen VI to drive lung cancer progression.","authors":"Shike Wang, Houfu Guo, Reo Fukushima, Masahiko Terajima, Min Liu, Guan-Yu Xiao, Lenka Koudelková, Chao Wu, Xin Liu, Jiang Yu, Emma Burris, Jun Xu, Alvise Schiavinato, William K Russell, Mitsuo Yamauchi, Xiaochao Tan, Jonathan M Kurie","doi":"10.1172/JCI189197","DOIUrl":"10.1172/JCI189197","url":null,"abstract":"Lysyl hydroxylase 2 (LH2) is highly expressed in multiple tumor types and accelerates disease progression by hydroxylating lysine residues on fibrillar collagen telopeptides to generate stable collagen cross links in tumor stroma. Here, we show that a galactosylhydroxylysyl glucosyltransferase (GGT) domain on LH2-modified type-VI collagen (Col6) to promote lung adenocarcinoma (LUAD) growth and metastasis. In tumors generated by LUAD cells lacking LH2 GGT domain activity, stroma was less stiff, and stable types of collagen cross links were reduced. Mass spectrometric analysis of total and glycosylated peptides in parental and GGT-inactive tumor samples identified Col6 chain α3 (Col6a3), a component of the Col6 heterotrimeric molecule, as a candidate LH2 substrate. In gain- and loss-of-function studies, high Col6a3 levels increased tumor growth and metastatic activity and enhanced the proliferative, migratory, and invasive activities of LUAD cells. LH2 coimmunoprecipitated with Col6a3, and LH2 glucosylated Col6 in an in vitro reaction. Glucosylation increased the integrin-binding and promigratory activities of Col6 in LUAD cells. Col6a3 K2049 was deglucosylated in GGT-inactive tumor samples, and mutagenesis of Col6a3 K2049 phenocopied Col6a3 deficiency or LH2 GGT domain inactivation in LUAD cells. Thus, LH2 glucosylates Col6 to drive LUAD progression. These findings show that the GGT domain of LH2 is protumorigenic, identify Col6 as a candidate effector, and provide a rationale to develop pharmacological strategies that target LH2's GGT domain in cancer cells.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":"135 7","pages":""},"PeriodicalIF":13.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11957695/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ACAT1 regulates tertiary lymphoid structures and correlates with immunotherapy response in non-small cell lung cancer. ACAT1调节三级淋巴样结构并与非小细胞肺癌的免疫治疗反应相关。

IF 13.3 1区医学

Journal of Clinical Investigation Pub Date : 2025-04-01 DOI: 10.1172/JCI181517

Mengxia Jiao, Yifan Guo, Hongyu Zhang, Haoyu Wen, Peng Chen, Zhiqiang Wang, Baichao Yu, Kameina Zhuma, Yuchen Zhang, Jingbo Qie, Yun Xing, Pengyuan Zhao, Zihe Pan, Luman Wang, Dan Zhang, Fei Li, Yijiu Ren, Chang Chen, Yiwei Chu, Jie Gu, Ronghua Liu

{"title":"ACAT1 regulates tertiary lymphoid structures and correlates with immunotherapy response in non-small cell lung cancer.","authors":"Mengxia Jiao, Yifan Guo, Hongyu Zhang, Haoyu Wen, Peng Chen, Zhiqiang Wang, Baichao Yu, Kameina Zhuma, Yuchen Zhang, Jingbo Qie, Yun Xing, Pengyuan Zhao, Zihe Pan, Luman Wang, Dan Zhang, Fei Li, Yijiu Ren, Chang Chen, Yiwei Chu, Jie Gu, Ronghua Liu","doi":"10.1172/JCI181517","DOIUrl":"10.1172/JCI181517","url":null,"abstract":"Tertiary lymphoid structures (TLS) in the tumor microenvironment (TME) are emerging solid-tumor indicators of prognosis and response to immunotherapy. Considering that tumorigenesis requires metabolic reprogramming and subsequent TME remodeling, the discovery of TLS metabolic regulators is expected to produce immunotherapeutic targets. To identify such metabolic regulators, we constructed a metabolism-focused sgRNA library and performed an in vivo CRISPR screening in an orthotopic lung tumor mouse model. Combined with The Cancer Genome Atlas database analysis of TLS-related metabolic hub genes, we found that the loss of Acat1 in tumor cells sensitized tumors to anti-PD1 treatment, accompanied by increased TLS in the TME. Mechanistic studies revealed that ACAT1 resulted in mitochondrial protein hypersuccinylation in lung tumor cells and subsequently enhanced mitochondrial oxidative metabolism, which impeded TLS formation. Elimination of ROS by NAC or Acat1 knockdown promoted B cell aggregation and TLS construction. Consistently, data from tissue microassays of 305 patients with lung cancer showed that TLS were more abundant in non-small cell lung cancer (NSCLC) tissues with lower ACAT1 expression. Intratumoral ACAT1 expression was associated with poor immunotherapy outcomes in patients with NSCLC. In conclusion, our results identified ACAT1 as a metabolic regulator of TLS and a promising immunotherapeutic target in NSCLC.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":"135 7","pages":""},"PeriodicalIF":13.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11957694/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752838","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Endothelial MICU1 protects against vascular inflammation and atherosclerosis by inhibiting mitochondrial calcium uptake. 内皮MICU1通过抑制线粒体钙摄取来防止血管炎症和动脉粥样硬化。

IF 13.3 1区医学

Journal of Clinical Investigation Pub Date : 2025-04-01 DOI: 10.1172/JCI181928

Lu Sun, Ruixue Leng, Monan Liu, Meiming Su, Qingze He, Zhidan Zhang, Zhenghong Liu, Zhihua Wang, Hui Jiang, Li Wang, Shuai Guo, Yiming Xu, Yuqing Huo, Clint L Miller, Maciej Banach, Yu Huang, Paul C Evans, Jaroslav Pelisek, Giovanni G Camici, Bradford C Berk, Stefan Offermanns, Junbo Ge, Suowen Xu, Jianping Weng

{"title":"Endothelial MICU1 protects against vascular inflammation and atherosclerosis by inhibiting mitochondrial calcium uptake.","authors":"Lu Sun, Ruixue Leng, Monan Liu, Meiming Su, Qingze He, Zhidan Zhang, Zhenghong Liu, Zhihua Wang, Hui Jiang, Li Wang, Shuai Guo, Yiming Xu, Yuqing Huo, Clint L Miller, Maciej Banach, Yu Huang, Paul C Evans, Jaroslav Pelisek, Giovanni G Camici, Bradford C Berk, Stefan Offermanns, Junbo Ge, Suowen Xu, Jianping Weng","doi":"10.1172/JCI181928","DOIUrl":"10.1172/JCI181928","url":null,"abstract":"Mitochondrial dysfunction fuels vascular inflammation and atherosclerosis. Mitochondrial calcium uptake 1 (MICU1) maintains mitochondrial Ca2+ homeostasis. However, the role of MICU1 in vascular inflammation and atherosclerosis remains unknown. Here, we report that endothelial MICU1 prevents vascular inflammation and atherosclerosis by maintaining mitochondrial homeostasis. We observed that vascular inflammation was aggravated in endothelial cell-specific Micu1 knockout mice (Micu1ECKO) and attenuated in endothelial cell-specific Micu1 transgenic mice (Micu1ECTg). Furthermore, hypercholesterolemic Micu1ECKO mice also showed accelerated development of atherosclerosis, while Micu1ECTg mice were protected against atherosclerosis. Mechanistically, MICU1 depletion increased mitochondrial Ca2+ influx, thereby decreasing the expression of the mitochondrial deacetylase sirtuin 3 (SIRT3) and the ensuing deacetylation of superoxide dismutase 2 (SOD2), leading to the burst of mitochondrial reactive oxygen species (mROS). Of clinical relevance, we observed decreased MICU1 expression in the endothelial layer covering human atherosclerotic plaques and in human aortic endothelial cells exposed to serum from patients with coronary artery diseases (CAD). Two-sample Wald ratio Mendelian randomization further revealed that increased expression of MICU1 was associated with decreased risk of CAD and coronary artery bypass grafting (CABG). Our findings support MICU1 as an endogenous endothelial resilience factor that protects against vascular inflammation and atherosclerosis by maintaining mitochondrial Ca2+ homeostasis.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":"135 7","pages":""},"PeriodicalIF":13.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11957702/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752848","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

ACAT1 regulates tertiary lymphoid structures: A target for enhancing immunotherapy in non-small cell lung cancer. ACAT1调节三级淋巴样结构：增强非小细胞肺癌免疫治疗的靶点。

IF 13.3 1区医学

Journal of Clinical Investigation Pub Date : 2025-04-01 DOI: 10.1172/JCI191094

Sophie O'Keefe, Qiwei Wang

引用次数: 0

Lipid peroxidation and immune activation: TRAF3's double-edged strategy against glioblastoma. 脂质过氧化和免疫激活：TRAF3对胶质母细胞瘤的双刃剑策略。

IF 13.3 1区医学

Journal of Clinical Investigation Pub Date : 2025-04-01 DOI: 10.1172/JCI190471

Tzu-Yi Chia, Nishanth S Sadagopan, Jason Miska

引用次数: 0

Meal-feeding promotes skeletal growth by ghrelin-dependent enhancement of growth hormone rhythmicity. 膳食喂养通过生长素依赖性生长激素节律性增强促进骨骼生长。

IF 13.3 1区医学

Journal of Clinical Investigation Pub Date : 2025-04-01 eCollection Date: 2025-06-16 DOI: 10.1172/JCI189202

Amanda Ke Hornsby, Richard C Brown, Thomas W Tilston, Harry A Smith, Alfonso Moreno-Cabañas, Bradley Arms-Williams, Anna L Hopkins, Katie D Taylor, Simran Kr Rogaly, Lois Hm Wells, Jamie J Walker, Jeffrey S Davies, Yuxiang Sun, Jeffrey M Zigman, James A Betts, Timothy Wells

{"title":"Meal-feeding promotes skeletal growth by ghrelin-dependent enhancement of growth hormone rhythmicity.","authors":"Amanda Ke Hornsby, Richard C Brown, Thomas W Tilston, Harry A Smith, Alfonso Moreno-Cabañas, Bradley Arms-Williams, Anna L Hopkins, Katie D Taylor, Simran Kr Rogaly, Lois Hm Wells, Jamie J Walker, Jeffrey S Davies, Yuxiang Sun, Jeffrey M Zigman, James A Betts, Timothy Wells","doi":"10.1172/JCI189202","DOIUrl":"10.1172/JCI189202","url":null,"abstract":"The physiological effect of ultradian temporal feeding patterns remains a major unanswered question in nutritional science. We have used automated and nasogastric feeding to address this question in male rodents and human volunteers. While grazing and meal-feeding reduced food intake in parallel (compared with ad libitum-fed rodents), body length and tibial epiphysial plate width were maintained in meal-fed rodents via the action of ghrelin and its receptor, GHS-R. Grazing and meal-feeding initially suppressed elevated preprandial ghrelin levels in rats, followed by either a sustained elevation in ghrelin in grazing rats or preprandial ghrelin surges in meal-fed rats. Episodic growth hormone (GH) secretion was largely unaffected in grazing rats, but meal-feeding tripled GH secretion, with burst height augmented and 2 additional bursts of GH per day. Continuous nasogastric infusion of enteral feed in humans failed to suppress circulating ghrelin, producing continuously elevated circulating GH levels with minimal rhythmicity. In contrast, bolus enteral infusion elicited postprandial ghrelin troughs accompanied by reduced circulating GH, with enhanced ultradian rhythmicity. Taken together, our data imply that the contemporary shift from regular meals to snacking behavior may be detrimental to optimal skeletal growth outcomes by sustaining circulating ghrelin at levels associated with undernourishment and diminishing GH pulsatility.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":" ","pages":""},"PeriodicalIF":13.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12165789/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764153","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metabolic dysfunction-associated steatotic liver disease and the gut microbiome: pathogenic insights and therapeutic innovations. 代谢功能障碍相关的脂肪变性肝病和肠道微生物组：致病的见解和治疗的创新。

IF 13.3 1区医学

Journal of Clinical Investigation Pub Date : 2025-04-01 DOI: 10.1172/JCI186423

Bernd Schnabl, Christopher J Damman, Rotonya M Carr

{"title":"Metabolic dysfunction-associated steatotic liver disease and the gut microbiome: pathogenic insights and therapeutic innovations.","authors":"Bernd Schnabl, Christopher J Damman, Rotonya M Carr","doi":"10.1172/JCI186423","DOIUrl":"10.1172/JCI186423","url":null,"abstract":"Metabolic dysfunction-associated steatotic liver disease (MASLD) is a major cause of liver disease worldwide, and our understanding of its pathogenesis continues to evolve. MASLD progresses from steatosis to steatohepatitis, fibrosis, and cirrhosis, and this Review explores how the gut microbiome and their metabolites contribute to MASLD pathogenesis. We explore the complexity and importance of the intestinal barrier function and how disruptions of the intestinal barrier and dysbiosis work in concert to promote the onset and progression of MASLD. The Review focuses on specific bacterial, viral, and fungal communities that impact the trajectory of MASLD and how specific metabolites (including ethanol, bile acids, short chain fatty acids, and other metabolites) contribute to disease pathogenesis. Finally, we underscore how knowledge of the interaction between gut microbes and the intestinal barrier may be leveraged for MASLD microbial-based therapeutics. Here, we include a discussion of the therapeutic potential of prebiotics, probiotics, postbiotics, and microbial-derived metabolites.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":"135 7","pages":""},"PeriodicalIF":13.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11957707/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752892","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cxcr3 promotes protection from colorectal cancer liver metastasis by driving NK cell infiltration and plasticity. Cxcr3通过驱动NK细胞浸润和可塑性，促进结直肠癌肝转移的保护作用。

IF 13.3 1区医学

Journal of Clinical Investigation Pub Date : 2025-04-01 eCollection Date: 2025-06-02 DOI: 10.1172/JCI184036

Eleonora Russo, Chiara D'Aquino, Chiara Di Censo, Mattia Laffranchi, Luana Tomaipitinca, Valerio Licursi, Stefano Garofalo, Johann Promeuschel, Giovanna Peruzzi, Francesca Sozio, Anna Kaffke, Cecilia Garlanda, Ulf Panzer, Cristina Limatola, Christian Aj Vosshenrich, Silvano Sozzani, Giuseppe Sciumè, Angela Santoni, Giovanni Bernardini

{"title":"Cxcr3 promotes protection from colorectal cancer liver metastasis by driving NK cell infiltration and plasticity.","authors":"Eleonora Russo, Chiara D'Aquino, Chiara Di Censo, Mattia Laffranchi, Luana Tomaipitinca, Valerio Licursi, Stefano Garofalo, Johann Promeuschel, Giovanna Peruzzi, Francesca Sozio, Anna Kaffke, Cecilia Garlanda, Ulf Panzer, Cristina Limatola, Christian Aj Vosshenrich, Silvano Sozzani, Giuseppe Sciumè, Angela Santoni, Giovanni Bernardini","doi":"10.1172/JCI184036","DOIUrl":"10.1172/JCI184036","url":null,"abstract":"The antimetastatic activity of NK cells is well established in several cancer types, but the mechanisms underlying NK cell metastasis infiltration and acquisition of antitumor characteristics remain unclear. Herein, we investigated the cellular and molecular factors required to facilitate the generation of an ILC1-like CD49a+ NK cell population within the liver metastasis (LM) environment of colorectal cancer (CRC). We show that CD49a+ NK cells had the highest cytotoxic capacity among metastasis-infiltrating NK cells in the MC38 mouse model. Furthermore, the chemokine receptor CXCR3 promoted CD49a+ NK cell accumulation and persistence in metastasis where NK cells colocalize with macrophages in CXCL9- and CXCL10-rich areas. By mining a published scRNA-seq dataset of a cohort of patients with CRC who were treatment naive, we confirmed the accumulation of CXCR3+NK cells in metastatic samples. Conditional deletion of Cxcr3 in NKp46+ cells and antibody-mediated depletion of metastasis-associated macrophages impaired CD49a+NK cell development, indicating that CXCR3 and macrophages contribute to efficient NK cell localization and polarization in LM. Conversely, CXCR3neg NK cells maintained a CD49a- phenotype in metastasis with reduced parenchymal infiltration and tumor killing capacity. Furthermore, CD49a+ NK cell accumulation was impaired in an independent SL4-induced CRC metastasis model, which fails to accumulate CXCL9+ macrophages. Together, our results highlight a role for CXCR3/ligand axis in promoting macrophage-dependent NK cell accumulation and functional sustenance in CRC LM.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":" ","pages":""},"PeriodicalIF":13.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12126236/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143764151","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Human genetics of metabolic dysfunction-associated steatotic liver disease: from variants to cause to precision treatment. 代谢功能障碍相关脂肪变性肝病的人类遗传学：从变异到病因再到精确治疗

IF 13.3 1区医学

Journal of Clinical Investigation Pub Date : 2025-04-01 DOI: 10.1172/JCI186424

Vincent L Chen, Annapurna Kuppa, Antonino Oliveri, Yanhua Chen, Prabhu Ponnandy, Puja B Patel, Nicholette D Palmer, Elizabeth K Speliotes

{"title":"Human genetics of metabolic dysfunction-associated steatotic liver disease: from variants to cause to precision treatment.","authors":"Vincent L Chen, Annapurna Kuppa, Antonino Oliveri, Yanhua Chen, Prabhu Ponnandy, Puja B Patel, Nicholette D Palmer, Elizabeth K Speliotes","doi":"10.1172/JCI186424","DOIUrl":"10.1172/JCI186424","url":null,"abstract":"Metabolic dysfunction-associated steatotic liver disease (MASLD) is characterized by increased hepatic steatosis with cardiometabolic disease and is a leading cause of advanced liver disease. We review here the genetic basis of MASLD. The genetic variants most consistently associated with hepatic steatosis implicate genes involved in lipoprotein input or output, glucose metabolism, adiposity/fat distribution, insulin resistance, or mitochondrial/ER biology. The distinct mechanisms by which these variants promote hepatic steatosis result in distinct effects on cardiometabolic disease that may be best suited to precision medicine. Recent work on gene-environment interactions has shown that genetic risk is not fixed and may be exacerbated or attenuated by modifiable (diet, exercise, alcohol intake) and nonmodifiable environmental risk factors. Some steatosis-associated variants, notably those in patatin-like phospholipase domain-containing 3 (PNPLA3) and transmembrane 6 superfamily member 2 (TM6SF2), are associated with risk of developing adverse liver-related outcomes and provide information beyond clinical risk stratification tools, especially in individuals at intermediate to high risk for disease. Future work to better characterize disease heterogeneity by combining genetics with clinical risk factors to holistically predict risk and develop therapies based on genetic risk is required.","PeriodicalId":15469,"journal":{"name":"Journal of Clinical Investigation","volume":"135 7","pages":""},"PeriodicalIF":13.3,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11957700/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143752882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HoxBlinc: a key driver of chromatin dynamics in NUP98 fusion-driven leukemia. HoxBlinc: NUP98融合驱动白血病中染色质动力学的关键驱动因素。

IF 13.3 1区医学

Journal of Clinical Investigation Pub Date : 2025-04-01 DOI: 10.1172/JCI191355

Jian Xu, Wei Du

引用次数: 0