IF 5.9 2区医学

Oncogenesis Pub Date : 2024-06-21 DOI: 10.1038/s41389-024-00524-3

Jiazhong Guo, Yunpeng Zhao, Huacong Sui, Lei Liu, Fanrong Liu, Lingxiao Yang, Fengyuan Gao, Jinfu Wang, Yilin Zhu, Lingbing Li, Xiangqing Song, Peng Li, Zhongxian Tian, Peichao Li, Xiaogang Zhao

{"title":"USP21-mediated G3BP1 stabilization accelerates proliferation and metastasis of esophageal squamous cell carcinoma via activating Wnt/β-Catenin signaling.","authors":"Jiazhong Guo, Yunpeng Zhao, Huacong Sui, Lei Liu, Fanrong Liu, Lingxiao Yang, Fengyuan Gao, Jinfu Wang, Yilin Zhu, Lingbing Li, Xiangqing Song, Peng Li, Zhongxian Tian, Peichao Li, Xiaogang Zhao","doi":"10.1038/s41389-024-00524-3","DOIUrl":"10.1038/s41389-024-00524-3","url":null,"abstract":"Lacking effective therapeutic targets heavily restricts the improvement of clinical prognosis for patients diagnosed with esophageal squamous cell carcinoma (ESCC). Ubiquitin Specific Peptidase 21 (USP21) is dysregulated in plenty of human cancers, however, its potential function and relevant molecular mechanisms in ESCC malignant progression as well as its value in clinical translation remain largely unknown. Here, in vitro and in vivo experiments revealed that aberrant upregulation of USP21 accelerated the proliferation and metastasis of ESCC in a deubiquitinase-dependent manner. Mechanistically, we found that USP21 binds to, deubiquitinates, and stabilizes the G3BP Stress Granule Assembly Factor 1 (G3BP1) protein, which is required for USP21-mediated ESCC progression. Further molecular studies demonstrated that the USP21/G3BP1 axis played a tumor-promoting role in ESCC progression by activating the Wnt/β-Catenin signaling pathway. Additionally, disulfiram (DSF), an inhibitor against USP21 deubiquitylation activity, markedly abolished the USP21-mediated stability of G3BP1 protein and significantly displayed an anti-tumor effect on USP21-driving ESCC progression. Finally, the regulatory axis of USP21/G3BP1 was demonstrated to be aberrantly activated in ESCC tumor tissues and closely associated with advanced clinical stages and unfavorable prognoses, which provides a promising therapeutic strategy targeting USP21/G3BP1 axis for ESCC patients.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":null,"pages":null},"PeriodicalIF":5.9,"publicationDate":"2024-06-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11192907/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141437268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Activated platelet-derived exosomal LRG1 promotes multiple myeloma cell growth. 活化的血小板衍生外泌体 LRG1 可促进多发性骨髓瘤细胞的生长。

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-06-13 DOI: 10.1038/s41389-024-00522-5

Meng Gao, Hang Dong, Siyi Jiang, Fangping Chen, Yunfeng Fu, Yanwei Luo

{"title":"Activated platelet-derived exosomal LRG1 promotes multiple myeloma cell growth.","authors":"Meng Gao, Hang Dong, Siyi Jiang, Fangping Chen, Yunfeng Fu, Yanwei Luo","doi":"10.1038/s41389-024-00522-5","DOIUrl":"10.1038/s41389-024-00522-5","url":null,"abstract":"The hypercoagulable state is a hallmark for patients with multiple myeloma (MM) and is associated with disease progression. Activated platelets secrete exosomes and promote solid tumor growth. However, the role of platelet-derived exosomes in MM is not fully clear. We aim to study the underlying mechanism of how platelet-derived exosomes promote MM cell growth. Flow cytometry, Western blot, proteome analysis, co-immunoprecipitation, immunofluorescence staining, and NOD/SCID mouse subcutaneous transplantation model were performed to investigate the role of exosomal LRG1 on multiple myeloma cell growth. Peripheral blood platelets in MM patients were in a highly activated state, and platelet-rich plasma from MM patients significantly promoted cell proliferation and decreased apoptotic cells in U266 and RPMI8226 cells. Leucine-rich-alpha-2-glycoprotein 1 (LRG1) was significantly enriched in MM platelet-derived exosomes. Blocking LRG1 in recipient cells using LRG1 antibody could significantly eliminate the proliferation-promoting effect of platelet-derived exosomes on MM cells. And high exosomal LRG1 was associated with poor prognosis of patients with MM. Mechanistic studies revealed that LRG1 interacted with Olfactomedin 4 (OLFM4) to accelerate MM progression by activating the epithelial-to-mesenchymal transition (EMT) signaling pathway and promoting angiogenesis. Our results revealed that blocking LRG1 is a promising therapeutic strategy for the treatment of MM.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11176168/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141317934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Comprehensive multi-omics analysis of breast cancer reveals distinct long-term prognostic subtypes. 乳腺癌多组学综合分析揭示了不同的长期预后亚型。

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-06-13 DOI: 10.1038/s41389-024-00521-6

Abhibhav Sharma, Julia Debik, Bjørn Naume, Hege Oma Ohnstad, Tone F Bathen, Guro F Giskeødegård

{"title":"Comprehensive multi-omics analysis of breast cancer reveals distinct long-term prognostic subtypes.","authors":"Abhibhav Sharma, Julia Debik, Bjørn Naume, Hege Oma Ohnstad, Tone F Bathen, Guro F Giskeødegård","doi":"10.1038/s41389-024-00521-6","DOIUrl":"10.1038/s41389-024-00521-6","url":null,"abstract":"Breast cancer (BC) is a leading cause of cancer-related death worldwide. The diverse nature and heterogeneous biology of BC pose challenges for survival prediction, as patients with similar diagnoses often respond differently to treatment. Clinically relevant BC intrinsic subtypes have been established through gene expression profiling and are implemented in the clinic. While these intrinsic subtypes show a significant association with clinical outcomes, their long-term survival prediction beyond 5 years often deviates from expected clinical outcomes. This study aimed to identify naturally occurring long-term prognostic subgroups of BC based on an integrated multi-omics analysis. This study incorporates a clinical cohort of 335 untreated BC patients from the Oslo2 study with long-term follow-up (>12 years). Multi-Omics Factor Analysis (MOFA+) was employed to integrate transcriptomic, proteomic, and metabolomic data obtained from the tumor tissues. Our analysis revealed three prominent multi-omics clusters of BC patients with significantly different long-term prognoses (p = 0.005). The multi-omics clusters were validated in two independent large cohorts, METABRIC and TCGA. Importantly, a lack of prognostic association to long-term follow-up above 12 years in the previously established intrinsic subtypes was shown for these cohorts. Through a systems-biology approach, we identified varying enrichment levels of cell-cycle and immune-related pathways among the prognostic clusters. Integrated multi-omics analysis of BC revealed three distinct clusters with unique clinical and biological characteristics. Notably, these multi-omics clusters displayed robust associations with long-term survival, outperforming the established intrinsic subtypes.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11176181/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141317935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

DAB2IP inhibits glucose uptake by modulating HIF-1α ubiquitination under hypoxia in breast cancer. DAB2IP 在乳腺癌缺氧状态下通过调节 HIF-1α 泛素化抑制葡萄糖摄取

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-06-11 DOI: 10.1038/s41389-024-00523-4

Hongliang Dong, Weiyi Jia, Weijian Meng, Rui Zhang, Zhihong Qi, Zhuo Chen, Sophia Xie, Jiang Min, Liang Liu, Jie Shen

{"title":"DAB2IP inhibits glucose uptake by modulating HIF-1α ubiquitination under hypoxia in breast cancer.","authors":"Hongliang Dong, Weiyi Jia, Weijian Meng, Rui Zhang, Zhihong Qi, Zhuo Chen, Sophia Xie, Jiang Min, Liang Liu, Jie Shen","doi":"10.1038/s41389-024-00523-4","DOIUrl":"10.1038/s41389-024-00523-4","url":null,"abstract":"Metabolic reprogramming has become increasingly important in tumor biology research. The glucose metabolic pathway is a major energy source and is often dysregulated in breast cancer. DAB2IP is widely reported to be a tumor suppressor that acts as a scaffold protein to suppress tumor malignancy in breast cancer. Interestingly, DAB2IP has also been found to be a potential regulator of glucose uptake; however, the exact mechanism remains unclear. In this study, we found that DAB2IP inhibited glucose uptake under hypoxia conditions in breast cancer cells by suppressing HIF-1α signals. Mechanically, DAB2IP interacted with the E3 ubiquitin ligase STUB1 via its PER domain, thus triggering STUB1 mediated HIF-1α ubiquitylation and degradation, and inhibit glucose metabolism and tumor progression. Deleting the PER domain abrogated the DAB2IP-related inhibitory effects on glucose uptake, intracellular ATP production, and lactic acid production in breast cancer cells. These findings elucidate the biological roles of DAB2IP in cancer-related glucose metabolism as well as a novel mechanism by which STUB1-driven HIF-1α ubiquitylated degradation is regulated in breast cancer.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11166643/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141306489","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Retraction Note: PI3K/Akt pathway and Nanog maintain cancer stem cells in sarcomas. 撤稿说明：PI3K/Akt通路和Nanog可维持肉瘤中的癌症干细胞。

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-05-29 DOI: 10.1038/s41389-024-00519-0

Changhwan Yoon, Jun Lu, Brendan C Yi, Kevin K Chang, M Celeste Simon, Sandra Ryeom, Sam S Yoon

引用次数: 0

Retraction Note: Platelet-derived growth factor receptor-α and -β promote cancer stem cell phenotypes in sarcomas. 撤稿说明：血小板衍生生长因子受体-α和-β可促进肉瘤中癌症干细胞表型的形成。

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-05-29 DOI: 10.1038/s41389-024-00520-7

Kevin K Chang, Changhwan Yoon, Brendan C Yi, William D Tap, M Celeste Simon, Sam S Yoon

引用次数: 0

Mitotic MTH1 inhibitor TH1579 induces PD-L1 expression and inflammatory response through the cGAS-STING pathway 有丝分裂 MTH1 抑制剂 TH1579 通过 cGAS-STING 通路诱导 PD-L1 表达和炎症反应

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-05-25 DOI: 10.1038/s41389-024-00518-1

Jianyu Shen, Emilio Guillén Mancina, Shenyu Chen, Theodora Manolakou, Helge Gad, Ulrika Warpman Berglund, Kumar Sanjiv, Thomas Helleday

{"title":"Mitotic MTH1 inhibitor TH1579 induces PD-L1 expression and inflammatory response through the cGAS-STING pathway","authors":"Jianyu Shen, Emilio Guillén Mancina, Shenyu Chen, Theodora Manolakou, Helge Gad, Ulrika Warpman Berglund, Kumar Sanjiv, Thomas Helleday","doi":"10.1038/s41389-024-00518-1","DOIUrl":"https://doi.org/10.1038/s41389-024-00518-1","url":null,"abstract":"The mitotic MTH1 inhibitor TH1579 is a dual inhibitor that inhibits mitosis and incorporation of oxidative DNA damage and leads to cancer-specific cell death. The response to immune checkpoint inhibitor (ICI) treatment is often augmented by DNA damaging agents through the cGAS-STING pathway. This study investigates whether TH1579 can improve the efficacy of immune checkpoint blockades through its immunomodulatory properties. Various human and murine cancer cell lines were treated with mitotic MTH1i TH1579, and the expression of PD-L1 and T-cell infiltration-related chemokines was analysed by flow cytometry and real-time qPCR. Syngeneic mouse models were established to examine the combined effect of TH1579 and PD-L1 blockade. In our investigation, we found that TH1579 upregulates PD-L1 expression at both the protein and mRNA levels in human cancer cell lines. However, in murine cell lines, the increase was less pronounced. An in vivo experiment in a syngeneic mouse melanoma model showed that TH1579 treatment significantly increased the efficacy of atezolizumab, an anti-PD-L1 antibody, compared to vehicle or atezolizumab monotherapy. Furthermore, TH1579 exhibited immune-modulatory properties, elevating cytokines such as IFN-β and chemokines including CCL5 and CXCL10, in a cGAS-STING pathway-dependent manner. In conclusion, TH1579 has the potential to improve ICI treatment by modulating immune checkpoint-related proteins and pathways.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141147822","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

An E3 ligase TRIM1 promotes colorectal cancer progression via K63-linked ubiquitination and activation of HIF1α. E3连接酶TRIM1通过与K63连接的泛素化和激活HIF1α促进结直肠癌的进展。

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-05-20 DOI: 10.1038/s41389-024-00517-2

Liuliu Shi, Xianglan Fang, Lijie Du, Jin Yang, Juan Xue, Xiaokai Yue, Duoshuang Xie, Yuanjian Hui, Kun Meng

{"title":"An E3 ligase TRIM1 promotes colorectal cancer progression via K63-linked ubiquitination and activation of HIF1α.","authors":"Liuliu Shi, Xianglan Fang, Lijie Du, Jin Yang, Juan Xue, Xiaokai Yue, Duoshuang Xie, Yuanjian Hui, Kun Meng","doi":"10.1038/s41389-024-00517-2","DOIUrl":"10.1038/s41389-024-00517-2","url":null,"abstract":"Accumulating studies have shown that E3 ligases play crucial roles in regulating cellular biological processes and signaling pathways during carcinogenesis via ubiquitination. Tripartite-motif (TRIM) ubiquitin E3 ligases consist of over 70 members. However, the clinical significance and their contributions to tumorigenesis remain largely unknown. In this study, we analyzed the RNA-sequencing expression of TRIM E3 ligases in colorectal cancer (CRC) and identified 10 differentially expressed genes, among which TRIM1 expression predicted poor prognosis of CRC patients. We demonstrated that TRIM1 expression is positively associated with CRC pathological stages, and higher expression is positively correlated with infiltrating levels of immune cells and immunotherapy biomarkers. TRIM1 expression promotes the proliferation and migration of colorectal cancer cells in vitro and in vivo. Transcriptional analysis showed that TRIM1 is responsible for metabolism promotion and immune suppression. Mechanistically, we found that TRIM1 binds HIF1α and mediates its K63-linked ubiquitination, which is required for HIF1α nuclear translocation and subsequent activation. Ubiquitination occurs at Lys214 in the loop between the two PAS domains of HIF1α, and mutation of Lys214 severely disturbs the function of HIF1α. Besides, HIF1α ubiquitination enhances its binding with proteins involved in cellular trafficking and nucleocytoplasmic transport pathway. Collectively, our results indicate TRIM1's role in predicting prognosis and reveal how TRIM1 functions to upregulate HIF1α expression and promote tumor cell proliferation.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-05-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11106307/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141071647","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

NAC1 transcriptional activation of LDHA induces hepatitis B virus immune evasion leading to cirrhosis and hepatocellular carcinoma development NAC1 对 LDHA 的转录激活诱导乙型肝炎病毒免疫逃避，导致肝硬化和肝细胞癌的发展

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-05-04 DOI: 10.1038/s41389-024-00515-4

Wenbiao Chen, Liliangzi Guo, Huixuan Xu, Yong Dai, Jun Yao, Lisheng Wang

{"title":"NAC1 transcriptional activation of LDHA induces hepatitis B virus immune evasion leading to cirrhosis and hepatocellular carcinoma development","authors":"Wenbiao Chen, Liliangzi Guo, Huixuan Xu, Yong Dai, Jun Yao, Lisheng Wang","doi":"10.1038/s41389-024-00515-4","DOIUrl":"https://doi.org/10.1038/s41389-024-00515-4","url":null,"abstract":"Our study aimed to elucidate the molecular mechanisms underlying NAC1 (nucleus accumbens associated 1) transcriptional regulation of LDHA and its role in HBV immune evasion, thus contributing to the development of cirrhosis and hepatocellular carcinoma (HCC). Utilizing public datasets, we performed differential gene expression and weighted gene co-expression network analysis (WGCNA) on HBV-induced cirrhosis/HCC data. We identified candidate genes by intersecting differentially expressed genes with co-expression modules. We validated these genes using the TCGA database, conducting survival analysis to pinpoint key genes affecting HBV-HCC prognosis. We also employed the TIMER database for immune cell infiltration data and analyzed correlations with identified key genes to uncover potential immune escape pathways. In vitro, we investigated the impact of NAC1 and LDHA on immune cell apoptosis and HBV immune evasion. In vivo, we confirmed these findings using an HBV-induced cirrhosis model. Bioinformatics analysis revealed 676 genes influenced by HBV infection, with 475 genes showing differential expression in HBV-HCC. NAC1 emerged as a key gene, potentially mediating HBV immune escape through LDHA transcriptional regulation. Experimental data demonstrated that NAC1 transcriptionally activates LDHA, promoting immune cell apoptosis and HBV immune evasion. Animal studies confirmed these findings, linking NAC1-mediated LDHA activation to cirrhosis and HCC development. NAC1, highly expressed in HBV-infected liver cells, likely drives HBV immune escape by activating LDHA expression, inhibiting CD8 + T cells, and promoting cirrhosis and HCC development.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-05-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140826988","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Phenotyping of cancer-associated somatic mutations in the BCL2 transmembrane domain BCL2跨膜结构域癌症相关体细胞突变的表型分析

IF 6.2 2区医学

Oncogenesis Pub Date : 2024-04-26 DOI: 10.1038/s41389-024-00516-3

Diego Leiva, Estefanía Lucendo, Alicia Belén García-Jareño, Mónica Sancho, Mar Orzáez

{"title":"Phenotyping of cancer-associated somatic mutations in the BCL2 transmembrane domain","authors":"Diego Leiva, Estefanía Lucendo, Alicia Belén García-Jareño, Mónica Sancho, Mar Orzáez","doi":"10.1038/s41389-024-00516-3","DOIUrl":"https://doi.org/10.1038/s41389-024-00516-3","url":null,"abstract":"The BCL2 family of proteins controls cell death by modulating the permeabilization of the mitochondrial outer membrane through a fine-tuned equilibrium of interactions among anti- and pro-apoptotic members. The upregulation of anti-apoptotic BCL2 proteins represents an unfavorable prognostic factor in many tumor types due to their ability to shift the equilibrium toward cancer cell survival. Furthermore, cancer-associated somatic mutations in BCL2 genes interfere with the protein interaction network, thereby promoting cell survival. A range of studies have documented how these mutations affect the interactions between the cytosolic domains of BCL2 and evaluate the impact on cell death; however, as the BCL2 transmembrane interaction network remains poorly understood, somatic mutations affecting transmembrane regions have been classified as pathogenic-based solely on prediction algorithms. We comprehensively investigated cancer-associated somatic mutations affecting the transmembrane domain of BCL2 proteins and elucidated their effect on membrane insertion, hetero-interactions with the pro-apoptotic protein BAX, and modulation of cell death in cancer cells. Our findings reveal how specific mutations disrupt switchable interactions, alter the modulation of apoptosis, and contribute to cancer cell survival. These results provide experimental evidence to distinguish BCL2 transmembrane driver mutations from passenger mutations and provide new insight regarding selecting precision anti-tumor treatments.","PeriodicalId":19489,"journal":{"name":"Oncogenesis","volume":null,"pages":null},"PeriodicalIF":6.2,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140803172","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Oncogenesis最新文献