Oncogene最新文献_第9页

Deciphering cancer complexity: perspective on hematopoietic remodeling-mediated immunosuppression 解读癌症的复杂性：造血重塑介导的免疫抑制的观点。

IF 6.9 1区医学

Oncogene Pub Date : 2025-04-07 DOI: 10.1038/s41388-025-03361-9

Qian Liao, Zheng Jin, Haixia Long, Bo Zhu

引用次数: 0

Aurora Kinase A and B inhibition abrogates 'Neosis', a non-mitotic cell division of GBM residual cells and prevents GBM recurrence. 极光激酶A和B的抑制消除了‘Neosis’， GBM残余细胞的非有丝分裂细胞分裂，并防止GBM复发。

IF 6.9 1区医学

Oncogene Pub Date : 2025-04-07 DOI: 10.1038/s41388-025-03372-6

Tejashree Mahaddalkar, Archisman Banerjee, Madhura Ketkar, Rahul Thorat, Nilesh Gardi, Shilpee Dutt

{"title":"Aurora Kinase A and B inhibition abrogates 'Neosis', a non-mitotic cell division of GBM residual cells and prevents GBM recurrence.","authors":"Tejashree Mahaddalkar, Archisman Banerjee, Madhura Ketkar, Rahul Thorat, Nilesh Gardi, Shilpee Dutt","doi":"10.1038/s41388-025-03372-6","DOIUrl":"10.1038/s41388-025-03372-6","url":null,"abstract":"Glioblastoma (GBM) has a dismal median survival of 15 months owing to therapy resistance and inevitable recurrence. Using our cellular models of GBM radiation resistance, we had shown that GBM recurrence is due to survival and proliferation of residual disease cells enriched in multinucleated giant cells (MNGCs). However, MNGC division mechanism remained elusive. Here, using live-cell imaging we found daughter cells emerge from MNGCs by cytoplasmic pinching. Lack of DNA condensation, absence of spindle poles and acto-myosin contractile ring in dividing-MNGCs confirmed non-mitotic division of MNGCs. Furthermore, MNGCs harboured DNA damage, senescence phenotype, repeated atypical division after radiation exposure, characteristics of unconventional division called 'Neosis'. Molecularly, WGCNA co-expression network analysis of RNA-Sequencing from parent, non-dividing MNGCs and dividing-MNGCs identified significantly high expression of aurora kinases (AurA and AurB) specifically in dividing-MNGCs. Pharmacological and genetic inhibition of aurora kinases abrogated MNGC neosis, preventing GBM recurrence in vitro and in vivo in an orthotopic GBM mouse model. Together, this study demonstrates that MNGCs divide by neosis, an atypical division mediated by AurA and AurB and identify aurora kinases as a potential molecular target to inhibit neosis and prevent GBM recurrence.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143803443","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}

引用次数: 0

Dichotomous roles of ACBD3 in NSCLC growth and metastasis. ACBD3 在 NSCLC 生长和转移中的二分作用

IF 6.9 1区医学

Oncogene Pub Date : 2025-04-06 DOI: 10.1038/s41388-025-03360-w

Xiaochao Tan, Chao Wu, Priyam Banerjee, Shike Wang, Derrick L Cardin, Yuting Xu, Chad J Creighton, William K Russell

{"title":"Dichotomous roles of ACBD3 in NSCLC growth and metastasis.","authors":"Xiaochao Tan, Chao Wu, Priyam Banerjee, Shike Wang, Derrick L Cardin, Yuting Xu, Chad J Creighton, William K Russell","doi":"10.1038/s41388-025-03360-w","DOIUrl":"https://doi.org/10.1038/s41388-025-03360-w","url":null,"abstract":"Lung cancer continues to be the leading cause of cancer-related deaths globally. Unraveling the regulators behind lung cancer growth and its metastatic spread, along with understanding the underlying mechanisms, is crucial for developing novel and effective therapeutic strategies. While much research has focused on identifying potential oncogenes or tumor suppressors, the roles of certain genes can vary depending on the context and may even exhibit contradictory effects. In this study, we demonstrate that acyl-CoA binding domain containing 3 (ACBD3), a Golgi resident protein, promotes primary lung cancer growth by recruiting phosphatidylinositol (PI)-4-kinase IIIβ (PI4KB) to the Golgi, thereby enhancing oncogenic secretion in chromosome 1q-amplified lung cancer cells. Conversely, in chromosome 1q-diploid lung cancer cells, ACBD3 acts as a suppressor of lung cancer metastasis by inhibiting the NOTCH signaling pathway and reducing cancer cell motility. This highlights the intricacy of cancer progression and cautions against simplistic approaches targeting individual oncogenes for cancer therapy.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795989","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}

引用次数: 0

CDX2 downregulation regulates intrinsic WNT pathway activation, dictating metastasis in APC and CTNNB1 wildtype colorectal cancer. CDX2下调WNT通路激活，决定APC和CTNNB1野生型结直肠癌的转移。

IF 6.9 1区医学

Oncogene Pub Date : 2025-04-06 DOI: 10.1038/s41388-025-03365-5

Valérie M Wouters, Roxan F C P A Helderman, Kate Cameron, Sander R van der Hooff, Arezo Torang, Saskia van den Bergh, Rene Jackstadt, Owen J Sansom, Sanne M van Neerven, Jan Paul Medema

{"title":"CDX2 downregulation regulates intrinsic WNT pathway activation, dictating metastasis in APC and CTNNB1 wildtype colorectal cancer.","authors":"Valérie M Wouters, Roxan F C P A Helderman, Kate Cameron, Sander R van der Hooff, Arezo Torang, Saskia van den Bergh, Rene Jackstadt, Owen J Sansom, Sanne M van Neerven, Jan Paul Medema","doi":"10.1038/s41388-025-03365-5","DOIUrl":"https://doi.org/10.1038/s41388-025-03365-5","url":null,"abstract":"Colorectal cancer (CRC) can be divided into 4 subtypes of which consensus molecular subtype 4 (CMS4) is associated with metastasis and poor survival. Previously, we reported that the KPN mouse model resembles human CMS4. Strikingly, although tumor formation in this model is slow and limited, effective metastasis is observed. To understand this aggressive behavior, we compared two distinct in vitro KPN models, organoids and tumoroids. The organoid model only carries the original mutations, while the tumoroids are derived from in vivo grown tumors that underwent selection during development. Here, we reveal that tumoroids harbor endogenous WNT pathway activity, which can be driven by tankyrase activity and Cdx2 downregulation. Importantly, WNT pathway activation was heterogeneous in nature, subject to regulation and allowed for a mixture of WNT-driven and YAP-driven cells within tumoroids. This unique type of WNT pathway activation is not crucial for colonic tumor growth, but results in metastatic spreading. Intriguingly, these findings reflect a specific subset of aggressive human CMS4 cancers that display low CDX2 expression and lack of classical WNT pathway mutations, while having a higher tendency to metastasize. Together, these data propose a novel mechanism for WNT pathway activation that drives metastasis formation in aggressive CRC.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-04-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795988","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}

引用次数: 0

Interaction of PHGDH with IGF2BP1 facilitates m6A-dependent stabilization of TCF7L2 mRNA to confer multidrug resistance in gastric cancer. PHGDH与IGF2BP1的相互作用促进了m6a依赖性TCF7L2 mRNA的稳定，从而赋予胃癌多药耐药。

IF 6.9 1区医学

Oncogene Pub Date : 2025-04-05 DOI: 10.1038/s41388-025-03374-4

Shuyi Chen, Tingyu Li, Dan Liu, Yi Liu, Zhaobo Long, Ying Wu, Yue Zhong, Jun Zhao, Tong Wu, Wenfang He, Tianyu Cao, Daiming Fan, Kaichun Wu, Yuanyuan Lu, Xiaodi Zhao

{"title":"Interaction of PHGDH with IGF2BP1 facilitates m6A-dependent stabilization of TCF7L2 mRNA to confer multidrug resistance in gastric cancer.","authors":"Shuyi Chen, Tingyu Li, Dan Liu, Yi Liu, Zhaobo Long, Ying Wu, Yue Zhong, Jun Zhao, Tong Wu, Wenfang He, Tianyu Cao, Daiming Fan, Kaichun Wu, Yuanyuan Lu, Xiaodi Zhao","doi":"10.1038/s41388-025-03374-4","DOIUrl":"10.1038/s41388-025-03374-4","url":null,"abstract":"Multidrug resistance (MDR) remains a significant barrier to effective chemotherapy and results in a poor prognosis for gastric cancer (GC). Exploring the mechanism of MDR is highly important for identifying biomarkers for MDR and developing new treatment strategies. In this study, integrative analyses of multiomics and bioinformatics data were combined with experimental validation to explore the mechanism of MDR in GC. We found that phosphoglycerate dehydrogenase (PHGDH), the key rate-limiting enzyme in the serine synthesis pathway, was significantly upregulated in MDR GC cells. PHGDH was found to perform a noncanonical function to promote MDR by activating the Wnt/β-catenin signaling pathway, and this effect is mediated by transcription factor 7-like 2 (TCF7L2), a pivotal co-activator of β-catenin in the Wnt pathway. Specifically, PHGDH stabilizes TCF7L2 mRNA by interacting with insulin-like growth factor 2 mRNA binding protein 1 (IGF2BP1), a key m6A reader, in an m6A-dependent manner, thereby increasing the expression of TCF7L2. Moreover, TCF7L2 binds to the promoter of PHGDH and regulates its expression, which forms a positive feedback loop. This PHGDH/IGF2BP1-TCF7L2 loop contributes to GC MDR and is correlated with a poor prognosis of GC patients.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-04-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788760","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}

引用次数: 0

Retraction Note: Down-regulation of cathepsin B expression impairs the invasive and tumorigenic potential of human glioblastoma cells 注：组织蛋白酶B表达的下调会削弱人胶质母细胞瘤细胞的侵袭性和致瘤性潜能。

IF 6.9 1区医学

Oncogene Pub Date : 2025-04-04 DOI: 10.1038/s41388-025-03379-z

Sanjeeva Mohanam, Sushma L. Jasti, Sudha R. Kondraganti, Nirmala Chandrasekar, Sajani S. Lakka, Yoshiaki Kin, Gregory N. Fuller, Alfred W. K. Yung, Anthanassios P. Kyritsis, Dzung H. Dinh, William C. Olivero, Meena Gujrati, Francis Ali-Osman, Jasti S. Rao

引用次数: 0

TP53INP2 promotes mitophagic degradation of YAP to impede dedifferentiated liposarcoma development. TP53INP2促进YAP的自噬降解以阻止去分化脂肪肉瘤的发展。

IF 6.9 1区医学

Oncogene Pub Date : 2025-04-04 DOI: 10.1038/s41388-025-03358-4

Yixuan Wang, Ying Huang, Liwei Wang, Zhixiu Chen, Lin Zhou, Feng Xiang, Guoyu Li, Jiawen Yang, Rui Chen, Qiang Xu, Yan Shen

{"title":"TP53INP2 promotes mitophagic degradation of YAP to impede dedifferentiated liposarcoma development.","authors":"Yixuan Wang, Ying Huang, Liwei Wang, Zhixiu Chen, Lin Zhou, Feng Xiang, Guoyu Li, Jiawen Yang, Rui Chen, Qiang Xu, Yan Shen","doi":"10.1038/s41388-025-03358-4","DOIUrl":"https://doi.org/10.1038/s41388-025-03358-4","url":null,"abstract":"Dedifferentiated liposarcoma (DDLPS) accounts for 15-20% of liposarcoma (LPS) and has high rates of local recurrence and distant metastasis. Hyperactivation of yes-associated protein (YAP) has been implicated in DDLPS development. However, the mechanisms that drive aberrant YAP signaling remain largely unknown. Here, we show that tumor protein p53 inducible nuclear protein 2 (TP53INP2) is a potential negative modulator of the malignant progression of DDLPS. The TP53INP2 protein expression level in tumor tissues from 79 patients with DDLPS decreased progressively. Compared with primary tumors, recurrent tumors also exhibited reduced TP53INP2 expression. More importantly, low TP53INP2 expression is correlated with poor prognosis. TP53INP2 gain- or loss-of-function experiments in DDLPS cell lines showed profound inhibitory effects on processes and properties linked with cancer malignancy, such as proliferation, migration, stemness and dedifferentiation. Mechanistically, TP53INP2 is located mainly in mitochondria and promotes mitophagic degradation of YAP in a VDAC1-dependent manner. The WW domain in YAP and the PPTY motif in VDAC1 are required for their interaction. Taken together, these data demonstrate that TP53INP2 represses the malignant progression of DDLPS by inactivating YAP via a mitophagy-dependent mechanism and that TP53INP2 may constitute a novel prognostic biomarker for advanced DDLPS.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788763","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}

引用次数: 0

Syntaxin-6 mediated autophagy confers lenvatinib resistance in hepatocellular carcinoma. Syntaxin-6介导的自噬使肝细胞癌对lenvatinib产生耐药性。

IF 6.9 1区医学

Oncogene Pub Date : 2025-04-03 DOI: 10.1038/s41388-025-03371-7

Guo-Pei Zhang, Ze-Bing Song, De-Hua Chen, Yang Yu, Fei-Feng Wu, Ming Kuang, Shao-Qiang Li

{"title":"Syntaxin-6 mediated autophagy confers lenvatinib resistance in hepatocellular carcinoma.","authors":"Guo-Pei Zhang, Ze-Bing Song, De-Hua Chen, Yang Yu, Fei-Feng Wu, Ming Kuang, Shao-Qiang Li","doi":"10.1038/s41388-025-03371-7","DOIUrl":"10.1038/s41388-025-03371-7","url":null,"abstract":"Lenvatinib is the first-line therapy for inoperable HCC. However, intrinsic and acquired drug resistance occurs during the treatment period. Autophagy is an adaptive response that favors tumor survival under stress. In the present study, we aim to reveal the unknown autophagic engagement in lenvatinib resistance. Lenvatinib-resistant HCC cell lines and xenograft mouse HCC models were established to identify the key regulator of lenvatinib resistance in HCC. By in vitro functional restoration assays and autophagic flux detection, we demonstrated that the Syntaxin-6 (STX6) -mediated autophagy induced lenvatinib resistance of HCC cells. Mechanistically, Co-immunoprecipitation assay and mass spectrometry indicated that the interactions of STX6 with Beclin1, VTI1A, and VAMP3 facilitated autophagy, leading to the lenvatinib resistance. Additionally, STX6 enhanced the ability of proliferation, migration, and invasion of HCC in vitro and in vivo. Clinically, STX6 expression was significantly elevated in HCC tissues compared to it in para-tumor tissues. High STX6 expression predicted poor outcomes for patients following resection. Moreover, high expression of STX6 displayed low preventive efficacy of lenvatinib as a postoperative adjuvant treatment for HCC patients with a high risk of recurrence. Collectively, we identified that STX6-mediated autophagy plays a crucial role in lenvatinib resistance in HCC, providing a potential therapeutic target to overcome lenvatinib resistance for HCC patients.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772777","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}

引用次数: 0

PKM2 crotonylation reprograms glycolysis in VSMCs, contributing to phenotypic switching. PKM2巴豆酰化重编程vsmc中的糖酵解，导致表型转换。

IF 6.9 1区医学

Oncogene Pub Date : 2025-04-03 DOI: 10.1038/s41388-025-03353-9

Shan-Hu Cao, Ru-Yuan Ma, Tong Cao, Tao Hu, Shu Yang, Zhi-Yan Ren, Jiang-Ling Niu, Ming-Qi Zheng, Mei Han, Li-Hua Dong

{"title":"PKM2 crotonylation reprograms glycolysis in VSMCs, contributing to phenotypic switching.","authors":"Shan-Hu Cao, Ru-Yuan Ma, Tong Cao, Tao Hu, Shu Yang, Zhi-Yan Ren, Jiang-Ling Niu, Ming-Qi Zheng, Mei Han, Li-Hua Dong","doi":"10.1038/s41388-025-03353-9","DOIUrl":"10.1038/s41388-025-03353-9","url":null,"abstract":"Post-translational modifications (PTMs) of pyruvate kinase M2 (PKM2) play a vital role in regulating its activity and function. Recently, we found PKM2 can undergo crotonylation in vascular smooth muscle cell (VSMC) phenotypic switching. However, the role of PKM2 crotonylation remains unknown. Here, we verify a crucial role of PKM2 crotonylation in VSMC metabolic reprogramming. In PDGF-BB-induced synthetic VSMCs, PKM2 crotonylation was upregulated and promotes its nuclear translocation, thereby facilitating the expression of Glut1 and Ldha. Furthermore, crotonylation facilitated the dimeric formation of PKM2. Then we identified the highly conserved crotonylation site at K305 across different species. The crotonylation of PKM2 was compromised by PKM2 K305 mutation, resulting in the suppression of PKM2 dimeric configuration and nuclear relocation, and ultimately reducing glycolysis rate. Furthermore, PKM2 K305 crotonylation was necessary for VSMC phenotypic switching in vitro and intimal hyperplasia in vivo via infection of PKM2 recombinant adenovirus. In summary, PKM2 K305 crotonylation facilitates VSMC aerobic glycolysis by enhancing PKM2 dimeric form.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780183","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}

引用次数: 0

Suprabasin promotes gastric cancer liver metastasis via hepatic stellate cells-mediated EGF/CCL2/JAK2 intercellular signaling pathways. Suprabasin通过肝星状细胞介导的EGF/CCL2/JAK2细胞间信号通路促进胃癌肝转移。

IF 6.9 1区医学

Oncogene Pub Date : 2025-04-03 DOI: 10.1038/s41388-025-03370-8

Difeng Li, Zhiqing Gao, Zhuojun Zhang, Han Chen, Ruiming Tang, Lihuan Zhou, Yingmin Ye, Jiaqian Lin, Ping Zhou, Chanjuan Wang, Xiaoli Feng, Yaoming He, Zijie Meng, Mingzhu Zheng, Wenjie Lu, Zhengfu Feng, Lan Wang, Yuanyuan Pei, Jianan Yang, Tianyu Tao, Xin Zhang, Lili Jiang

{"title":"Suprabasin promotes gastric cancer liver metastasis via hepatic stellate cells-mediated EGF/CCL2/JAK2 intercellular signaling pathways.","authors":"Difeng Li, Zhiqing Gao, Zhuojun Zhang, Han Chen, Ruiming Tang, Lihuan Zhou, Yingmin Ye, Jiaqian Lin, Ping Zhou, Chanjuan Wang, Xiaoli Feng, Yaoming He, Zijie Meng, Mingzhu Zheng, Wenjie Lu, Zhengfu Feng, Lan Wang, Yuanyuan Pei, Jianan Yang, Tianyu Tao, Xin Zhang, Lili Jiang","doi":"10.1038/s41388-025-03370-8","DOIUrl":"10.1038/s41388-025-03370-8","url":null,"abstract":"Gastric cancer is among the most prevalent gastrointestinal tumors, with liver metastasis significantly worsening patient outcomes. While hepatic stellate cell activation is crucial in hepatocellular carcinoma progression and liver metastasis, its role in gastric cancer liver metastasis is not well understood. In this study, we identified Suprabasin (SBSN) as a key oncogene driving gastric cancer liver metastasis. SBSN was upregulated in gastric cancer tissues and further elevated in liver metastasis, correlating with poor prognosis. Mechanistically, SBSN promoted proliferation, migration, and invasion of gastric cancer cells by activating the STAT3 signaling pathway, as shown in vitro and in vivo. Using a co-culture model of gastric cancer cells and hepatic stellate cell line LX-2, we found that increased SBSN expression in gastric cancer cells triggered EGF secretion, activating LX-2 cells through the EGF/EGFR axis. Activated LX-2 cells then secreted CCL2, initiating the CCL2/CCR2/JAK2 signaling pathway in gastric cancer cells, facilitating their migration to the liver and promoting colonization and growth. Our findings highlight the prognostic significance of SBSN in gastric cancer and liver metastasis, suggesting it as a potential biomarker for disease progression. The SBSN-mediated EGF/EGFR and CCL2/CCR2/JAK2 signaling axes are critical for LX-2 activation and gastric cancer cell migration, offering a rationale for targeting SBSN in treating gastric cancer liver metastasis.","PeriodicalId":19524,"journal":{"name":"Oncogene","volume":" ","pages":""},"PeriodicalIF":6.9,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780294","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}

引用次数: 0