Cancer research最新文献

{"title":"Bone voyage: OPN's path from skeleton to systemic immunosuppression","authors":"Kyoko Hashimoto, Kazuo Okamoto, Hiroshi Takayanagi","doi":"10.1158/0008-5472.can-25-2702","DOIUrl":"https://doi.org/10.1158/0008-5472.can-25-2702","url":null,"abstract":"Immune checkpoint blockade (ICB) therapy has revolutionized cancer treatment across multiple tumor types. However, some patients receive limited benefit, and the underlying mechanisms of resistance remain a formidable challenge, spurring intensive research efforts. A recent study published in Cancer Cell reveals that bone metastases actively suppress systemic anti-tumor immunity and contribute to ICB resistance. Analysis of clinical cohorts showed that patients with bone metastases exhibit reduced responsiveness to ICBs. Mechanistically, the study demonstrated that intraosseous tumors enhance osteopontin (OPN) production by osteoclasts. Circulating OPN was found to impair differentiation of progenitor exhausted T cells (Tpex), a subset correlated with ICB responsiveness, in distant tumor sites, thereby blunting anti-tumor immune response. Importantly, osteoclast-specific depletion of OPN or inhibition of osteoclastogenesis restored T cell function and enhanced ICB efficacy in preclinical cancer models, suggesting that targeting osteoclasts overcomes ICB resistance in patients with bone metastases. This study offers novel insights into the role of OPN, revealing its capacity to traverse from the skeletal microenvironment to distant sites, orchestrating widespread immunosuppression that extend well beyond the bone itself. As a pioneering investigation, it delineates the immunosuppression mechanism mediated by the osteoimmune axis and represents a significant advancement in the emerging field of osteoimmunology.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":"10 1","pages":""},"PeriodicalIF":11.2,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144520595","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 C-terminal Kinase Domain-Binding and Suppression Motif Prevents Constitutive Activation of FGFR2.","authors":"Daniel Zingg,Chi-Chuan Lin,Julia Yemelyanenko,Lukasz Wieteska,Sjors M Kas,Onno B Bleijerveld,Xue Chao,Jinhyuk Bhin,Catrin Lutz,Ellen Wientjens,Sjoerd Klarenbeek,Giulia Zanetti,Stefano Annunziato,Bjørn Siteur,Eline van der Burg,Anne Paulien Drenth,Marieke van de Ven,Lodewyk F A Wessels,Maarten Altelaar,John E Ladbury,Jos Jonkers","doi":"10.1158/0008-5472.can-24-3349","DOIUrl":"https://doi.org/10.1158/0008-5472.can-24-3349","url":null,"abstract":"Genetic alterations in receptor tyrosine kinase (RTK) genes can generate potent oncogenic drivers. Truncation of the fibroblast growth factor receptor 2 (FGFR2) gene by its last exon 18 (E18) is caused by structural alterations, such as focal amplifications and gene fusions/rearrangements, as well as by mutations. All the E18-truncating FGFR2 variants (FGFR2ΔE18) act as strong driver alterations in cancer, and they commonly encode a receptor lacking the carboxy (C)-terminal tail. Here, we analyzed a compendium of Fgfr2-E18 variants to uncover the mechanism by which loss of the C-tail renders FGFR2 oncogenic. While permutation of previously annotated C-terminal FGFR motifs did not recapitulate the tumorigenicity of FGFR2ΔE18, the functional annotation efforts led to the discovery of a C-terminal phenylalanine-serine motif that mediates binding of the C-tail to the kinase domain and thereby suppresses FGFR2 kinase activity. Permutation of this kinase domain-binding and suppression (KDBS) motif in conjunction with other FGFR2-regulatory C-terminal sites fully phenocopied the oncogenic competence of FGFR2ΔE18. Together, these findings delineate how the C-terminal tail prevents FGFR2 from aberrant oncogenic activation.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":"16 1","pages":""},"PeriodicalIF":11.2,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144478758","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":"Tumor-Specific MHC-II Activates CD4+ and CD8+ T cells in Head and Neck Squamous Cell Carcinoma to Boost Immunotherapy Efficacy","authors":"Yuying Zhang, Jinbang Li, Xiaoyu Guo, Zhao Gao, Junchen Pan, Sheng Nong, Jiyuan Ma, Gang Chen, Jiali Zhang","doi":"10.1158/0008-5472.can-24-4383","DOIUrl":"https://doi.org/10.1158/0008-5472.can-24-4383","url":null,"abstract":"Neoadjuvant immunotherapy is a first-line treatment for recurrent and metastatic head and neck squamous cell carcinoma. However, only a fraction of advanced HNSCC patients benefit from immunotherapy. Identifying accurate and accessible biomarkers is essential for optimal patient selection. Herein, we integrated single-cell RNA-sequencing and T cell receptor-sequencing to comprehensively characterize the tumor immune microenvironment (TIME) of HNSCC biopsies prior to a phase II neoadjuvant immunotherapy clinical trial. Tumor-specific MHC-II (tsMHC-II) was identified as a superior predictor of response to neoadjuvant immunotherapy in HNSCC compared to PD-L1. Mechanistically, tsMHC-II ignited a hot TIME and enhanced the effect of PD-1 blockade by recruiting T cells through the induction of chemokines, particularly CCL5. Moreover, tsMHC-II triggered a Th1 response and activated CD4+ and CD8+ T cell expansion, suppressing HNSCC growth in a CD4+ T-cell-dependent manner. Simultaneously, tsMHC-II facilitated an increase in PD-1+CD4+ T cells and a modest elevation in tumor PD-L1, thereby enhancing sensitivity to anti-PD-1 therapy. This study highlights that tsMHC-II, by generating an inflamed TIME, is crucial in enhancing the effectiveness of neoadjuvant immunotherapy in HNSCC.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":"36 1","pages":""},"PeriodicalIF":11.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144335023","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":"Ceramide-Induced Metabolic Stress Depletes Fumarate and Drives Mitophagy to Mediate Tumor Suppression","authors":"Natalia V. Oleinik, Firdevs Cansu. Atilgan, Mohamed Faisal Kassir, Han Gyul Lee, Alhaji H. Janneh, Wyatt Wofford, Chase Walton, Zdzislaw M. Szulc, Elizabeth G. Hill, Alexander V. Alekseyenko, Huseyin Cimen, Jessica H. Hartman, Christina Voelkel-Johnson, Michael B. Lilly, John J. Lemasters, Norma Frizzell, Xue-Zhong Yu, Shikhar Mehrotra, Besim Ogretmen","doi":"10.1158/0008-5472.can-24-4042","DOIUrl":"https://doi.org/10.1158/0008-5472.can-24-4042","url":null,"abstract":"Bioactive ceramide induces cell death in part by promoting mitophagy. C18-ceramide levels are commonly reduced in head and neck squamous cell carcinoma (HNSCC), which correlates with poor prognosis, suggesting the potential of harnessing ceramide for cancer treatment. Here, we evaluated the ability of the ceramide analog LCL768 to induce mitophagy and metabolic stress in HNSCC. Mechanistically, LCL768 induced CerS1-mediated endogenous C18-ceramide accumulation in mitochondria to mediate mitophagy, which did not require the CerS1 transporter p17/PERMIT but was dependent on DRP1 activation via nitrosylation at C644. DRP1 facilitated anchoring of the endoplasmic reticulum (ER) and mitochondrial membranes by promoting the association between phosphatidylethanolamine in the ER and cardiolipin in mitochondrial membranes. Mutations of Drp1 that prevented its binding to ER and mitochondrial membranes blocked CerS1/C18-ceramide mitochondrial accumulation, inhibiting LCL768-mediated mitophagy. In addition, LCL768-driven mitophagy altered mitochondrial metabolism, resulting in fumarate depletion and leading to tumor suppression in vivo. Exogenous fumarate supplementation prevented LCL768-mediated mitophagy, mitochondrial trafficking of CerS1, ER-mitochondrial tethering, and tumor suppression in mice. Fumarate metabolism was associated with PARKIN succination at a catalytic cysteine (Cys431), inhibiting its association with PINK1 and ubiquitin and thereby preventing mitophagy. LCL768-induced fumarate depletion attenuated PARKIN succination to promote PARKIN activation and mitophagy, indicating a feed-forward mechanism that regulates mitophagy and fumarate metabolism through PARKIN succination. These data provide a mechanism whereby LCL768/CerS1-C18-ceramide-mediated mitophagy and tumor suppression are regulated by Drp1 nitrosylation, fumarate depletion, and PARKIN succination, providing a metabolic stress signature for lethal mitophagy.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":"44 1","pages":""},"PeriodicalIF":11.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144334901","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":"Dietary Fiber Lacks a Consistent Effect on Immune Checkpoint Blockade Efficacy Across Diverse Murine Tumor Models","authors":"Asael Roichman, Gabriela Reyes-Castellanos, Ziqing Chen, Zihong Chen, Sarah J. Mitchell, Michael R. MacArthur, Akshada Sawant, Llewelyn Levett, Jesse R. Powers, Victoria Burgo, Maria Gomez-Jenkins, Maria Ibrahim, Xincheng Xu, Beianka Tomlinson, Xiang Hang, Eric G. Pamer, Yong Wei, Yibin Kang, Eileen P. White, Joshua D. Rabinowitz","doi":"10.1158/0008-5472.can-24-4378","DOIUrl":"https://doi.org/10.1158/0008-5472.can-24-4378","url":null,"abstract":"Immune checkpoint blockade (ICB) has transformed cancer treatment, but success rates remain limited. Recent research suggests that dietary fiber enhances ICB efficacy through microbiome-dependent mechanisms. However, prior studies in mice compared grain-based chow (high-fiber) to low-fiber purified diet, but these diets also differed in other dimensions, including phytochemicals. Therefore, further work is needed to establish the robustness of the effect of fiber on ICB across cancer types and dietary contexts. Here, we investigated gut microbiome composition, metabolite levels, and ICB activity in mice fed grain-based chow or purified diets with differing quantities of isolated fibers (cellulose and inulin). Compared to dietary fiber content, consumption of chow versus purified diet had a greater effect on the gut microbiome and a much stronger impact on the metabolome. Studies in multiple tumor models revealed that fiber has a weaker impact on ICB (anti-PD-1) efficacy than previously reported. While diet impacted ICB in some models, the effect was not directionally consistent. None of the models tested displayed the pattern expected if fiber controlled ICB efficacy: strong efficacy in both chow and high-fiber purified diet but low efficacy in low-fiber purified diet. Thus, dietary fiber appears to have limited or inconsistent effects on ICB efficacy in mouse models, and other dietary factors that correlate with fiber intake may underlie clinical correlations between fiber consumption and immunotherapy efficacy.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":"6 1","pages":""},"PeriodicalIF":11.2,"publicationDate":"2025-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144334903","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":"XPO1R749Q Mutations Co-occur with POLE Mutations in Cancer and can be Targeted to Overcome Chemoresistance","authors":"Tulasigeri M. Totiger, Wannasiri Chiraphapphaiboon, Yasmine Baca, Sana Chaudhry, Ryan Q. Notti, Skye Montoya, Monika Chojnacka, Gabriel Gaidosh, Jumana Afaghani, Maurizio Affer, Christopher Armstrong, Paul M. Kavanaugh, Efe Karaca, Jenna Zabroski, Michael Lewis, Alyssa Maye, Jacob Jahn, Rajesh K. Soni, Daniel Bilbao, Phil Walker, Andrew Elliott, Emil Lou, Wafik S. El-Deiry, Jose Antonio Rodriguez, Hai Dang Nguyen, Justin Taylor","doi":"10.1158/0008-5472.can-24-3112","DOIUrl":"https://doi.org/10.1158/0008-5472.can-24-3112","url":null,"abstract":"XPO1 is a nuclear export receptor that is essential for cell survival. Previous genomic analyses have identified recurrent XPO1 hotspot mutations in cancer. Here, we conducted a large-scale genomic analysis of 217,570 cancer patients to identify and characterize XPO1 variants from real-world patient tumors. XPO1 harbored a R749Q mutation in various solid tumors, with a clear enrichment in endometrial and colorectal cancers, and XPO1R749Q mutations significantly co-occurred with POLE mutations. Analysis of isogenic colon cancer cell lines revealed that XPO1R749Q localized more in the cytoplasm than wildtype XPO1, with enhanced export of a large number of proteins. Structural modeling of XPO1R749Q suggested an increase in RanGTP affinity, which is consistent with enhanced protein export. A compound library screen using over 200 FDA-approved anticancer drugs indicated a general trend towards chemoresistance, specifically to topoisomerase I inhibition, in XPO1R749Q mutant cells. Mechanistically, XPO1R749Q mutant cells exhibited enhanced DNA damage response via RPA phosphorylation in response to topoisomerase I inhibition. Combining XPO1 and topoisomerase I inhibitors reduced DNA damage-induced RPA phosphorylation and mediated synergistic antitumor effects in cells harboring the XPO1R749Q mutation. Finally, the combination of selinexor and irinotecan overcame chemotherapeutic resistance in xenograft mouse models, prolonging survival. These findings suggest that XPO1 alterations in cancer are selected for in POLE mutant tumors and may confer resistance to DNA-damaging chemotherapies, which have implications for patients with tumors bearing XPO1R749Q and for XPO1 inhibitor development in cancer.","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":"44 1","pages":""},"PeriodicalIF":11.2,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144319744","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":"SLC3A2-Mediated Lysine Uptake by Cancer Cells Restricts T-cell Activity in Hepatocellular Carcinoma.","authors":"Yating Chang, Naizhen Wang, Shaopeng Li, Jiaqi Zhang, Yipeng Rao, Zilong Xu, Lu Li, Hongning Wu, Jun Chen, Yanhua Lin, Xiaoxuan Huang, Pingguo Liu, Jun Zhang, Yueting Liao, Chaolong Lin, Chenghao Huang, Ningshao Xia","doi":"10.1158/0008-5472.CAN-24-3180","DOIUrl":"10.1158/0008-5472.CAN-24-3180","url":null,"abstract":"<p><p>Abnormal amino acid metabolism supports cancer cell proliferation, invasion, and immune evasion in hepatocellular carcinoma (HCC). Previous research exploring amino acid metabolism in HCC has primarily focused on the impact of metabolic reprogramming on tumor cells. In this study, we focused on the role of amino acid metabolism dysregulation in the cross-talk between HCC and T cells. HCC cells disrupted lysine uptake in T cells, leading to impaired T-cell immunity. Lysine deprivation decreased STAT3 levels in T cells, inhibiting T-cell proliferation and effector function and ultimately promoting tumor progression. Mechanistically, HCC cells outcompeted T cells for lysine by expressing high levels of the lysine transporter solute carrier family 3 member 2 (SLC3A2). Clinically, elevated SLC3A2 expression correlated with poor survival and was linked to dysregulated T-cell functional gene signatures in patients with HCC. Furthermore, the multikinase inhibitor lenvatinib induced a c-Myc-SLC3A2 regulatory axis that limited the efficacy of lenvatinib treatment. Lysine supplementation enhanced tumor sensitivity to combined treatment with lenvatinib and anti-PD-1 immunotherapy. These findings suggest that lysine supplementation is a potential therapeutic strategy for treating HCC and enhancing the sensitivity of HCC to tyrosine kinase inhibitors and immune checkpoint blockade.</p><p><strong>Significance: </strong>Hepatocellular carcinoma cells impair T-cell activity by consuming lysine, which can be targeted with SLC3A2 inhibition or lysine supplementation as a therapeutic strategy to enhance antitumor immunity and treatment efficacy.</p>","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":" ","pages":"2250-2267"},"PeriodicalIF":12.5,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691304","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":"Age-Associated Modulation of TREM1/2-Expressing Macrophages Promotes Melanoma Progression and Metastasis.","authors":"Marzia Scortegagna, Rabi Murad, Parinaz Bina, Yongmei Feng, Rebecca A Porritt, Alexey V Terskikh, Xiao Tian, Peter D Adams, Kristiina Vuori, Ze'ev A Ronai","doi":"10.1158/0008-5472.CAN-24-4317","DOIUrl":"10.1158/0008-5472.CAN-24-4317","url":null,"abstract":"<p><p>Aging is a known risk factor for melanoma, yet mechanisms underlying melanoma progression and metastasis in older populations remain largely unexplored. Aging might alter phenotypes of cells in the melanoma microenvironment, selecting for populations that support metastatic progression. In this study, we have demonstrated that age engenders the development of an immunosuppressive tumor microenvironment, which is linked to phenotypes associated with melanoma metastasis. Among cellular populations enriched by aging were macrophages with a tolerogenic phenotype expressing TREM2 and dysfunctional CD8+ T cells with an exhausted phenotype, whereas macrophages with a profibrotic phenotype expressing TREM1 were depleted. Notably, TREM1 inhibition decreased melanoma growth in young but not in old mice, whereas TREM2 inhibition prevented lung metastasis in aged mice. These data identify age-related targets associated with melanoma metastasis and may guide age-dependent immunotherapeutic strategies.</p><p><strong>Significance: </strong>TREM2 is elevated in melanoma-associated macrophages of aged mice and humans and can be inhibited to block melanoma metastasis, highlighting the role of the microenvironment in promoting aging-related metastasis.</p>","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":" ","pages":"2218-2233"},"PeriodicalIF":12.5,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143691290","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":"Spatial Profiling Identifies Regionally Distinct Microenvironments and Targetable Immunosuppressive Mechanisms in Pediatric Osteosarcoma Pulmonary Metastases.","authors":"Jason Eigenbrood, Nathan Wong, Paul Mallory, Janice S Pereira, Demond Williams, Douglass W Morris-Ii, Jessica A Beck, James C Cronk, Carly M Sayers, Monica Mendez, Linus Kaiser, Julie Galindo, Jatinder Singh, Ashley Cardamone, Milind Pore, Michael Kelly, Amy K LeBlanc, Jennifer Cotter, Rosandra N Kaplan, Troy A McEachron","doi":"10.1158/0008-5472.CAN-24-3723","DOIUrl":"10.1158/0008-5472.CAN-24-3723","url":null,"abstract":"<p><p>Osteosarcoma is the most common malignant bone tumor in young patients and remains a significant clinical challenge, particularly at the metastatic stage. Studies detailing the immunosuppressive mechanisms within the metastatic osteosarcoma microenvironment are needed to elucidate the cellular communities in the metastatic microenvironment that support metastatic growth and to identify therapeutic approaches to target the cross-talk between cancer cells and their microenvironment. In this study, we performed spatial transcriptional profiling on a cohort of osteosarcoma pulmonary metastases from pediatric patients. The data revealed a conserved spatial gene expression pattern resembling a foreign body granuloma, characterized by peripheral inflammatory signaling, fibrocollagenous encapsulation, lymphocyte exclusion, and peritumoral macrophage accumulation. The intratumoral microenvironment of these lesions, however, lacked inflammatory signaling. Exploration of spatially distinct drug-gene interactions identified the CXCR4 signaling axis, which displayed spatial heterogeneity and complexity, as a potential therapeutic target that bridges both the intra- and extratumoral microenvironments. Collectively, this study reveals that metastatic osteosarcoma comprises multiple regionally distinct immunosuppressive microenvironments.</p><p><strong>Significance: </strong>Exploration of spatially resolved microenvironments in metastatic osteosarcoma tissues reveals how the tissue architecture promotes immunosuppression and identifies actionable processes to enhance immunotherapy efficacy.</p>","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":" ","pages":"2320-2337"},"PeriodicalIF":12.5,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12170161/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771215","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}

{"title":"Editor's Note: Lactate Dehydrogenase B Is Critical for Hyperactive mTOR-Mediated Tumorigenesis.","authors":"Xiaojun Zha,Fang Wang,Ying Wang,Shaozong He,Yanling Jing,Xueyan Wu,Hongbing Zhang","doi":"10.1158/0008-5472.can-25-1562","DOIUrl":"https://doi.org/10.1158/0008-5472.can-25-1562","url":null,"abstract":"","PeriodicalId":9441,"journal":{"name":"Cancer research","volume":"13 1","pages":"2339"},"PeriodicalIF":11.2,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144295859","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}