Cancer discovery最新文献_第9页

Multiplexed In Vivo Screen Pinpoints Drivers of Breast Cancer Aneuploidies. 多重体内筛选确定乳腺癌非整倍体的驱动因素。

IF 29.5 1区医学

Cancer discovery Pub Date : 2026-09-01 DOI: 10.1158/2159-8290.CD-RW2026-069

引用次数: 0

Insights on Future Directions in Cancer Research from the AACR Trailblazer Cancer Research Grant Awardees. 美国癌症研究协会开拓者癌症研究基金获得者对癌症研究未来方向的见解。

IF 29.5 1区医学

Cancer discovery Pub Date : 2026-09-01 DOI: 10.1158/2159-8290.CD-26-1356

Ana Luísa Correia, Karen O Dixon, J Justin Milner, Nathan H Parker, Theodore L Roth, Jonathan M Tsai, Jessalyn M Ubellacker, Natalie I Vokes, Samir Zaidi, Effie Apostolou, Adrienne Boire, Carla J Chibwesha, Yifat Merbl, Aaron M Newman, Tuomas Tammela

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Mitochondrial Complex I at the Crossroads of NK cell Dysfunction in Glioblastoma 线粒体复合体I在胶质母细胞瘤中NK细胞功能障碍的十字路口

IF 28.2 1区医学

Cancer discovery Pub Date : 2026-09-01 DOI: 10.1158/2159-8290.cd-26-1267

Silvia Tiberti, Katayoun Rezvani, May Daher

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Arginine Suppresses Tumorigenesis by Enhancing Antigen Presentation. 精氨酸通过增强抗原呈递抑制肿瘤发生。

IF 29.5 1区医学

Cancer discovery Pub Date : 2026-09-01 DOI: 10.1158/2159-8290.CD-RW2026-072

引用次数: 0

PHGDH-High Dormant Tumor Cells Evade Immunity and Drive Metastasis. 高phgdh休眠肿瘤细胞逃避免疫和驱动转移。

IF 29.5 1区医学

Cancer discovery Pub Date : 2026-09-01 DOI: 10.1158/2159-8290.CD-RW2026-073

引用次数: 0

The Evolution of Polyclonal Competition in Aging Hematopoiesis. 衰老造血过程中多克隆竞争的演化。

IF 29.5 1区医学

Cancer discovery Pub Date : 2026-09-01 DOI: 10.1158/2159-8290.CD-25-0990

Nathaniel V Mon Père, Francesco Terenzi, Benjamin Werner

{"title":"The Evolution of Polyclonal Competition in Aging Hematopoiesis.","authors":"Nathaniel V Mon Père, Francesco Terenzi, Benjamin Werner","doi":"10.1158/2159-8290.CD-25-0990","DOIUrl":"10.1158/2159-8290.CD-25-0990","url":null,"abstract":"Clonal hematopoiesis (CH)-the expansion of genetic variants in blood-is a prime example of somatic evolution. Although it often precedes malignant transformation, many aspects of this process remain unknown. We show that a model of polyclonal competition, in which selectively advantaged clones continually occur and compete, explains observed CH dynamics throughout human life. We quantify the fitness distribution and occurrence rate of clonal expansions using either variant trajectories or hematopoietic stem cell (HSC) genetic heterogeneity. Inferences on both data converge. Approximately 3 fit clones enter the HSC pool per year, yet rarely more than 5 achieve >1.5% frequency throughout life. The fittest clones emerge predominantly later in life in accordance with a multistep evolutionary process. DNMT3A variants were enriched for single-hit clones, whereas TET2, ASXL1, JAK2, SF3B1, and SRSF2 showed enrichment for multihit evolution. These findings suggest that precursors of hematologic malignancies are identifiable prior to transformation and may facilitate early intervention strategies.Significance: We study the evolution of CH through longitudinal variant trajectories and HSC genetic heterogeneity. Clonal interference and a multistep evolutionary process become evident. Clones further advanced on the path to malignant transformation are identifiable, and propensities for multiple hits differ among most commonly mutated CH variants.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":" ","pages":"1765-1779"},"PeriodicalIF":29.5,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13531000/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147834243","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

Endogenous Metabolite Glues Can Be Therapeutically Exploited. 内源性代谢物胶可用于治疗。

IF 29.5 1区医学

Cancer discovery Pub Date : 2026-09-01 DOI: 10.1158/2159-8290.CD-RW2026-074

引用次数: 0

Tumor-Secreted ADAMTSL4 Activates Latent TGFβ1 to Drive Cancer Cachexia 肿瘤分泌ADAMTSL4激活潜伏tgf - β1驱动癌症恶病质

IF 28.2 1区医学

Cancer discovery Pub Date : 2026-09-01 DOI: 10.1158/2159-8290.cd-26-0045

Juliano Machado, Vignesh Karthikaisamy, Hermine Mohr, Doris Kaltenecker, Pia Benedikt, Pauline Morigny, Amit Mhamane, Julia Geppert, Amy Rose Fumo, Kerstin Haase, Estefania Simoes, Joanna D.C.C. Lima, Anastasia Georgiadi, Achim Krüger, José Pinhata Otoch, Marc E. Martignoni, Vickie E. Baracos, Mariam Jamal-Hanjani, Marilia C.L. Seelaender, Olga Prokopchuk, Julia Szendrödi, Maria Rohm, Stephan Herzig, Mauricio Berriel Diaz

{"title":"Tumor-Secreted ADAMTSL4 Activates Latent TGFβ1 to Drive Cancer Cachexia","authors":"Juliano Machado, Vignesh Karthikaisamy, Hermine Mohr, Doris Kaltenecker, Pia Benedikt, Pauline Morigny, Amit Mhamane, Julia Geppert, Amy Rose Fumo, Kerstin Haase, Estefania Simoes, Joanna D.C.C. Lima, Anastasia Georgiadi, Achim Krüger, José Pinhata Otoch, Marc E. Martignoni, Vickie E. Baracos, Mariam Jamal-Hanjani, Marilia C.L. Seelaender, Olga Prokopchuk, Julia Szendrödi, Maria Rohm, Stephan Herzig, Mauricio Berriel Diaz","doi":"10.1158/2159-8290.cd-26-0045","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-26-0045","url":null,"abstract":"Cancer cachexia is a devastating wasting syndrome with no approved therapies. In this study, we identify the tumor-derived glycoprotein ADAMTSL4 as a circulating factor associated with body weight loss in preclinical cachexia models and patients with colorectal and lung cancers. In mice, Adamtsl4 overexpression converted non–cachexia-inducing tumors into cachexia-inducing tumors, whereas its deletion in cachexia-inducing tumors spared fat and muscle, blunted muscle atrophy signatures, and reduced cachexia severity. ADAMTSL4 engages the latency-associated peptide (LAP) of TGFβ1, promoting local activation of TGFβ1 at muscle cell membranes. Genetic blockade of proTGFβ1 or pharmacologic inhibition of TGFβ signaling reduced ADAMTSL4-dependent wasting in adipocytes and muscle cells. Suppression of tumor-derived ADAMTSL4 attenuated skeletal muscle fibrosis in mice. Together, the association between increased circulating ADAMTSL4 levels and TGFβ–driven muscle atrophy and fibrosis gene signatures in patients with cachectic cancer identifies ADAMTSL4 as an upstream regulator of TGFβ1 and a potential therapeutic target in cancer cachexia. Significance: Cancer cachexia lacks effective therapies and remains a major cause of cancer-related morbidity and mortality. We identify tumor-derived ADAMTSL4 as an upstream regulator of latent TGFβ activation via LAP engagement that promotes multiorgan wasting and fibrosis-related remodeling. Targeting ADAMTSL4 may provide a selective therapeutic strategy without systemic TGFβ pathway blockade.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"74 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2026-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148860834","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

Malignant Transition in Three Dimensions 三维恶性转移

IF 28.2 1区医学

Cancer discovery Pub Date : 2026-09-01 DOI: 10.1158/2159-8290.cd-26-1266

Zehua Jing, Mingyao Li

引用次数: 0

AI Model Predicts Cancer Development, Diagnoses Tumors 人工智能模型预测癌症发展，诊断肿瘤

IF 28.2 1区医学

Cancer discovery Pub Date : 2026-08-21 DOI: 10.1158/2159-8290.cd-nw2026-0083

引用次数: 0