Nature cancer最新文献

Author Correction: Evolving landscape of nasopharyngeal carcinoma therapy. 作者更正：鼻咽癌治疗的发展前景。

IF 28.5 1区医学

Nature cancer Pub Date : 2025-10-10 DOI: 10.1038/s43018-025-01064-4

Kar Wei Chin, Wan-Qin Chong, Boon Cher Goh, Brigette B Y Ma

引用次数: 0

Primary tumor chromatin landscape governs metastatic organotropism. 原发肿瘤染色质结构决定转移性器官倾向。

IF 28.5 1区医学

Nature cancer Pub Date : 2025-10-10 DOI: 10.1038/s43018-025-01048-4

Amy C Gladstein, David M Feldser

引用次数: 0

A cellular and spatial atlas of TP53-associated tissue remodeling defines a multicellular tumor ecosystem in lung adenocarcinoma. tp53相关组织重塑的细胞和空间图谱定义了肺腺癌的多细胞肿瘤生态系统。

IF 28.5 1区医学

Nature cancer Pub Date : 2025-10-07 DOI: 10.1038/s43018-025-01053-7

William Zhao, Thinh T Nguyen, Atharva Bhagwat, Akhil Kumar, Bruno Giotti, Benjamin Kepecs, Jason L Weirather, Navin R Mahadevan, Asa Segerstolpe, Komal Dolasia, Jamshid Abdul-Ghafar, Naomi R Besson, Stephanie M Jones, Brian Y Soong, Chendi Li, Sebastien Vigneau, Michal Slyper, Isaac Wakiro, Mei-Ju Su, Karla Helvie, Allison Frangieh, Judit Jane-Valbuena, Orr Ashenberg, Mark Awad, Asaf Rotem, Raphael Bueno, Orit Rozenblatt-Rosen, Kathleen Pfaff, Scott Rodig, Aaron N Hata, Aviv Regev, Bruce E Johnson, Alexander M Tsankov

{"title":"A cellular and spatial atlas of TP53-associated tissue remodeling defines a multicellular tumor ecosystem in lung adenocarcinoma.","authors":"William Zhao, Thinh T Nguyen, Atharva Bhagwat, Akhil Kumar, Bruno Giotti, Benjamin Kepecs, Jason L Weirather, Navin R Mahadevan, Asa Segerstolpe, Komal Dolasia, Jamshid Abdul-Ghafar, Naomi R Besson, Stephanie M Jones, Brian Y Soong, Chendi Li, Sebastien Vigneau, Michal Slyper, Isaac Wakiro, Mei-Ju Su, Karla Helvie, Allison Frangieh, Judit Jane-Valbuena, Orr Ashenberg, Mark Awad, Asaf Rotem, Raphael Bueno, Orit Rozenblatt-Rosen, Kathleen Pfaff, Scott Rodig, Aaron N Hata, Aviv Regev, Bruce E Johnson, Alexander M Tsankov","doi":"10.1038/s43018-025-01053-7","DOIUrl":"10.1038/s43018-025-01053-7","url":null,"abstract":"Tumor protein p53 (TP53) is the most frequently mutated gene across many cancers and is associated with shorter overall survival in lung adenocarcinoma (LUAD). Here, to define how TP53 mutations affect the LUAD tumor microenvironment (TME), we constructed a multiomic cellular and spatial atlas of 23 treatment-naive human lung tumors. We found that TP53-mutant malignant cells lose alveolar identity and upregulate highly proliferative and entropic gene expression programs consistently across LUAD tumors from resectable clinical samples, genetically engineered mouse models, and cell lines harboring a wide spectrum of TP53 mutations. We further identified a multicellular tumor niche composed of SPP1+ macrophages and collagen-expressing fibroblasts that coincides with hypoxic, prometastatic expression programs in TP53-mutant tumors. Spatially correlated angiostatic and immune checkpoint interactions, including CD274-PDCD1 and PVR-TIGIT, are also enriched in TP53-mutant LUAD tumors and likely engender a more favorable response to checkpoint blockade therapy. Our systematic approach can be used to investigate genotype-associated TMEs in other cancers.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145244765","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

Hijacked brain-gut polysynaptic pathway promotes colorectal cancer growth. 劫持脑肠多突触通路促进结直肠癌生长。

IF 28.5 1区医学

Nature cancer Pub Date : 2025-10-07 DOI: 10.1038/s43018-025-01050-w

引用次数: 0

Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia. 在急性髓系白血病中，SLAMF6的异常表达构成了一种可靶向的免疫逃逸机制。

IF 28.5 1区医学

Nature cancer Pub Date : 2025-10-03 DOI: 10.1038/s43018-025-01054-6

Carl Sandén, Niklas Landberg, Pablo Peña-Martínez, Hanna Thorsson, Shruti Daga, Noelia Puente-Moncada, Maria Rodriguez-Zabala, Sofia von Palffy, Marianne Rissler, Vladimir Lazarevic, Gunnar Juliusson, Mats Ohlin, Axel Hyrenius-Wittsten, Christina Orsmark-Pietras, Henrik Lilljebjörn, Helena Ågerstam, Thoas Fioretos

{"title":"Aberrant expression of SLAMF6 constitutes a targetable immune escape mechanism in acute myeloid leukemia.","authors":"Carl Sandén, Niklas Landberg, Pablo Peña-Martínez, Hanna Thorsson, Shruti Daga, Noelia Puente-Moncada, Maria Rodriguez-Zabala, Sofia von Palffy, Marianne Rissler, Vladimir Lazarevic, Gunnar Juliusson, Mats Ohlin, Axel Hyrenius-Wittsten, Christina Orsmark-Pietras, Henrik Lilljebjörn, Helena Ågerstam, Thoas Fioretos","doi":"10.1038/s43018-025-01054-6","DOIUrl":"https://doi.org/10.1038/s43018-025-01054-6","url":null,"abstract":"Immunotherapy has shown limited success in acute myeloid leukemia (AML), indicating an incomplete understanding of the underlying immunoregulatory mechanisms. Here we identify an immune evasion mechanism present in 60% of AML cases, wherein primitive AML cells aberrantly express the lymphoid surface protein SLAMF6 (signaling lymphocyte activation molecule family member 6). Knockout of SLAMF6 in AML cells enables T cell activation and highly efficient killing of leukemia cells in coculture systems, demonstrating that SLAMF6 protects AML cells from recognition and elimination by the immune system in a mode analogous to the programmed cell death protein-ligand (PDL1/PD1) axis. Targeting SLAMF6 with an antibody against the SLAMF6 dimerization site inhibits the SLAMF6-SLAMF6 interaction and induces T cell activation and killing of AML cells both in vitro and in humanized in vivo models. In conclusion, we show that aberrant expression of SLAMF6 is a common and targetable immune escape mechanism that could pave the way for immunotherapy in AML.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-10-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145225533","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

Radiopharma pipeline builds ahead of key data. 放射性药物管线在关键数据之前建立。

IF 28.5 1区医学

Nature cancer Pub Date : 2025-10-01 DOI: 10.1038/s43018-025-01044-8

Melanie Senior

引用次数: 0

SMAD4 induces opposite effects on metastatic growth from pancreatic tumors depending on the organ of residence. SMAD4对胰腺肿瘤转移生长的影响取决于居住器官。

IF 28.5 1区医学

Nature cancer Pub Date : 2025-09-25 DOI: 10.1038/s43018-025-01047-5

Kaloyan M Tsanov, Francisco M Barriga, Yu-Jui Ho, Direna Alonso-Curbelo, Geulah Livshits, Sha Tian, Richard P Koche, Timour Baslan, Janelle Simon, Alexandra N Wuest, José Reyes, Jin Park, Wei Luan, John E Wilkinson, Umesh Bhanot, Jordana Ray-Kirton, Ignas Masilionis, Nevenka Dimitrova, Christine A Iacobuzio-Donahue, Ronan Chaligné, Dana Pe'er, Joan Massagué, Scott W Lowe

{"title":"SMAD4 induces opposite effects on metastatic growth from pancreatic tumors depending on the organ of residence.","authors":"Kaloyan M Tsanov, Francisco M Barriga, Yu-Jui Ho, Direna Alonso-Curbelo, Geulah Livshits, Sha Tian, Richard P Koche, Timour Baslan, Janelle Simon, Alexandra N Wuest, José Reyes, Jin Park, Wei Luan, John E Wilkinson, Umesh Bhanot, Jordana Ray-Kirton, Ignas Masilionis, Nevenka Dimitrova, Christine A Iacobuzio-Donahue, Ronan Chaligné, Dana Pe'er, Joan Massagué, Scott W Lowe","doi":"10.1038/s43018-025-01047-5","DOIUrl":"10.1038/s43018-025-01047-5","url":null,"abstract":"The role of driver gene mutations in sustaining tumor growth at metastatic sites is poorly understood. SMAD4 inactivation is a paradigm of such mutations and a hallmark of pancreatic ductal adenocarcinoma (PDAC). To determine whether metastatic tumors are dependent on SMAD4 inactivation, we developed a mouse model of PDAC that enables spatiotemporal control of Smad4 expression. While Smad4 inactivation in the premalignant pancreas facilitated the formation of primary tumors, Smad4 reactivation in metastatic disease suppressed liver metastases but promoted lung metastases. These divergent effects were underpinned by organ-biased differences in the tumor cells' chromatin state that emerged in the premalignant pancreas and were distinguished by the dominance of KLF4 versus RUNX1 transcription factors. Our results show how epigenetic states favored by the organ of residence can influence the output of driver mutations in metastatic tumors, which has implications for interpreting tumor genetics and therapeutically targeting metastatic disease.","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":28.5,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149984","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

Evolving landscape of nasopharyngeal carcinoma therapy 鼻咽癌治疗的发展前景。

IF 28.5 1区医学

Nature cancer Pub Date : 2025-09-19 DOI: 10.1038/s43018-025-01045-7

Kar Wei Chin, Wan-Qin Chong, Boon Cher Goh, Brigette B. Y. Ma

引用次数: 0

Key highlights from the ESMO Targeted Anticancer Therapies Asia Congress 2025 ESMO靶向抗癌治疗2025亚洲大会的主要亮点。

IF 28.5 1区医学

Nature cancer Pub Date : 2025-09-12 DOI: 10.1038/s43018-025-01046-6

Vincenzo Giacco

引用次数: 0

Past, present and future of drug conjugates for cancer therapy 癌症治疗药物偶联物的过去、现在和未来。