Nature Reviews Cancer最新文献

{"title":"Protection against tumour formation","authors":"Anna Dart","doi":"10.1038/s41568-024-00762-y","DOIUrl":"10.1038/s41568-024-00762-y","url":null,"abstract":"Ciwinska et al. asked whether natural tissue remodelling can drive mutant cell expansion and identified three protective mechanisms in the healthy mouse mammary gland that constrain the ability of mutant cells to transform and give rise to cancer.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"24 11","pages":"741-741"},"PeriodicalIF":72.5,"publicationDate":"2024-10-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142374139","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":"Modelling and deciphering tumour metabolism in CRISPR screens.","authors":"Johannes Zuber, Wilhelm Palm","doi":"10.1038/s41568-024-00758-8","DOIUrl":"https://doi.org/10.1038/s41568-024-00758-8","url":null,"abstract":"","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":" ","pages":""},"PeriodicalIF":72.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361822","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":"Macrophages and T cells in metabolic disorder-associated cancers","authors":"Daniel Taranto, Daan J. Kloosterman, Leila Akkari","doi":"10.1038/s41568-024-00743-1","DOIUrl":"10.1038/s41568-024-00743-1","url":null,"abstract":"Cancer and metabolic disorders have emerged as major global health challenges, reaching epidemic levels in recent decades. Often viewed as separate issues, metabolic disorders are shown by mounting evidence to heighten cancer risk and incidence. The intricacies underlying this connection are still being unraveled and encompass a complex interplay between metabolites, cancer cells and immune cells within the tumour microenvironment (TME). Here, we outline the interplay between metabolic and immune cell dysfunction in the context of three highly prevalent metabolic disorders, namely obesity; two associated liver diseases, metabolic dysfunction-associated steatotic liver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH); and type 2 diabetes. We focus primarily on macrophages and T cells, the critical roles of which in dictating inflammatory response and immune surveillance in metabolic disorder-associated cancers are widely reported. Moreover, considering the ever-increasing number of patients prescribed with metabolism disorder-altering drugs and diets in recent years, we discuss how these therapies modulate systemic and local immune phenotypes, consequently impacting cancer malignancy. Collectively, unraveling the determinants of metabolic disorder-associated immune landscape and their role in fuelling cancer malignancy will provide a framework essential to therapeutically address these highly prevalent diseases. Metabolic disorders, such as obesity, metabolic dysfunction-associated steatotic liver disease (MASLD), metabolic dysfunction-associated steatohepatitis (MASH) and type 2 diabetes, are increasingly recognized as significant contributors to cancer development. Here, Taranto, Kloosterman and Akkari explore the influence of metabolic disorders on tumour progression through the metabolic interactions of macrophages and T cells to alter immune function and cancer outcomes.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"24 11","pages":"744-767"},"PeriodicalIF":72.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142361821","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":"Defining precancer: a grand challenge for the cancer community","authors":"Jessica Faupel-Badger, Indu Kohaar, Manisha Bahl, Andrew T. Chan, Joshua D. Campbell, Li Ding, Angelo M. De Marzo, Anirban Maitra, Daniel T. Merrick, Ernest T. Hawk, Ignacio I. Wistuba, Irene M. Ghobrial, Scott M. Lippman, Karen H. Lu, Mark Lawler, Neil E. Kay, Thea D. Tlsty, Timothy R. Rebbeck, Sudhir Srivastava, the Precancer Think Tank Team","doi":"10.1038/s41568-024-00744-0","DOIUrl":"10.1038/s41568-024-00744-0","url":null,"abstract":"The term ‘precancer’ typically refers to an early stage of neoplastic development that is distinguishable from normal tissue owing to molecular and phenotypic alterations, resulting in abnormal cells that are at least partially self-sustaining and function outside of normal cellular cues that constrain cell proliferation and survival. Although such cells are often histologically distinct from both the corresponding normal and invasive cancer cells of the same tissue origin, defining precancer remains a challenge for both the research and clinical communities. Once sufficient molecular and phenotypic changes have occurred in the precancer, the tissue is identified as a ‘cancer’ by a histopathologist. While even diagnosing cancer can at times be challenging, the determination of invasive cancer is generally less ambiguous and suggests a high likelihood of and potential for metastatic disease. The ‘hallmarks of cancer’ set out the fundamental organizing principles of malignant transformation but exactly how many of these hallmarks and in what configuration they define precancer has not been clearly and consistently determined. In this Expert Recommendation, we provide a starting point for a conceptual framework for defining precancer, which is based on molecular, pathological, clinical and epidemiological criteria, with the goal of advancing our understanding of the initial changes that occur and opportunities to intervene at the earliest possible time point. In this Expert Recommendation, Faupel-Badger and colleagues present a conceptual framework to define precancer and advance our understanding of the earliest changes that occur in the progression to overt cancer, providing novel opportunities to intervene to prevent or treat their emergence.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"24 11","pages":"792-809"},"PeriodicalIF":72.5,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142360107","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":"A standing platform for cancer drug development using ctDNA-based evidence of recurrence","authors":"Arielle J. Medford, Ariel B. Carmeli, Alexandra Ritchie, Nikhil Wagle, Levi Garraway, Eric S. Lander, Aparna Parikh","doi":"10.1038/s41568-024-00742-2","DOIUrl":"10.1038/s41568-024-00742-2","url":null,"abstract":"The time required to conduct clinical trials limits the rate at which we can evaluate and deliver new treatment options to patients with cancer. New approaches to increase trial efficiency while maintaining rigor would benefit patients, especially in oncology, in which adjuvant trials hold promise for intercepting metastatic disease, but typically require large numbers of patients and many years to complete. We envision a standing platform — an infrastructure to support ongoing identification and trial enrolment of patients with cancer with early molecular evidence of disease (MED) after curative-intent therapy for early-stage cancer, based on the presence of circulating tumour DNA. MED strongly predicts subsequent recurrence, with the vast majority of patients showing radiographic evidence of disease within 18 months. Such a platform would allow efficient testing of many treatments, from small exploratory studies to larger pivotal trials. Trials enrolling patients with MED but without radiographic evidence of disease have the potential to advance drug evaluation because they can be smaller (given high probability of recurrence) and faster (given short time to recurrence) than conventional adjuvant trials. Circulating tumour DNA may also provide a valuable early biomarker of treatment effect, which would allow small signal-finding trials. In this Perspective, we discuss how such a platform could be established. Efficient clinical trials are crucial for advancing cancer care. In this Perspective, the authors propose a platform that leverages circulating tumour DNA to identify patients with early-stage cancer at high risk of recurrence and enrol them onto therapeutic clinical trials. This approach would enable faster, smaller trials and streamline evaluation of drugs aimed at preventing disease recurrence and increasing cure.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"24 11","pages":"810-821"},"PeriodicalIF":72.5,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142329983","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":"VIBRANT: mapping cell phenotypes using vibrational spectroscopy","authors":"Xinwen Liu","doi":"10.1038/s41568-024-00749-9","DOIUrl":"10.1038/s41568-024-00749-9","url":null,"abstract":"In this Tools of the Trade article, Xinwen Liu describes the development of VIBRANT, a vibrational spectroscopy method for high-content phenotypic profiling, and highlights its use to predict drug mechanisms of action or identify potential drug candidates.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"24 12","pages":"826-826"},"PeriodicalIF":72.5,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142245346","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 recruitment of metastasis-associated monocytes","authors":"Suhn Hyung Kim, Keehoon Jung","doi":"10.1038/s41568-024-00753-z","DOIUrl":"10.1038/s41568-024-00753-z","url":null,"abstract":"In this Journal Club, Kim and Jung discuss a study that demonstrates the role of CCL2 in recruiting monocytes to the metastasic site.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"24 11","pages":"743-743"},"PeriodicalIF":72.5,"publicationDate":"2024-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142245347","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":"Managing cancer following the World Trade Center disaster","authors":"Rachel Zeig-Owens, David J. Prezant","doi":"10.1038/s41568-024-00730-6","DOIUrl":"10.1038/s41568-024-00730-6","url":null,"abstract":"The World Trade Center (WTC) disaster exposed individuals to carcinogens, leading to elevated cancer rates. Responders who received care through the WTC Health Program have higher survival rates. Twenty-three years post-disaster, we summarize cancer incidence and outcome studies in this population and highlight the importance of a dedicated health programme response.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"24 11","pages":"737-738"},"PeriodicalIF":72.5,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142166193","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 evolutionary theory of cancer: challenges and potential solutions","authors":"Lucie Laplane, Carlo C. Maley","doi":"10.1038/s41568-024-00734-2","DOIUrl":"10.1038/s41568-024-00734-2","url":null,"abstract":"The clonal evolution model of cancer was developed in the 1950s–1970s and became central to cancer biology in the twenty-first century, largely through studies of cancer genetics. Although it has proven its worth, its structure has been challenged by observations of phenotypic plasticity, non-genetic forms of inheritance, non-genetic determinants of clone fitness and non-tree-like transmission of genes. There is even confusion about the definition of a clone, which we aim to resolve. The performance and value of the clonal evolution model depends on the empirical extent to which evolutionary processes are involved in cancer, and on its theoretical ability to account for those evolutionary processes. Here, we identify limits in the theoretical performance of the clonal evolution model and provide solutions to overcome those limits. Although we do not claim that clonal evolution can explain everything about cancer, we show how many of the complexities that have been identified in the dynamics of cancer can be integrated into the model to improve our current understanding of cancer. Clonal evolution is now a central theoretical framework in cancer research. In this Perspective, Laplane and Maley identify challenges to that theory such that some non-evolutionary phenomena in cancer cannot be captured by the theory. They also outline how other challenges, including non-genetic heredity, phenotypic plasticity, reticulate evolution and clone diversity, can be included in an expanded cancer evolutionary theory.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"24 10","pages":"718-733"},"PeriodicalIF":72.5,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142160471","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":"Creating a dietary vulnerability","authors":"Daniela Senft","doi":"10.1038/s41568-024-00751-1","DOIUrl":"10.1038/s41568-024-00751-1","url":null,"abstract":"In a recent Nature paper, Ruggero and colleagues found that fasting and ketogenic diets induce metabolic rewiring through a translational mechanism involving MNK-mediated phosphorylation of eIF4E, which enhances ketogenesis. This process creates a metabolic vulnerability in pancreatic cancer that could be therapeutically exploited.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"24 10","pages":"652-652"},"PeriodicalIF":72.5,"publicationDate":"2024-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142160470","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}