Pub Date : 2023-02-08DOI: 10.1038/s41568-023-00551-z
Gabrielle Brewer
In this study, Jung-Garcia et al. use in vitro and in vivo modelling to demonstrate the role of LAP1 in promoting melanoma cell invasion and highlight its link to metastatic dissemination.
{"title":"LAP1 squeezes out ahead","authors":"Gabrielle Brewer","doi":"10.1038/s41568-023-00551-z","DOIUrl":"10.1038/s41568-023-00551-z","url":null,"abstract":"In this study, Jung-Garcia et al. use in vitro and in vivo modelling to demonstrate the role of LAP1 in promoting melanoma cell invasion and highlight its link to metastatic dissemination.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 3","pages":"114-114"},"PeriodicalIF":78.5,"publicationDate":"2023-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9363138","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}
Pub Date : 2023-02-06DOI: 10.1038/s41568-022-00546-2
Simon T. Barry, Dmitry I. Gabrilovich, Owen J. Sansom, Andrew D. Campbell, Jennifer P. Morton
Myeloid cells are pivotal within the immunosuppressive tumour microenvironment. The accumulation of tumour-modified myeloid cells derived from monocytes or neutrophils — termed ‘myeloid-derived suppressor cells’ — and tumour-associated macrophages is associated with poor outcome and resistance to treatments such as chemotherapy and immune checkpoint inhibitors. Unfortunately, there has been little success in large-scale clinical trials of myeloid cell modulators, and only a few distinct strategies have been used to target suppressive myeloid cells clinically so far. Preclinical and translational studies have now elucidated specific functions for different myeloid cell subpopulations within the tumour microenvironment, revealing context-specific roles of different myeloid cell populations in disease progression and influencing response to therapy. To improve the success of myeloid cell-targeted therapies, it will be important to target tumour types and patient subsets in which myeloid cells represent the dominant driver of therapy resistance, as well as to determine the most efficacious treatment regimens and combination partners. This Review discusses what we can learn from work with the first generation of myeloid modulators and highlights recent developments in modelling context-specific roles for different myeloid cell subtypes, which can ultimately inform how to drive more successful clinical trials. Myeloid cells in the tumour microenvironment strongly influence tumour progression, and targeting these cells has been a key clinical focus. In this Review, Barry et al. discuss preclinical and clinical data on myeloid-targeting therapies, with a focus on how understanding context-specific effects might aid the design of successful clinical trials for these drugs.
{"title":"Therapeutic targeting of tumour myeloid cells","authors":"Simon T. Barry, Dmitry I. Gabrilovich, Owen J. Sansom, Andrew D. Campbell, Jennifer P. Morton","doi":"10.1038/s41568-022-00546-2","DOIUrl":"10.1038/s41568-022-00546-2","url":null,"abstract":"Myeloid cells are pivotal within the immunosuppressive tumour microenvironment. The accumulation of tumour-modified myeloid cells derived from monocytes or neutrophils — termed ‘myeloid-derived suppressor cells’ — and tumour-associated macrophages is associated with poor outcome and resistance to treatments such as chemotherapy and immune checkpoint inhibitors. Unfortunately, there has been little success in large-scale clinical trials of myeloid cell modulators, and only a few distinct strategies have been used to target suppressive myeloid cells clinically so far. Preclinical and translational studies have now elucidated specific functions for different myeloid cell subpopulations within the tumour microenvironment, revealing context-specific roles of different myeloid cell populations in disease progression and influencing response to therapy. To improve the success of myeloid cell-targeted therapies, it will be important to target tumour types and patient subsets in which myeloid cells represent the dominant driver of therapy resistance, as well as to determine the most efficacious treatment regimens and combination partners. This Review discusses what we can learn from work with the first generation of myeloid modulators and highlights recent developments in modelling context-specific roles for different myeloid cell subtypes, which can ultimately inform how to drive more successful clinical trials. Myeloid cells in the tumour microenvironment strongly influence tumour progression, and targeting these cells has been a key clinical focus. In this Review, Barry et al. discuss preclinical and clinical data on myeloid-targeting therapies, with a focus on how understanding context-specific effects might aid the design of successful clinical trials for these drugs.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 4","pages":"216-237"},"PeriodicalIF":78.5,"publicationDate":"2023-02-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9280435","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}
Pub Date : 2023-02-02DOI: 10.1038/s41568-023-00550-0
Daniela Senft
This study shows how the selective immune pressure in early-stage tumours drives interferon-γ-dependent metabolic reprogramming in cancer cells to mediate immune escape.
{"title":"T cells feed into cancer immune escape","authors":"Daniela Senft","doi":"10.1038/s41568-023-00550-0","DOIUrl":"10.1038/s41568-023-00550-0","url":null,"abstract":"This study shows how the selective immune pressure in early-stage tumours drives interferon-γ-dependent metabolic reprogramming in cancer cells to mediate immune escape.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 3","pages":"113-113"},"PeriodicalIF":78.5,"publicationDate":"2023-02-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9391742","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}
Pub Date : 2023-01-30DOI: 10.1038/s41568-022-00544-4
Antoinette van Weverwijk, Karin E. de Visser
Tumours display an astonishing variation in the spatial distribution, composition and activation state of immune cells, which impacts their progression and response to immunotherapy. Shedding light on the mechanisms that govern the diversity and function of immune cells in the tumour microenvironment will pave the way for the development of more tailored immunomodulatory strategies for the benefit of patients with cancer. Cancer cells, by virtue of their paracrine and juxtacrine communication mechanisms, are key contributors to intertumour heterogeneity in immune contextures. In this Review, we discuss how cancer cell-intrinsic features, including (epi)genetic aberrations, signalling pathway deregulation and altered metabolism, play a key role in orchestrating the composition and functional state of the immune landscape, and influence the therapeutic benefit of immunomodulatory strategies. Moreover, we highlight how targeting cancer cell-intrinsic parameters or their downstream immunoregulatory pathways is a viable strategy to manipulate the tumour immune milieu in favour of antitumour immunity. This Review outlines how the profound intertumoural heterogeneity in immune landscapes of tumours is shaped by cancer cell-intrinsic alterations and highlights how the crosstalk between these two continuously evolving systems not only challenges therapy success of immunomodulatory drugs but also provides the basis for new therapeutic strategies to overcome immune evasion.
{"title":"Mechanisms driving the immunoregulatory function of cancer cells","authors":"Antoinette van Weverwijk, Karin E. de Visser","doi":"10.1038/s41568-022-00544-4","DOIUrl":"10.1038/s41568-022-00544-4","url":null,"abstract":"Tumours display an astonishing variation in the spatial distribution, composition and activation state of immune cells, which impacts their progression and response to immunotherapy. Shedding light on the mechanisms that govern the diversity and function of immune cells in the tumour microenvironment will pave the way for the development of more tailored immunomodulatory strategies for the benefit of patients with cancer. Cancer cells, by virtue of their paracrine and juxtacrine communication mechanisms, are key contributors to intertumour heterogeneity in immune contextures. In this Review, we discuss how cancer cell-intrinsic features, including (epi)genetic aberrations, signalling pathway deregulation and altered metabolism, play a key role in orchestrating the composition and functional state of the immune landscape, and influence the therapeutic benefit of immunomodulatory strategies. Moreover, we highlight how targeting cancer cell-intrinsic parameters or their downstream immunoregulatory pathways is a viable strategy to manipulate the tumour immune milieu in favour of antitumour immunity. This Review outlines how the profound intertumoural heterogeneity in immune landscapes of tumours is shaped by cancer cell-intrinsic alterations and highlights how the crosstalk between these two continuously evolving systems not only challenges therapy success of immunomodulatory drugs but also provides the basis for new therapeutic strategies to overcome immune evasion.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 4","pages":"193-215"},"PeriodicalIF":78.5,"publicationDate":"2023-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9279313","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}
Pub Date : 2023-01-19DOI: 10.1038/s41568-022-00543-5
David A. Guertin, Kathryn E. Wellen
Few metabolites can claim a more central and versatile role in cell metabolism than acetyl coenzyme A (acetyl-CoA). Acetyl-CoA is produced during nutrient catabolism to fuel the tricarboxylic acid cycle and is the essential building block for fatty acid and isoprenoid biosynthesis. It also functions as a signalling metabolite as the substrate for lysine acetylation reactions, enabling the modulation of protein functions in response to acetyl-CoA availability. Recent years have seen exciting advances in our understanding of acetyl-CoA metabolism in normal physiology and in cancer, buoyed by new mouse models, in vivo stable-isotope tracing approaches and improved methods for measuring acetyl-CoA, including in specific subcellular compartments. Efforts to target acetyl-CoA metabolic enzymes are also advancing, with one therapeutic agent targeting acetyl-CoA synthesis receiving approval from the US Food and Drug Administration. In this Review, we give an overview of the regulation and cancer relevance of major metabolic pathways in which acetyl-CoA participates. We further discuss recent advances in understanding acetyl-CoA metabolism in normal tissues and tumours and the potential for targeting these pathways therapeutically. We conclude with a commentary on emerging nodes of acetyl-CoA metabolism that may impact cancer biology. Acetyl coenzyme A (acetyl-CoA) is a key metabolite in carbohydrate and lipid metabolism and plays a role in signalling through protein acetylation, and the dysregulation of these pathways is a hallmark of various cancers. In this Review, Guertin and Wellen give an overview of acetyl-CoA metabolism in health and in cancer and discuss emerging therapeutic strategies for targeting metabolic pathways involving acetyl-CoA.
{"title":"Acetyl-CoA metabolism in cancer","authors":"David A. Guertin, Kathryn E. Wellen","doi":"10.1038/s41568-022-00543-5","DOIUrl":"10.1038/s41568-022-00543-5","url":null,"abstract":"Few metabolites can claim a more central and versatile role in cell metabolism than acetyl coenzyme A (acetyl-CoA). Acetyl-CoA is produced during nutrient catabolism to fuel the tricarboxylic acid cycle and is the essential building block for fatty acid and isoprenoid biosynthesis. It also functions as a signalling metabolite as the substrate for lysine acetylation reactions, enabling the modulation of protein functions in response to acetyl-CoA availability. Recent years have seen exciting advances in our understanding of acetyl-CoA metabolism in normal physiology and in cancer, buoyed by new mouse models, in vivo stable-isotope tracing approaches and improved methods for measuring acetyl-CoA, including in specific subcellular compartments. Efforts to target acetyl-CoA metabolic enzymes are also advancing, with one therapeutic agent targeting acetyl-CoA synthesis receiving approval from the US Food and Drug Administration. In this Review, we give an overview of the regulation and cancer relevance of major metabolic pathways in which acetyl-CoA participates. We further discuss recent advances in understanding acetyl-CoA metabolism in normal tissues and tumours and the potential for targeting these pathways therapeutically. We conclude with a commentary on emerging nodes of acetyl-CoA metabolism that may impact cancer biology. Acetyl coenzyme A (acetyl-CoA) is a key metabolite in carbohydrate and lipid metabolism and plays a role in signalling through protein acetylation, and the dysregulation of these pathways is a hallmark of various cancers. In this Review, Guertin and Wellen give an overview of acetyl-CoA metabolism in health and in cancer and discuss emerging therapeutic strategies for targeting metabolic pathways involving acetyl-CoA.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 3","pages":"156-172"},"PeriodicalIF":78.5,"publicationDate":"2023-01-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9826019","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}
Pub Date : 2023-01-11DOI: 10.1038/s41568-023-00548-8
Daniela Senft
To understand malignant progression, Yuan et al. delineate the complex crosstalk between cancer stem cells and their microenvironment that is initiated by oncogenic RAS.
{"title":"Leptin fuels non-genetic skin tumour progression","authors":"Daniela Senft","doi":"10.1038/s41568-023-00548-8","DOIUrl":"10.1038/s41568-023-00548-8","url":null,"abstract":"To understand malignant progression, Yuan et al. delineate the complex crosstalk between cancer stem cells and their microenvironment that is initiated by oncogenic RAS.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 2","pages":"56-56"},"PeriodicalIF":78.5,"publicationDate":"2023-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10834629","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}
Pub Date : 2023-01-10DOI: 10.1038/s41568-022-00541-7
Robert K. Bradley, Olga Anczuków
Dysregulated RNA splicing is a molecular feature that characterizes almost all tumour types. Cancer-associated splicing alterations arise from both recurrent mutations and altered expression of trans-acting factors governing splicing catalysis and regulation. Cancer-associated splicing dysregulation can promote tumorigenesis via diverse mechanisms, contributing to increased cell proliferation, decreased apoptosis, enhanced migration and metastatic potential, resistance to chemotherapy and evasion of immune surveillance. Recent studies have identified specific cancer-associated isoforms that play critical roles in cancer cell transformation and growth and demonstrated the therapeutic benefits of correcting or otherwise antagonizing such cancer-associated mRNA isoforms. Clinical-grade small molecules that modulate or inhibit RNA splicing have similarly been developed as promising anticancer therapeutics. Here, we review splicing alterations characteristic of cancer cell transcriptomes, dysregulated splicing’s contributions to tumour initiation and progression, and existing and emerging approaches for targeting splicing for cancer therapy. Finally, we discuss the outstanding questions and challenges that must be addressed to translate these findings into the clinic. This Review discusses the diverse ways in which cancer-associated RNA splicing dysregulation promotes tumour initiation and progression, existing and emerging approaches for targeting splicing for cancer therapy and outstanding questions and challenges in the field.
{"title":"RNA splicing dysregulation and the hallmarks of cancer","authors":"Robert K. Bradley, Olga Anczuków","doi":"10.1038/s41568-022-00541-7","DOIUrl":"10.1038/s41568-022-00541-7","url":null,"abstract":"Dysregulated RNA splicing is a molecular feature that characterizes almost all tumour types. Cancer-associated splicing alterations arise from both recurrent mutations and altered expression of trans-acting factors governing splicing catalysis and regulation. Cancer-associated splicing dysregulation can promote tumorigenesis via diverse mechanisms, contributing to increased cell proliferation, decreased apoptosis, enhanced migration and metastatic potential, resistance to chemotherapy and evasion of immune surveillance. Recent studies have identified specific cancer-associated isoforms that play critical roles in cancer cell transformation and growth and demonstrated the therapeutic benefits of correcting or otherwise antagonizing such cancer-associated mRNA isoforms. Clinical-grade small molecules that modulate or inhibit RNA splicing have similarly been developed as promising anticancer therapeutics. Here, we review splicing alterations characteristic of cancer cell transcriptomes, dysregulated splicing’s contributions to tumour initiation and progression, and existing and emerging approaches for targeting splicing for cancer therapy. Finally, we discuss the outstanding questions and challenges that must be addressed to translate these findings into the clinic. This Review discusses the diverse ways in which cancer-associated RNA splicing dysregulation promotes tumour initiation and progression, existing and emerging approaches for targeting splicing for cancer therapy and outstanding questions and challenges in the field.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 3","pages":"135-155"},"PeriodicalIF":78.5,"publicationDate":"2023-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10507189","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}
Pub Date : 2023-01-03DOI: 10.1038/s41568-022-00537-3
Yi-Jia Li, Chunyan Zhang, Antons Martincuks, Andreas Herrmann, Hua Yu
Reprogrammed metabolism is a hallmark of cancer. However, the metabolic dependency of cancer, from tumour initiation through disease progression and therapy resistance, requires a spectrum of distinct reprogrammed cellular metabolic pathways. These pathways include aerobic glycolysis, oxidative phosphorylation, reactive oxygen species generation, de novo lipid synthesis, fatty acid β-oxidation, amino acid (notably glutamine) metabolism and mitochondrial metabolism. This Review highlights the central roles of signal transducer and activator of transcription (STAT) proteins, notably STAT3, STAT5, STAT6 and STAT1, in orchestrating the highly dynamic metabolism not only of cancer cells but also of immune cells and adipocytes in the tumour microenvironment. STAT proteins are able to shape distinct metabolic processes that regulate tumour progression and therapy resistance by transducing signals from metabolites, cytokines, growth factors and their receptors; defining genetic programmes that regulate a wide range of molecules involved in orchestration of metabolism in cancer and immune cells; and regulating mitochondrial activity at multiple levels, including energy metabolism and lipid-mediated mitochondrial integrity. Given the central role of STAT proteins in regulation of metabolic states, they are potential therapeutic targets for altering metabolic reprogramming in cancer. Reprogrammed metabolism is a hallmark of cancer. Here, Li, Zhang and colleagues describe how signal transducer and activator of transcription (STAT) proteins alter cancer cell metabolism by sensing and transducing signals from the tumour environment and modulating signalling pathways, transcription factors, mitochondrial proteins and enzymes.
新陈代谢重编程是癌症的一个标志。然而，癌症的代谢依赖性，从肿瘤发生到疾病进展和耐药性，需要一系列不同的重编程细胞代谢途径。这些途径包括有氧糖酵解、氧化磷酸化、活性氧生成、新脂质合成、脂肪酸β-氧化、氨基酸（特别是谷氨酰胺）代谢和线粒体代谢。本综述强调了信号转导和激活转录（STAT）蛋白，特别是 STAT3、STAT5、STAT6 和 STAT1 在协调肿瘤微环境中癌细胞、免疫细胞和脂肪细胞高度动态的新陈代谢中的核心作用。STAT 蛋白能够通过以下方式形成调节肿瘤进展和耐药性的独特代谢过程：传递来自代谢物、细胞因子、生长因子及其受体的信号；确定基因程序，以调节参与协调癌症和免疫细胞代谢的各种分子；以及在多个水平上调节线粒体活性，包括能量代谢和脂质介导的线粒体完整性。鉴于 STAT 蛋白在调节代谢状态中的核心作用，它们是改变癌症代谢重编程的潜在治疗靶点。代谢重编程是癌症的一个特征。在这里，李、张及其同事描述了信号转导和激活转录（STAT）蛋白如何通过感知和传递来自肿瘤环境的信号以及调节信号通路、转录因子、线粒体蛋白和酶来改变癌细胞的新陈代谢。
{"title":"STAT proteins in cancer: orchestration of metabolism","authors":"Yi-Jia Li, Chunyan Zhang, Antons Martincuks, Andreas Herrmann, Hua Yu","doi":"10.1038/s41568-022-00537-3","DOIUrl":"10.1038/s41568-022-00537-3","url":null,"abstract":"Reprogrammed metabolism is a hallmark of cancer. However, the metabolic dependency of cancer, from tumour initiation through disease progression and therapy resistance, requires a spectrum of distinct reprogrammed cellular metabolic pathways. These pathways include aerobic glycolysis, oxidative phosphorylation, reactive oxygen species generation, de novo lipid synthesis, fatty acid β-oxidation, amino acid (notably glutamine) metabolism and mitochondrial metabolism. This Review highlights the central roles of signal transducer and activator of transcription (STAT) proteins, notably STAT3, STAT5, STAT6 and STAT1, in orchestrating the highly dynamic metabolism not only of cancer cells but also of immune cells and adipocytes in the tumour microenvironment. STAT proteins are able to shape distinct metabolic processes that regulate tumour progression and therapy resistance by transducing signals from metabolites, cytokines, growth factors and their receptors; defining genetic programmes that regulate a wide range of molecules involved in orchestration of metabolism in cancer and immune cells; and regulating mitochondrial activity at multiple levels, including energy metabolism and lipid-mediated mitochondrial integrity. Given the central role of STAT proteins in regulation of metabolic states, they are potential therapeutic targets for altering metabolic reprogramming in cancer. Reprogrammed metabolism is a hallmark of cancer. Here, Li, Zhang and colleagues describe how signal transducer and activator of transcription (STAT) proteins alter cancer cell metabolism by sensing and transducing signals from the tumour environment and modulating signalling pathways, transcription factors, mitochondrial proteins and enzymes.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 3","pages":"115-134"},"PeriodicalIF":78.5,"publicationDate":"2023-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9470793","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}
Pub Date : 2022-12-21DOI: 10.1038/s41568-022-00545-3
Joseph Willson
In a study in Nature, Wang et al. describe how circadian rhythms can impact tumour suppression through their effects on dendritic cells, a finding that could help to optimize clinical trials of cancer immunotherapies.
{"title":"Dendritic cells rise and shine","authors":"Joseph Willson","doi":"10.1038/s41568-022-00545-3","DOIUrl":"10.1038/s41568-022-00545-3","url":null,"abstract":"In a study in Nature, Wang et al. describe how circadian rhythms can impact tumour suppression through their effects on dendritic cells, a finding that could help to optimize clinical trials of cancer immunotherapies.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 2","pages":"55-55"},"PeriodicalIF":78.5,"publicationDate":"2022-12-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9223948","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}
Pub Date : 2022-12-15DOI: 10.1038/s41568-022-00542-6
Anna K. Casasent, Mathilde M. Almekinders, Charlotta Mulder, Proteeti Bhattacharjee, Deborah Collyar, Alastair M. Thompson, Jos Jonkers, Esther H. Lips, Jacco van Rheenen, E. Shelley Hwang, Serena Nik-Zainal, Nicholas E. Navin, Jelle Wesseling, Grand Challenge PRECISION Consortium
{"title":"Author Correction: Learning to distinguish progressive and non-progressive ductal carcinoma in situ","authors":"Anna K. Casasent, Mathilde M. Almekinders, Charlotta Mulder, Proteeti Bhattacharjee, Deborah Collyar, Alastair M. Thompson, Jos Jonkers, Esther H. Lips, Jacco van Rheenen, E. Shelley Hwang, Serena Nik-Zainal, Nicholas E. Navin, Jelle Wesseling, Grand Challenge PRECISION Consortium","doi":"10.1038/s41568-022-00542-6","DOIUrl":"10.1038/s41568-022-00542-6","url":null,"abstract":"","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 2","pages":"112-112"},"PeriodicalIF":78.5,"publicationDate":"2022-12-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s41568-022-00542-6.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9204360","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：