Pub Date : 2023-06-07DOI: 10.1038/s41568-023-00583-5
Mårten C. G. Winge, Laura N. Kellman, Konnie Guo, Jean Y. Tang, Susan M. Swetter, Sumaira Z. Aasi, Kavita Y. Sarin, Anne Lynn S. Chang, Paul A. Khavari
Human malignancies arise predominantly in tissues of epithelial origin, where the stepwise transformation from healthy epithelium to premalignant dysplasia to invasive neoplasia involves sequential dysregulation of biological networks that govern essential functions of epithelial homeostasis. Cutaneous squamous cell carcinoma (cSCC) is a prototype epithelial malignancy, often with a high tumour mutational burden. A plethora of risk genes, dominated by UV-induced sun damage, drive disease progression in conjunction with stromal interactions and local immunomodulation, enabling continuous tumour growth. Recent studies have identified subpopulations of SCC cells that specifically interact with the tumour microenvironment. These advances, along with increased knowledge of the impact of germline genetics and somatic mutations on cSCC development, have led to a greater appreciation of the complexity of skin cancer pathogenesis and have enabled progress in neoadjuvant immunotherapy, which has improved pathological complete response rates. Although measures for the prevention and therapeutic management of cSCC are associated with clinical benefit, the prognosis remains poor for advanced disease. Elucidating how the genetic mechanisms that drive cSCC interact with the tumour microenvironment is a current focus in efforts to understand, prevent and treat cSCC. This Review outlines risk factors and prevention strategies for cutaneous squamous cell carcinoma (cSCC) and highlights recent advances in the understanding of the impact of molecular and cellular intra-tumour heterogeneity that provide the basis for new therapeutic strategies to treat advanced cSCC.
{"title":"Advances in cutaneous squamous cell carcinoma","authors":"Mårten C. G. Winge, Laura N. Kellman, Konnie Guo, Jean Y. Tang, Susan M. Swetter, Sumaira Z. Aasi, Kavita Y. Sarin, Anne Lynn S. Chang, Paul A. Khavari","doi":"10.1038/s41568-023-00583-5","DOIUrl":"10.1038/s41568-023-00583-5","url":null,"abstract":"Human malignancies arise predominantly in tissues of epithelial origin, where the stepwise transformation from healthy epithelium to premalignant dysplasia to invasive neoplasia involves sequential dysregulation of biological networks that govern essential functions of epithelial homeostasis. Cutaneous squamous cell carcinoma (cSCC) is a prototype epithelial malignancy, often with a high tumour mutational burden. A plethora of risk genes, dominated by UV-induced sun damage, drive disease progression in conjunction with stromal interactions and local immunomodulation, enabling continuous tumour growth. Recent studies have identified subpopulations of SCC cells that specifically interact with the tumour microenvironment. These advances, along with increased knowledge of the impact of germline genetics and somatic mutations on cSCC development, have led to a greater appreciation of the complexity of skin cancer pathogenesis and have enabled progress in neoadjuvant immunotherapy, which has improved pathological complete response rates. Although measures for the prevention and therapeutic management of cSCC are associated with clinical benefit, the prognosis remains poor for advanced disease. Elucidating how the genetic mechanisms that drive cSCC interact with the tumour microenvironment is a current focus in efforts to understand, prevent and treat cSCC. This Review outlines risk factors and prevention strategies for cutaneous squamous cell carcinoma (cSCC) and highlights recent advances in the understanding of the impact of molecular and cellular intra-tumour heterogeneity that provide the basis for new therapeutic strategies to treat advanced cSCC.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 7","pages":"430-449"},"PeriodicalIF":78.5,"publicationDate":"2023-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10069568","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 : 2023-06-06DOI: 10.1038/s41568-023-00584-4
Ioannis Peppas, Anthony M. Ford, Caroline L. Furness, Mel F. Greaves
Acute lymphoblastic leukaemia (ALL) is the most common cancer of childhood. Here, we map emerging evidence suggesting that children with ALL at the time of diagnosis may have a delayed maturation of the gut microbiome compared with healthy children. This finding may be associated with early-life epidemiological factors previously identified as risk indicators for childhood ALL, including caesarean section birth, diminished breast feeding and paucity of social contacts. The consistently observed deficiency in short-chain fatty-acid-producing bacterial taxa in children with ALL has the potential to promote dysregulated immune responses and to, ultimately, increase the risk of transformation of preleukaemic clones in response to common infectious triggers. These data endorse the concept that a microbiome deficit in early life may contribute to the development of the major subtypes of childhood ALL and encourage the notion of risk-reducing microbiome-targeted intervention in the future. In this Perspective article, Mel Greaves and co-workers outline emerging evidence that suggests that children with newly diagnosed acute lymphoblastic leukaemia may have a delayed maturation of the gut microbiome compared with healthy children, a deficit that might be associated with early-life epidemiological factors and could contribute to the risk of transformation of preleukaemic clones in response to common infectious triggers.
急性淋巴细胞白血病(ALL)是最常见的儿童癌症。在这里,我们绘制了新出现的证据,这些证据表明,与健康儿童相比,确诊时患有急性淋巴细胞白血病的儿童的肠道微生物组可能会延迟成熟。这一发现可能与之前被确定为儿童 ALL 风险指标的早期流行病学因素有关,这些因素包括剖腹产、母乳喂养减少和社会交往稀少。在儿童白血病患者中持续观察到的短链脂肪酸细菌类群的缺乏有可能导致免疫反应失调,并最终增加白血病前期克隆在常见感染诱因下发生转化的风险。这些数据证实了生命早期微生物组缺失可能导致儿童 ALL 主要亚型发展的观点,并鼓励了未来以降低风险的微生物组为目标进行干预的理念。在这篇 "视角 "文章中,梅尔-格里夫斯(Mel Greaves)及其合作者概述了新出现的证据,这些证据表明,与健康儿童相比,新确诊的急性淋巴细胞白血病患儿的肠道微生物组可能会延迟成熟,这种缺陷可能与生命早期的流行病学因素有关,并可能导致白血病前期克隆在常见感染诱因下发生转化的风险。
{"title":"Gut microbiome immaturity and childhood acute lymphoblastic leukaemia","authors":"Ioannis Peppas, Anthony M. Ford, Caroline L. Furness, Mel F. Greaves","doi":"10.1038/s41568-023-00584-4","DOIUrl":"10.1038/s41568-023-00584-4","url":null,"abstract":"Acute lymphoblastic leukaemia (ALL) is the most common cancer of childhood. Here, we map emerging evidence suggesting that children with ALL at the time of diagnosis may have a delayed maturation of the gut microbiome compared with healthy children. This finding may be associated with early-life epidemiological factors previously identified as risk indicators for childhood ALL, including caesarean section birth, diminished breast feeding and paucity of social contacts. The consistently observed deficiency in short-chain fatty-acid-producing bacterial taxa in children with ALL has the potential to promote dysregulated immune responses and to, ultimately, increase the risk of transformation of preleukaemic clones in response to common infectious triggers. These data endorse the concept that a microbiome deficit in early life may contribute to the development of the major subtypes of childhood ALL and encourage the notion of risk-reducing microbiome-targeted intervention in the future. In this Perspective article, Mel Greaves and co-workers outline emerging evidence that suggests that children with newly diagnosed acute lymphoblastic leukaemia may have a delayed maturation of the gut microbiome compared with healthy children, a deficit that might be associated with early-life epidemiological factors and could contribute to the risk of transformation of preleukaemic clones in response to common infectious triggers.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 8","pages":"565-576"},"PeriodicalIF":78.5,"publicationDate":"2023-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10243253/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9873401","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}
Pub Date : 2023-06-05DOI: 10.1038/s41568-023-00578-2
Alexis J. Combes, Bushra Samad, Matthew F. Krummel
Tumours are surrounded by a host immune system that can suppress or promote tumour growth. The tumour microenvironment (TME) has often been framed as a singular entity, suggesting a single type of immune state that is defective and in need of therapeutic intervention. By contrast, the past few years have highlighted a plurality of immune states that can surround tumours. In this Perspective, we suggest that different TMEs have ‘archetypal’ qualities across all cancers — characteristic and repeating collections of cells and gene-expression profiles at the level of the bulk tumour. We discuss many studies that together support a view that tumours typically draw from a finite number (around 12) of ‘dominant’ immune archetypes. In considering the likely evolutionary origin and roles of these archetypes, their associated TMEs can be predicted to have specific vulnerabilities that can be leveraged as targets for cancer treatment with expected and addressable adverse effects for patients. In this Perspective, the authors suggest that different tumour microenvironments have ‘archetypal’ qualities across all cancers — characteristic and repeating collections of cells and gene-expression profiles at the level of the bulk tumour. They propose the existence of 12 dominant immune archetypes.
{"title":"Defining and using immune archetypes to classify and treat cancer","authors":"Alexis J. Combes, Bushra Samad, Matthew F. Krummel","doi":"10.1038/s41568-023-00578-2","DOIUrl":"10.1038/s41568-023-00578-2","url":null,"abstract":"Tumours are surrounded by a host immune system that can suppress or promote tumour growth. The tumour microenvironment (TME) has often been framed as a singular entity, suggesting a single type of immune state that is defective and in need of therapeutic intervention. By contrast, the past few years have highlighted a plurality of immune states that can surround tumours. In this Perspective, we suggest that different TMEs have ‘archetypal’ qualities across all cancers — characteristic and repeating collections of cells and gene-expression profiles at the level of the bulk tumour. We discuss many studies that together support a view that tumours typically draw from a finite number (around 12) of ‘dominant’ immune archetypes. In considering the likely evolutionary origin and roles of these archetypes, their associated TMEs can be predicted to have specific vulnerabilities that can be leveraged as targets for cancer treatment with expected and addressable adverse effects for patients. In this Perspective, the authors suggest that different tumour microenvironments have ‘archetypal’ qualities across all cancers — characteristic and repeating collections of cells and gene-expression profiles at the level of the bulk tumour. They propose the existence of 12 dominant immune archetypes.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 7","pages":"491-505"},"PeriodicalIF":78.5,"publicationDate":"2023-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9692236","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 : 2023-06-02DOI: 10.1038/s41568-023-00592-4
Eva C. Freckmann
In this Tool of the Trade article, Eva Freckmann describes the development of Traject3d, a workflow that enables the detection of heterogeneous phenotypes in 3D culture by analysing label-free multi-day time-lapse imaging.
{"title":"Traject3d for studying 3D cellular heterogeneity","authors":"Eva C. Freckmann","doi":"10.1038/s41568-023-00592-4","DOIUrl":"10.1038/s41568-023-00592-4","url":null,"abstract":"In this Tool of the Trade article, Eva Freckmann describes the development of Traject3d, a workflow that enables the detection of heterogeneous phenotypes in 3D culture by analysing label-free multi-day time-lapse imaging.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 9","pages":"577-577"},"PeriodicalIF":78.5,"publicationDate":"2023-06-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10060843","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 : 2023-05-31DOI: 10.1038/s41568-023-00576-4
Johannes Schwenck, Dominik Sonanini, Jonathan M. Cotton, Hans-Georg Rammensee, Christian la Fougère, Lars Zender, Bernd J. Pichler
Molecular imaging has experienced enormous advancements in the areas of imaging technology, imaging probe and contrast development, and data quality, as well as machine learning-based data analysis. Positron emission tomography (PET) and its combination with computed tomography (CT) or magnetic resonance imaging (MRI) as a multimodality PET–CT or PET–MRI system offer a wealth of molecular, functional and morphological data with a single patient scan. Despite the recent technical advances and the availability of dozens of disease-specific contrast and imaging probes, only a few parameters, such as tumour size or the mean tracer uptake, are used for the evaluation of images in clinical practice. Multiparametric in vivo imaging data not only are highly quantitative but also can provide invaluable information about pathophysiology, receptor expression, metabolism, or morphological and functional features of tumours, such as pH, oxygenation or tissue density, as well as pharmacodynamic properties of drugs, to measure drug response with a contrast agent. It can further quantitatively map and spatially resolve the intertumoural and intratumoural heterogeneity, providing insights into tumour vulnerabilities for target-specific therapeutic interventions. Failure to exploit and integrate the full potential of such powerful imaging data may lead to a lost opportunity in which patients do not receive the best possible care. With the desire to implement personalized medicine in the cancer clinic, the full comprehensive diagnostic power of multiplexed imaging should be utilized. In this Review, Schwenck et al. discuss how PET imaging of cancer has advanced through its combination with CT and MRI and the development of an array of imaging probes, and how these innovations now need to be fully integrated into the clinic to improve cancer diagnostics and guide therapy.
{"title":"Advances in PET imaging of cancer","authors":"Johannes Schwenck, Dominik Sonanini, Jonathan M. Cotton, Hans-Georg Rammensee, Christian la Fougère, Lars Zender, Bernd J. Pichler","doi":"10.1038/s41568-023-00576-4","DOIUrl":"10.1038/s41568-023-00576-4","url":null,"abstract":"Molecular imaging has experienced enormous advancements in the areas of imaging technology, imaging probe and contrast development, and data quality, as well as machine learning-based data analysis. Positron emission tomography (PET) and its combination with computed tomography (CT) or magnetic resonance imaging (MRI) as a multimodality PET–CT or PET–MRI system offer a wealth of molecular, functional and morphological data with a single patient scan. Despite the recent technical advances and the availability of dozens of disease-specific contrast and imaging probes, only a few parameters, such as tumour size or the mean tracer uptake, are used for the evaluation of images in clinical practice. Multiparametric in vivo imaging data not only are highly quantitative but also can provide invaluable information about pathophysiology, receptor expression, metabolism, or morphological and functional features of tumours, such as pH, oxygenation or tissue density, as well as pharmacodynamic properties of drugs, to measure drug response with a contrast agent. It can further quantitatively map and spatially resolve the intertumoural and intratumoural heterogeneity, providing insights into tumour vulnerabilities for target-specific therapeutic interventions. Failure to exploit and integrate the full potential of such powerful imaging data may lead to a lost opportunity in which patients do not receive the best possible care. With the desire to implement personalized medicine in the cancer clinic, the full comprehensive diagnostic power of multiplexed imaging should be utilized. In this Review, Schwenck et al. discuss how PET imaging of cancer has advanced through its combination with CT and MRI and the development of an array of imaging probes, and how these innovations now need to be fully integrated into the clinic to improve cancer diagnostics and guide therapy.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 7","pages":"474-490"},"PeriodicalIF":78.5,"publicationDate":"2023-05-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9697534","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 : 2023-05-25DOI: 10.1038/s41568-023-00589-z
Gabrielle Brewer
In this study, Insco et al. find patient-specific CDK13 mutations to impede RNA surveillance, leading to the accumulation and translation of prematurely terminated RNAs that drive malignancy in melanoma models.
{"title":"Impaired RNA clearance","authors":"Gabrielle Brewer","doi":"10.1038/s41568-023-00589-z","DOIUrl":"10.1038/s41568-023-00589-z","url":null,"abstract":"In this study, Insco et al. find patient-specific CDK13 mutations to impede RNA surveillance, leading to the accumulation and translation of prematurely terminated RNAs that drive malignancy in melanoma models.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 7","pages":"428-428"},"PeriodicalIF":78.5,"publicationDate":"2023-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9698427","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 : 2023-05-22DOI: 10.1038/s41568-023-00574-6
Blerida Banushi, Shannon R. Joseph, Benedict Lum, Jason J. Lee, Fiona Simpson
Endocytosis is a complex process whereby cell surface proteins, lipids and fluid from the extracellular environment are packaged, sorted and internalized into cells. Endocytosis is also a mechanism of drug internalization into cells. There are multiple routes of endocytosis that determine the fate of molecules, from degradation in the lysosomes to recycling back to the plasma membrane. The overall rates of endocytosis and temporal regulation of molecules transiting through endocytic pathways are also intricately linked with signalling outcomes. This process relies on an array of factors, such as intrinsic amino acid motifs and post-translational modifications. Endocytosis is frequently disrupted in cancer. These disruptions lead to inappropriate retention of receptor tyrosine kinases on the tumour cell membrane, changes in the recycling of oncogenic molecules, defective signalling feedback loops and loss of cell polarity. In the past decade, endocytosis has emerged as a pivotal regulator of nutrient scavenging, response to and regulation of immune surveillance and tumour immune evasion, tumour metastasis and therapeutic drug delivery. This Review summarizes and integrates these advances into the understanding of endocytosis in cancer. The potential to regulate these pathways in the clinic to improve cancer therapy is also discussed. In this Review, Banushi et al. discuss how endocytotic pathways impact many cancer processes including nutrient scavenging, metastasis and therapeutic drug delivery, and how knowledge of these pathways can be used to improve cancer therapy in the clinic.
{"title":"Endocytosis in cancer and cancer therapy","authors":"Blerida Banushi, Shannon R. Joseph, Benedict Lum, Jason J. Lee, Fiona Simpson","doi":"10.1038/s41568-023-00574-6","DOIUrl":"10.1038/s41568-023-00574-6","url":null,"abstract":"Endocytosis is a complex process whereby cell surface proteins, lipids and fluid from the extracellular environment are packaged, sorted and internalized into cells. Endocytosis is also a mechanism of drug internalization into cells. There are multiple routes of endocytosis that determine the fate of molecules, from degradation in the lysosomes to recycling back to the plasma membrane. The overall rates of endocytosis and temporal regulation of molecules transiting through endocytic pathways are also intricately linked with signalling outcomes. This process relies on an array of factors, such as intrinsic amino acid motifs and post-translational modifications. Endocytosis is frequently disrupted in cancer. These disruptions lead to inappropriate retention of receptor tyrosine kinases on the tumour cell membrane, changes in the recycling of oncogenic molecules, defective signalling feedback loops and loss of cell polarity. In the past decade, endocytosis has emerged as a pivotal regulator of nutrient scavenging, response to and regulation of immune surveillance and tumour immune evasion, tumour metastasis and therapeutic drug delivery. This Review summarizes and integrates these advances into the understanding of endocytosis in cancer. The potential to regulate these pathways in the clinic to improve cancer therapy is also discussed. In this Review, Banushi et al. discuss how endocytotic pathways impact many cancer processes including nutrient scavenging, metastasis and therapeutic drug delivery, and how knowledge of these pathways can be used to improve cancer therapy in the clinic.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 7","pages":"450-473"},"PeriodicalIF":78.5,"publicationDate":"2023-05-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9685405","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 : 2023-05-17DOI: 10.1038/s41568-023-00588-0
Daniela Senft
Sloan and colleagues demonstrate that anthracycline chemotherapy drives metastatic progression by stimulating a cancer cell-mediated increase in nerve fibre activity in the tumour microenvironment, which can be reversed by the use of β-blockers.
{"title":"Nerve-driven metastasis","authors":"Daniela Senft","doi":"10.1038/s41568-023-00588-0","DOIUrl":"10.1038/s41568-023-00588-0","url":null,"abstract":"Sloan and colleagues demonstrate that anthracycline chemotherapy drives metastatic progression by stimulating a cancer cell-mediated increase in nerve fibre activity in the tumour microenvironment, which can be reversed by the use of β-blockers.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 7","pages":"428-428"},"PeriodicalIF":78.5,"publicationDate":"2023-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9761262","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 : 2023-05-12DOI: 10.1038/s41568-023-00587-1
Gabrielle Brewer
In a recent study on castration-resistant prostate cancer, Cui et al. uncover a role for cancer-associated fibroblasts (CAFs) in inducing androgen synthesis in prostate cancer cells.
{"title":"CAFs promote CRPC","authors":"Gabrielle Brewer","doi":"10.1038/s41568-023-00587-1","DOIUrl":"10.1038/s41568-023-00587-1","url":null,"abstract":"In a recent study on castration-resistant prostate cancer, Cui et al. uncover a role for cancer-associated fibroblasts (CAFs) in inducing androgen synthesis in prostate cancer cells.","PeriodicalId":19055,"journal":{"name":"Nature Reviews Cancer","volume":"23 6","pages":"349-349"},"PeriodicalIF":78.5,"publicationDate":"2023-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9665208","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}