Pub Date : 2024-10-01DOI: 10.1038/s41568-024-00744-0
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
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.
{"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":72,"journal":{"name":"Energy & Environmental Science","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":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-30DOI: 10.1038/s41568-024-00742-2
Arielle J. Medford, Ariel B. Carmeli, Alexandra Ritchie, Nikhil Wagle, Levi Garraway, Eric S. Lander, Aparna Parikh
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.
开展临床试验所需的时间限制了我们为癌症患者评估和提供新治疗方案的速度。提高试验效率同时保持严谨性的新方法将使患者受益，尤其是在肿瘤学领域，辅助试验有望拦截转移性疾病，但通常需要大量患者和多年时间才能完成。我们设想建立一个常设平台--一个支持对早期癌症治愈性治疗后出现早期疾病分子证据（MED）的癌症患者进行持续识别和试验登记的基础设施，其基础是循环肿瘤 DNA 的存在。MED 可有力地预测随后的复发，绝大多数患者会在 18 个月内出现放射学上的疾病证据。有了这样一个平台，就可以对许多治疗方法进行高效测试，从小型探索性研究到大型关键性试验。招募有 MED 但无放射学疾病证据的患者参加的试验有可能推动药物评估，因为与传统的辅助试验相比，这些试验规模更小（因为复发概率高）、速度更快（因为复发时间短）。循环肿瘤 DNA 也可能为治疗效果提供有价值的早期生物标志物，从而允许进行小型信号搜索试验。在本视角中，我们将讨论如何建立这样一个平台。
{"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":72,"journal":{"name":"Energy & Environmental Science","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":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-19DOI: 10.1038/s41568-024-00749-9
Xinwen Liu
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.
在这篇 "贸易工具"（Tools of the Trade）文章中，刘新文介绍了用于高含量表型分析的振动光谱法 VIBRANT 的开发过程，并重点介绍了该方法在预测药物作用机制或确定潜在候选药物方面的应用。
{"title":"VIBRANT: mapping cell phenotypes using vibrational spectroscopy","authors":"Xinwen Liu","doi":"10.1038/s41568-024-00749-9","DOIUrl":"https://doi.org/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":72,"journal":{"name":"Energy & Environmental Science","volume":"93 1","pages":""},"PeriodicalIF":78.5,"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":"材料科学","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":72,"journal":{"name":"Energy & Environmental Science","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":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-11DOI: 10.1038/s41568-024-00730-6
Rachel Zeig-Owens, David J. Prezant
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.
{"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":72,"journal":{"name":"Energy & Environmental Science","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":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-10DOI: 10.1038/s41568-024-00734-2
Lucie Laplane, Carlo C. Maley
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.
{"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":72,"journal":{"name":"Energy & Environmental Science","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":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-10DOI: 10.1038/s41568-024-00751-1
Daniela Senft
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.
{"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":72,"journal":{"name":"Energy & Environmental Science","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":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Solid tumours comprise cancer cells that engage in continuous interactions with non-malignant cells and with acellular components, forming the tumour microenvironment (TME). The TME has crucial and diverse roles in tumour progression and metastasis, and substantial efforts have been dedicated into understanding the functions of different cell types within the TME. These efforts highlighted the importance of non-cell-autonomous signalling in cancer, mediating interactions between the cancer cells, the immune microenvironment and the non-immune stroma. Much of this non-cell-autonomous signalling is mediated through acellular components of the TME, known as the extracellular matrix (ECM), and controlled by the cells that secrete and remodel the ECM — the cancer-associated fibroblasts (CAFs). In this Review, we delve into the complex crosstalk among cancer cells, CAFs and immune cells, highlighting the effects of CAF-induced ECM remodelling on T cell functions and offering insights into the potential of targeting ECM components to improve cancer therapies. In this Review, Arpinati et al. summarize how the extracellular matrix, produced primarily by cancer-associated fibroblasts, impacts tumour progression, metastasis and therapy response through modulation of T cell-mediated antitumour immunity and propose routes to target these mechanisms therapeutically.
{"title":"CAF-induced physical constraints controlling T cell state and localization in solid tumours","authors":"Ludovica Arpinati, Giulia Carradori, Ruth Scherz-Shouval","doi":"10.1038/s41568-024-00740-4","DOIUrl":"10.1038/s41568-024-00740-4","url":null,"abstract":"Solid tumours comprise cancer cells that engage in continuous interactions with non-malignant cells and with acellular components, forming the tumour microenvironment (TME). The TME has crucial and diverse roles in tumour progression and metastasis, and substantial efforts have been dedicated into understanding the functions of different cell types within the TME. These efforts highlighted the importance of non-cell-autonomous signalling in cancer, mediating interactions between the cancer cells, the immune microenvironment and the non-immune stroma. Much of this non-cell-autonomous signalling is mediated through acellular components of the TME, known as the extracellular matrix (ECM), and controlled by the cells that secrete and remodel the ECM — the cancer-associated fibroblasts (CAFs). In this Review, we delve into the complex crosstalk among cancer cells, CAFs and immune cells, highlighting the effects of CAF-induced ECM remodelling on T cell functions and offering insights into the potential of targeting ECM components to improve cancer therapies. In this Review, Arpinati et al. summarize how the extracellular matrix, produced primarily by cancer-associated fibroblasts, impacts tumour progression, metastasis and therapy response through modulation of T cell-mediated antitumour immunity and propose routes to target these mechanisms therapeutically.","PeriodicalId":72,"journal":{"name":"Energy & Environmental Science","volume":"24 10","pages":"676-693"},"PeriodicalIF":72.5,"publicationDate":"2024-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142160472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-06DOI: 10.1038/s41568-024-00746-y
Radhika Mathur
In this Tools of the Trade article, Radhika Mathur describes the development of a novel 3D whole-tumour sampling approach for glioblastoma, which can be used to elucidate tumour heterogeneity.
{"title":"Overcoming heterogeneity with 3D whole-tumour sampling","authors":"Radhika Mathur","doi":"10.1038/s41568-024-00746-y","DOIUrl":"https://doi.org/10.1038/s41568-024-00746-y","url":null,"abstract":"In this Tools of the Trade article, Radhika Mathur describes the development of a novel 3D whole-tumour sampling approach for glioblastoma, which can be used to elucidate tumour heterogeneity.","PeriodicalId":72,"journal":{"name":"Energy & Environmental Science","volume":"9 1","pages":""},"PeriodicalIF":78.5,"publicationDate":"2024-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142160473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-05DOI: 10.1038/s41568-024-00748-w
Anna Dart
Pan et al. performed a large-scale, cluster-randomized controlled trial to assess whether eradicating Helicobacter pylori in asymptomatic individuals would be beneficial in preventing gastric cancer.
Pan 等人进行了一项大规模的分组随机对照试验，以评估根除无症状者体内的幽门螺杆菌是否有益于预防胃癌。
{"title":"Intercepting gastric cancer","authors":"Anna Dart","doi":"10.1038/s41568-024-00748-w","DOIUrl":"10.1038/s41568-024-00748-w","url":null,"abstract":"Pan et al. performed a large-scale, cluster-randomized controlled trial to assess whether eradicating Helicobacter pylori in asymptomatic individuals would be beneficial in preventing gastric cancer.","PeriodicalId":72,"journal":{"name":"Energy & Environmental Science","volume":"24 10","pages":"651-651"},"PeriodicalIF":72.5,"publicationDate":"2024-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142137935","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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