Energy & Environmental Science最新文献_第3页

Encoding spatial tumour dynamics with Starfysh 用 Starfysh 对空间肿瘤动态进行编码

IF 78.5 1区材料科学

Energy & Environmental Science Pub Date : 2024-10-11 DOI: 10.1038/s41568-024-00764-w

Siyu He

引用次数: 0

Compressive stresses in cancer: characterization and implications for tumour progression and treatment 癌症中的压缩应力：特征描述及其对肿瘤进展和治疗的影响

IF 72.5 1区材料科学

Energy & Environmental Science Pub Date : 2024-10-10 DOI: 10.1038/s41568-024-00745-z

Julia A. Linke, Lance L. Munn, Rakesh K. Jain

{"title":"Compressive stresses in cancer: characterization and implications for tumour progression and treatment","authors":"Julia A. Linke, Lance L. Munn, Rakesh K. Jain","doi":"10.1038/s41568-024-00745-z","DOIUrl":"10.1038/s41568-024-00745-z","url":null,"abstract":"Beyond their many well-established biological aberrations, solid tumours create an abnormal physical microenvironment that fuels cancer progression and confers treatment resistance. Mechanical forces impact tumours across a range of biological sizes and timescales, from rapid events at the molecular level involved in their sensing and transmission, to slower and larger-scale events, including clonal selection, epigenetic changes, cell invasion, metastasis and immune response. Owing to challenges with studying these dynamic stimuli in biological systems, the mechanistic understanding of the effects and pathways triggered by abnormally elevated mechanical forces remains elusive, despite clear correlations with cancer pathophysiology, aggressiveness and therapeutic resistance. In this Review, we examine the emerging and diverse roles of physical forces in solid tumours and provide a comprehensive framework for understanding solid stress mechanobiology. We first review the physiological importance of mechanical forces, especially compressive stresses, and discuss their defining characteristics, biological context and relative magnitudes. We then explain how abnormal compressive stresses emerge in tumours and describe the experimental challenges in investigating these mechanically induced processes. Finally, we discuss the clinical translation of mechanotherapeutics that alleviate solid stresses and their potential to synergize with chemotherapy, radiotherapy and immunotherapies. In this Review, Linke, Munn and Jain provide a framework for understanding solid stress mechanobiology, examine the emerging and diverse roles of elevated compressive stresses in solid tumours, and highlight the potential for targeting mechanical abnormalities in cancer.","PeriodicalId":72,"journal":{"name":"Energy & Environmental Science","volume":"24 11","pages":"768-791"},"PeriodicalIF":72.5,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142397861","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}

引用次数: 0

Male melanoma comes of age 男性黑色素瘤进入成熟期

IF 72.5 1区材料科学

Energy & Environmental Science Pub Date : 2024-10-10 DOI: 10.1038/s41568-024-00766-8

Daniela Senft

引用次数: 0

Cancer-induced systemic pre-conditioning of distant organs: building a niche for metastatic cells 癌症诱导的远处器官系统性预处理：为转移细胞建立生态位

IF 78.5 1区材料科学

Energy & Environmental Science Pub Date : 2024-10-10 DOI: 10.1038/s41568-024-00752-0

Nicolas Rabas, Rute M. M. Ferreira, Stefania Di Blasio, Ilaria Malanchi

{"title":"Cancer-induced systemic pre-conditioning of distant organs: building a niche for metastatic cells","authors":"Nicolas Rabas, Rute M. M. Ferreira, Stefania Di Blasio, Ilaria Malanchi","doi":"10.1038/s41568-024-00752-0","DOIUrl":"https://doi.org/10.1038/s41568-024-00752-0","url":null,"abstract":"<p>From their early genesis, tumour cells integrate with the surrounding normal cells to form an abnormal structure that is tightly integrated with the host organism via blood and lymphatic vessels and even neural associations. Using these connections, emerging cancers send a plethora of mediators that efficiently perturb the entire organism and induce changes in distant tissues. These perturbations serendipitously favour early metastatic establishment by promoting a more favourable tissue environment (niche) that supports the persistence of disseminated tumour cells within a foreign tissue. Because the establishment of early metastatic niches represents a key limiting step for metastasis, the creation of a more suitable pre-conditioned tissue strongly enhances metastatic success. In this Review, we provide an updated view of the mechanisms and mediators of primary tumours described so far that induce a pro-metastatic conditioning of distant organs, which favours early metastatic niche formation. We reflect on the nature of cancer-induced systemic conditioning, considering that non-cancer-dependent perturbations of tissue homeostasis are also able to trigger pro-metastatic conditioning. We argue that a more holistic view of the processes catalysing metastatic progression is needed to identify preventive or therapeutic opportunities.</p>","PeriodicalId":72,"journal":{"name":"Energy & Environmental Science","volume":"8 1","pages":""},"PeriodicalIF":78.5,"publicationDate":"2024-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142397859","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}

引用次数: 0

Steering research on mRNA splicing in cancer towards clinical translation 引导癌症中 mRNA 剪接的研究向临床转化

IF 78.5 1区材料科学

Energy & Environmental Science Pub Date : 2024-10-09 DOI: 10.1038/s41568-024-00750-2

Olga Anczukow, Frédéric H.-T. Allain, Brittany L. Angarola, Douglas L. Black, Angela N. Brooks, Chonghui Cheng, Ana Conesa, Edie I. Crosse, Eduardo Eyras, Ernesto Guccione, Sydney X. Lu, Karla M. Neugebauer, Priyanka Sehgal, Xiao Song, Zuzana Tothova, Juan Valcárcel, Kevin M. Weeks, Gene W. Yeo, Andrei Thomas-Tikhonenko

{"title":"Steering research on mRNA splicing in cancer towards clinical translation","authors":"Olga Anczukow, Frédéric H.-T. Allain, Brittany L. Angarola, Douglas L. Black, Angela N. Brooks, Chonghui Cheng, Ana Conesa, Edie I. Crosse, Eduardo Eyras, Ernesto Guccione, Sydney X. Lu, Karla M. Neugebauer, Priyanka Sehgal, Xiao Song, Zuzana Tothova, Juan Valcárcel, Kevin M. Weeks, Gene W. Yeo, Andrei Thomas-Tikhonenko","doi":"10.1038/s41568-024-00750-2","DOIUrl":"https://doi.org/10.1038/s41568-024-00750-2","url":null,"abstract":"<p>Splicing factors are affected by recurrent somatic mutations and copy number variations in several types of haematologic and solid malignancies, which is often seen as prima facie evidence that splicing aberrations can drive cancer initiation and progression. However, numerous spliceosome components also ‘moonlight’ in DNA repair and other cellular processes, making their precise role in cancer difficult to pinpoint. Still, few would deny that dysregulated mRNA splicing is a pervasive feature of most cancers. Correctly interpreting these molecular fingerprints can reveal novel tumour vulnerabilities and untapped therapeutic opportunities. Yet multiple technological challenges, lingering misconceptions, and outstanding questions hinder clinical translation. To start with, the general landscape of splicing aberrations in cancer is not well defined, due to limitations of short-read RNA sequencing not adept at resolving complete mRNA isoforms, as well as the shallow read depth inherent in long-read RNA-sequencing, especially at single-cell level. Although individual cancer-associated isoforms are known to contribute to cancer progression, widespread splicing alterations could be an equally important and, perhaps, more readily actionable feature of human cancers. This is to say that in addition to ‘repairing’ mis-spliced transcripts, possible therapeutic avenues include exacerbating splicing aberration with small-molecule spliceosome inhibitors, targeting recurrent splicing aberrations with synthetic lethal approaches, and training the immune system to recognize splicing-derived neoantigens.</p>","PeriodicalId":72,"journal":{"name":"Energy & Environmental Science","volume":"65 1","pages":""},"PeriodicalIF":78.5,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142385076","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}

引用次数: 0

Four-pronged attack on PDAC 四管齐下打击 PDAC

IF 72.5 1区材料科学

Energy & Environmental Science Pub Date : 2024-10-08 DOI: 10.1038/s41568-024-00765-9

Gabrielle Brewer

引用次数: 0

Challenging the status quo to improve the translational potential of preclinical oncology studies 挑战现状，提高临床前肿瘤学研究的转化潜力

IF 78.5 1区材料科学

Energy & Environmental Science Pub Date : 2024-10-07 DOI: 10.1038/s41568-024-00756-w

Kate Connor, Anna Golebiewska, Annette T. Byrne

引用次数: 0

Protection against tumour formation 防止肿瘤形成

IF 72.5 1区材料科学

Energy & Environmental Science Pub Date : 2024-10-04 DOI: 10.1038/s41568-024-00762-y

Anna Dart

引用次数: 0

Modelling and deciphering tumour metabolism in CRISPR screens. 在 CRISPR 筛选中模拟和解读肿瘤代谢。

IF 72.5 1区材料科学

Energy & Environmental Science Pub Date : 2024-10-01 DOI: 10.1038/s41568-024-00758-8

Johannes Zuber, Wilhelm Palm

引用次数: 0

Macrophages and T cells in metabolic disorder-associated cancers 代谢紊乱相关癌症中的巨噬细胞和 T 细胞。

IF 72.5 1区材料科学

Energy & Environmental Science Pub Date : 2024-10-01 DOI: 10.1038/s41568-024-00743-1

Daniel Taranto, Daan J. Kloosterman, Leila Akkari

{"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":72,"journal":{"name":"Energy & Environmental Science","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":"材料科学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0