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Cellular Origins and Lineage Plasticity in Cancer. 癌症的细胞起源和血统可塑性
IF 5.4 2区 医学
Cold Spring Harbor perspectives in medicine Pub Date : 2024-06-03 DOI: 10.1101/cshperspect.a041389
Jason R Pitarresi, Ben Z Stanger
{"title":"Cellular Origins and Lineage Plasticity in Cancer.","authors":"Jason R Pitarresi, Ben Z Stanger","doi":"10.1101/cshperspect.a041389","DOIUrl":"10.1101/cshperspect.a041389","url":null,"abstract":"<p><p>All cancers arise from normal cells whose progeny acquire the cancer-initiating mutations and epigenetic modifications leading to frank tumorigenesis. The identity of those \"cells-of-origin\" has historically been a source of controversy across tumor types, as it has not been possible to witness the dynamic events giving rise to human tumors. Genetically engineered mouse models (GEMMs) of cancer provide an invaluable substitute, enabling researchers to interrogate the competence of various naive cellular compartments to initiate tumors in vivo. Researchers using these models have relied on lineage-specific promoters, knowledge of preneoplastic disease states in humans, and technical advances allowing more precise manipulations of the mouse germline. These approaches have given rise to the emerging view that multiple lineages within a given organ may generate tumors with similar histopathology. Here, we review some of the key studies leading to this conclusion in solid tumors and highlight the biological and clinical ramifications.</p>","PeriodicalId":10452,"journal":{"name":"Cold Spring Harbor perspectives in medicine","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11146313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10036673","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Next-Generation Modeling of Cancer Using Organoids. 癌症的类器官下一代模型。
IF 5.4 2区 医学
Cold Spring Harbor perspectives in medicine Pub Date : 2024-06-03 DOI: 10.1101/cshperspect.a041380
Jillian R Love, Wouter R Karthaus
{"title":"Next-Generation Modeling of Cancer Using Organoids.","authors":"Jillian R Love, Wouter R Karthaus","doi":"10.1101/cshperspect.a041380","DOIUrl":"10.1101/cshperspect.a041380","url":null,"abstract":"<p><p>In the last decade, organoid technology has become a cornerstone in cancer research. Organoids are long-term primary cell cultures, usually of epithelial origin, grown in a three-dimensional (3D) protein matrix and a fully defined medium. Organoids can be derived from many organs and cancer types and sites, encompassing both murine and human tissues. Importantly, they can be established from various stages during tumor evolution and recapitulate with high accuracy patient genomics and phenotypes in vitro, offering a platform for personalized medicine. Additionally, organoids are remarkably amendable for experimental manipulation. Taken together, these features make organoids a powerful tool with applications in basic cancer research and personalized medicine. Here, we will discuss the origins of organoid culture, applications in cancer research, and how cancer organoids can synergize with other models of cancer to drive basic discoveries as well as to translate these toward clinical solutions.</p>","PeriodicalId":10452,"journal":{"name":"Cold Spring Harbor perspectives in medicine","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-06-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11146310/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41132296","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Evolution of Mouse Models of Cancer: Past, Present, and Future. 癌症小鼠模型的演变：过去、现在和未来
IF 5.4 2区 医学
Cold Spring Harbor perspectives in medicine Pub Date : 2024-05-21 DOI: 10.1101/cshperspect.a041736
Cory Abate-Shen, Katerina Politi
{"title":"The Evolution of Mouse Models of Cancer: Past, Present, and Future.","authors":"Cory Abate-Shen, Katerina Politi","doi":"10.1101/cshperspect.a041736","DOIUrl":"https://doi.org/10.1101/cshperspect.a041736","url":null,"abstract":"<p><p>In the nearly 50 years since the original models of cancer first hit the stage, mouse models have become a major contributor to virtually all aspects of cancer research, and these have evolved well beyond simple transgenic or xenograft models to encompass a wide range of more complex models. As the sophistication of mouse models has increased, an explosion of new technologies has expanded the potential to both further develop and apply these models to address major challenges in cancer research. In the current era, cancer modeling has expanded to include nongermline genetically engineered mouse models (GEMMs), patient-derived models, organoids, and adaptations of the models better suited for cancer immunology research. New technologies that have transformed the field include the application of CRISPR-Cas9-mediated genome editing, in vivo imaging, and single-cell analysis to cancer modeling. Here, we provide a historical perspective on the evolution of mouse models of cancer, focusing on how far we have come in a relatively short time and how new technologies will shape the future development of mouse models of cancer.</p>","PeriodicalId":10452,"journal":{"name":"Cold Spring Harbor perspectives in medicine","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-05-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141075737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
How CRISPR Is Revolutionizing the Generation of New Models for Cancer Research. CRISPR 如何彻底改变癌症研究新模型的生成。
IF 5.4 2区 医学
Cold Spring Harbor perspectives in medicine Pub Date : 2024-05-02 DOI: 10.1101/cshperspect.a041384
Francisco J Sánchez Rivera, Lukas E Dow
{"title":"How CRISPR Is Revolutionizing the Generation of New Models for Cancer Research.","authors":"Francisco J Sánchez Rivera, Lukas E Dow","doi":"10.1101/cshperspect.a041384","DOIUrl":"10.1101/cshperspect.a041384","url":null,"abstract":"<p><p>Cancers arise through acquisition of mutations in genes that regulate core biological processes like cell proliferation and cell death. Decades of cancer research have led to the identification of genes and mutations causally involved in disease development and evolution, yet defining their precise function across different cancer types and how they influence therapy responses has been challenging. Mouse models have helped define the in vivo function of cancer-associated alterations, and genome-editing approaches using CRISPR have dramatically accelerated the pace at which these models are developed and studied. Here, we highlight how CRISPR technologies have impacted the development and use of mouse models for cancer research and discuss the many ways in which these rapidly evolving platforms will continue to transform our understanding of this disease.</p>","PeriodicalId":10452,"journal":{"name":"Cold Spring Harbor perspectives in medicine","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11065179/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10223194","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Role of Stroma in Cancer Metabolism. 中风在癌症代谢中的作用。
IF 7.8 2区 医学
Cold Spring Harbor perspectives in medicine Pub Date : 2024-05-02 DOI: 10.1101/cshperspect.a041540
Alec C Kimmelman, Mara H Sherman
{"title":"The Role of Stroma in Cancer Metabolism.","authors":"Alec C Kimmelman, Mara H Sherman","doi":"10.1101/cshperspect.a041540","DOIUrl":"10.1101/cshperspect.a041540","url":null,"abstract":"<p><p>The altered metabolism of tumor cells is a well-known hallmark of cancer and is driven by multiple factors such as mutations in oncogenes and tumor suppressor genes, the origin of the tissue where the tumor arises, and the microenvironment of the tumor. These metabolic changes support the growth of cancer cells by providing energy and the necessary building blocks to sustain proliferation. Targeting these metabolic alterations therapeutically is a potential strategy to treat cancer, but it is challenging due to the metabolic plasticity of tumors. Cancer cells have developed ways to scavenge nutrients through autophagy and macropinocytosis and can also form metabolic networks with stromal cells in the tumor microenvironment. Understanding the role of the tumor microenvironment in tumor metabolism is crucial for effective therapeutic targeting. This review will discuss tumor metabolism and the contribution of the stroma in supporting tumor growth through metabolic interactions.</p>","PeriodicalId":10452,"journal":{"name":"Cold Spring Harbor perspectives in medicine","volume":" ","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10925555/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10213395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Isocitrate Dehydrogenase Mutations in Cancer: Mechanisms of Transformation and Metabolic Liability. 癌症中的异柠檬酸脱氢酶突变：转化机制和代谢责任。
IF 5.4 2区 医学
Cold Spring Harbor perspectives in medicine Pub Date : 2024-05-02 DOI: 10.1101/cshperspect.a041537
Kathryn Gunn, Julie-Aurore Losman
{"title":"Isocitrate Dehydrogenase Mutations in Cancer: Mechanisms of Transformation and Metabolic Liability.","authors":"Kathryn Gunn, Julie-Aurore Losman","doi":"10.1101/cshperspect.a041537","DOIUrl":"10.1101/cshperspect.a041537","url":null,"abstract":"<p><p>Isocitrate dehydrogenase 1 and 2 (IDH1 and IDH2) are metabolic enzymes that interconvert isocitrate and 2-oxoglutarate (2OG). Gain-of-function mutations in <i>IDH1</i> and <i>IDH2</i> occur in a number of cancers, including acute myeloid leukemia, glioma, cholangiocarcinoma, and chondrosarcoma. These mutations cripple the wild-type activity of IDH and cause the enzymes to catalyze a partial reverse reaction in which 2OG is reduced but not carboxylated, resulting in production of the (<i>R</i>)-enantiomer of 2-hydroxyglutarate ((<i>R</i>)-2HG). (<i>R</i>)-2HG accumulation in <i>IDH-mutant</i> tumors results in profound dysregulation of cellular metabolism. The most well-characterized oncogenic effects of (<i>R</i>)-2HG involve the dysregulation of 2OG-dependent epigenetic tumor-suppressor enzymes. However, (<i>R</i>)-2HG has many other effects in <i>IDH-mutant</i> cells, some that promote transformation and others that induce metabolic dependencies. Herein, we review how cancer-associated <i>IDH</i> mutations impact epigenetic regulation and cellular metabolism and discuss how these effects can potentially be leveraged to therapeutically target <i>IDH-mutant</i> tumors.</p>","PeriodicalId":10452,"journal":{"name":"Cold Spring Harbor perspectives in medicine","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11065172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139402160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Gene Therapies for Retinitis Pigmentosa that Target Glucose Metabolism. 针对葡萄糖代谢的视网膜色素变性基因疗法。
IF 7.8 2区 医学
Cold Spring Harbor perspectives in medicine Pub Date : 2024-05-02 DOI: 10.1101/cshperspect.a041289
Yunlu Xue, Constance L Cepko
{"title":"Gene Therapies for Retinitis Pigmentosa that Target Glucose Metabolism.","authors":"Yunlu Xue, Constance L Cepko","doi":"10.1101/cshperspect.a041289","DOIUrl":"10.1101/cshperspect.a041289","url":null,"abstract":"<p><p>Retinitis pigmentosa is a blinding disease wherein rod photoreceptors are affected first, due to the expression of a disease gene, leading to the loss of dim light vision. In many cases, cones do not express the disease gene, yet they are also affected and eventually die, typically after most of the rods in their neighborhood have died. The cause of secondary cone death is unclear. Photoreceptors are one of the most energy-demanding cell types in the body and consume a high amount of glucose. At an early stage of degeneration, the cones appear to have a shortage of glucose to fuel their metabolism. This review focuses on gene therapy approaches that address this potential metabolic shortcoming.</p>","PeriodicalId":10452,"journal":{"name":"Cold Spring Harbor perspectives in medicine","volume":" ","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11065158/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9830052","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Developmental Dysregulation of Childhood Cancer 儿童癌症的发育失调
IF 5.4 2区 医学
Cold Spring Harbor perspectives in medicine Pub Date : 2024-05-01 DOI: 10.1101/cshperspect.a041580
Thomas R.W. Oliver, Sam Behjati
{"title":"Developmental Dysregulation of Childhood Cancer","authors":"Thomas R.W. Oliver, Sam Behjati","doi":"10.1101/cshperspect.a041580","DOIUrl":"https://doi.org/10.1101/cshperspect.a041580","url":null,"abstract":"Most childhood cancers possess distinct clinicopathological profiles from those seen in adulthood, reflecting their divergent mechanisms of carcinogenesis. Rather than depending on the decades-long, stepwise accumulation of changes within a mature cell that defines adult carcinomas, many pediatric malignancies emerge rapidly as the consequence of random errors during development. These errors—whether they be genetic, epigenetic, or microenvironmental—characteristically block maturation, resulting in phenotypically primitive neoplasms. Only an event that falls within a narrow set of spatiotemporal parameters will forge a malignant clone; if it occurs too soon then the event might be lethal, or negatively selected against, while if it is too late or in an incorrectly primed precursor cell then the necessary intracellular conditions for transformation will not be met. The precise characterization of these changes, through the study of normal tissues and tumors from patients and model systems, will be essential if we are to develop new strategies to diagnose, treat, and perhaps even prevent childhood cancer.","PeriodicalId":10452,"journal":{"name":"Cold Spring Harbor perspectives in medicine","volume":"145 1","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140835231","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Angiogenesis and Microvascular Permeability 血管生成和微血管通透性
IF 5.4 2区 医学
Cold Spring Harbor perspectives in medicine Pub Date : 2024-05-01 DOI: 10.1101/cshperspect.a041163
Ye Zeng, Bingmei M. Fu
{"title":"Angiogenesis and Microvascular Permeability","authors":"Ye Zeng, Bingmei M. Fu","doi":"10.1101/cshperspect.a041163","DOIUrl":"https://doi.org/10.1101/cshperspect.a041163","url":null,"abstract":"Angiogenesis, the formation of new blood microvessels, is a necessary physiological process for tissue generation and repair. Sufficient blood supply to the tissue is dependent on microvascular density, while the material exchange between the circulating blood and the surrounding tissue is controlled by microvascular permeability. We thus begin this article by reviewing the key signaling factors, particularly vascular endothelial growth factor (VEGF), which regulates both angiogenesis and microvascular permeability. We then review the role of angiogenesis in tissue growth (bone regeneration) and wound healing. Finally, we review angiogenesis as a pathological process in tumorigenesis, intraplaque hemorrhage, cerebral microhemorrhage, pulmonary fibrosis, and hepatic fibrosis. Since the glycocalyx is important for both angiogenesis and microvascular permeability, we highlight the role of the glycocalyx in regulating the interaction between tumor cells and endothelial cells (ECs) and VEGF-containing exosome release and uptake by tumor-associated ECs, all of which contribute to tumorigenesis and metastasis.","PeriodicalId":10452,"journal":{"name":"Cold Spring Harbor perspectives in medicine","volume":"5 1","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140835704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Toward a Unified Theory of Why Young People Develop Cancer 构建年轻人罹患癌症的统一理论
IF 5.4 2区 医学
Cold Spring Harbor perspectives in medicine Pub Date : 2024-05-01 DOI: 10.1101/cshperspect.a041658
Alex Kentsis
{"title":"Toward a Unified Theory of Why Young People Develop Cancer","authors":"Alex Kentsis","doi":"10.1101/cshperspect.a041658","DOIUrl":"https://doi.org/10.1101/cshperspect.a041658","url":null,"abstract":"Epidemiologic and genetic studies have now defined specific patterns of incidence and distinct molecular features of cancers in young versus aging people. Here, I review a general framework for the causes of cancer in children and young adults by relating somatic genetic mosaicism and developmental tissue mutagenesis. This framework suggests how aging-associated cancers such as carcinomas, glioblastomas, and myelodysplastic leukemias are causally distinct from cancers that predominantly affect children and young adults, including lymphoblastic and myeloid leukemias, sarcomas, neuroblastomas, medulloblastomas, and other developmental cancers. I discuss the oncogenic activities of known developmental mutators RAG1/2, AID, and PGBD5, and describe strategies needed to define missing developmental causes of young-onset cancers. Thus, a precise understanding of the mechanisms of tissue-specific somatic mosaicism, developmental mutators, and their control by human genetic variation and environmental exposures is needed for improved strategies for cancer screening, prevention, and treatment.","PeriodicalId":10452,"journal":{"name":"Cold Spring Harbor perspectives in medicine","volume":"10 1","pages":""},"PeriodicalIF":5.4,"publicationDate":"2024-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140835164","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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