Pub Date : 2024-10-01Epub Date: 2024-08-06DOI: 10.1016/j.trecan.2024.07.005
Steven A Frank, Itai Yanai
The traditional view of cancer emphasizes a genes-first process. Novel cancer traits arise by genetic mutations that spread to drive phenotypic change. However, recent data support a phenotypes-first process in which nonheritable cellular variability creates novel traits that later become heritably stabilized by genetic and epigenetic changes. Single-cell measurements reinforce the idea that phenotypes lead genotypes, showing how cancer evolution follows normal developmental plasticity and creates novel traits by recombining parts of different cellular developmental programs. In parallel, studies in evolutionary biology also support a phenotypes-first process driven by developmental plasticity and developmental recombination. These advances in cancer research and evolutionary biology mutually reinforce a revolution in our understanding of how cells and organisms evolve novel traits in response to environmental challenges.
{"title":"The origin of novel traits in cancer.","authors":"Steven A Frank, Itai Yanai","doi":"10.1016/j.trecan.2024.07.005","DOIUrl":"10.1016/j.trecan.2024.07.005","url":null,"abstract":"<p><p>The traditional view of cancer emphasizes a genes-first process. Novel cancer traits arise by genetic mutations that spread to drive phenotypic change. However, recent data support a phenotypes-first process in which nonheritable cellular variability creates novel traits that later become heritably stabilized by genetic and epigenetic changes. Single-cell measurements reinforce the idea that phenotypes lead genotypes, showing how cancer evolution follows normal developmental plasticity and creates novel traits by recombining parts of different cellular developmental programs. In parallel, studies in evolutionary biology also support a phenotypes-first process driven by developmental plasticity and developmental recombination. These advances in cancer research and evolutionary biology mutually reinforce a revolution in our understanding of how cells and organisms evolve novel traits in response to environmental challenges.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"880-892"},"PeriodicalIF":14.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141903028","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 : 2024-10-01Epub Date: 2024-08-30DOI: 10.1016/j.trecan.2024.07.002
Mercedes Herrera, Giulia Pretelli, Jayesh Desai, Elena Garralda, Lillian L Siu, Thiago M Steiner, Lewis Au
Bispecific antibodies (bsAbs) are engineered molecules designed to target two different epitopes or antigens. The mechanism of action is determined by the bsAb molecular targets and structure (or format), which can be manipulated to create variable and novel functionalities, including linking immune cells with tumor cells, or dual signaling pathway blockade. Several bsAbs have already changed the treatment landscape of hematological malignancies and select solid cancers. However, the mechanisms of resistance to these agents are understudied and the management of toxicities remains challenging. Herein, we review the principles in bsAb engineering, current understanding of mechanisms of action and resistance, data for clinical application, and provide a perspective on ongoing challenges and future developments in this field.
{"title":"Bispecific antibodies: advancing precision oncology.","authors":"Mercedes Herrera, Giulia Pretelli, Jayesh Desai, Elena Garralda, Lillian L Siu, Thiago M Steiner, Lewis Au","doi":"10.1016/j.trecan.2024.07.002","DOIUrl":"10.1016/j.trecan.2024.07.002","url":null,"abstract":"<p><p>Bispecific antibodies (bsAbs) are engineered molecules designed to target two different epitopes or antigens. The mechanism of action is determined by the bsAb molecular targets and structure (or format), which can be manipulated to create variable and novel functionalities, including linking immune cells with tumor cells, or dual signaling pathway blockade. Several bsAbs have already changed the treatment landscape of hematological malignancies and select solid cancers. However, the mechanisms of resistance to these agents are understudied and the management of toxicities remains challenging. Herein, we review the principles in bsAb engineering, current understanding of mechanisms of action and resistance, data for clinical application, and provide a perspective on ongoing challenges and future developments in this field.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"893-919"},"PeriodicalIF":14.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142112409","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 : 2024-10-01Epub Date: 2024-09-05DOI: 10.1016/j.trecan.2024.07.009
Elena Montauti, David Y Oh, Lawrence Fong
Advances in cancer immunotherapy have transformed cancer care and realized unprecedented responses in many patients. The growing arsenal of novel therapeutics - including immune checkpoint inhibition (ICI), adoptive T cell therapies (ACTs), and cancer vaccines - reflects the success of cancer immunotherapy. The therapeutic benefits of these treatment modalities are generally attributed to the enhanced quantity and quality of antitumor CD8+ T cell responses. Nevertheless, CD4+ T cells are now recognized to play key roles in both the priming and effector phases of the antitumor immune response. In addition to providing T cell help through co-stimulation and cytokine production, CD4+ T cells can also possess cytotoxicity either directly on MHC class II-expressing tumor cells or to other cells within the tumor microenvironment (TME). The presence of specific populations of CD4+ T cells, and their intrinsic plasticity, within the TME can represent an important determinant of clinical response to immune checkpoint inhibitors, vaccines, and chimeric antigen receptor (CAR) T cell therapies. Understanding how the antitumor functions of specific CD4+ T cell types are induced while limiting their protumorigenic attributes will enable more successful immunotherapies.
癌症免疫疗法的进步改变了癌症治疗,使许多患者获得了前所未有的治疗效果。包括免疫检查点抑制疗法(ICI)、收养 T 细胞疗法(ACTs)和癌症疫苗在内的新型疗法不断增加,反映了癌症免疫疗法的成功。这些治疗方法的疗效通常归功于抗肿瘤 CD8+ T 细胞应答数量和质量的提高。然而,现在人们认识到,CD4+ T 细胞在抗肿瘤免疫反应的起始阶段和效应阶段都发挥着关键作用。除了通过协同刺激和产生细胞因子为 T 细胞提供帮助外,CD4+ T 细胞还能直接对 MHC II 类表达的肿瘤细胞或肿瘤微环境(TME)中的其他细胞产生细胞毒性。TME 中特定 CD4+ T 细胞群的存在及其内在可塑性是决定免疫检查点抑制剂、疫苗和嵌合抗原受体(CAR)T 细胞疗法临床反应的重要因素。了解如何诱导特定 CD4+ T 细胞类型的抗肿瘤功能,同时限制它们的原发肿瘤属性,将使免疫疗法更加成功。
{"title":"CD4<sup>+</sup> T cells in antitumor immunity.","authors":"Elena Montauti, David Y Oh, Lawrence Fong","doi":"10.1016/j.trecan.2024.07.009","DOIUrl":"10.1016/j.trecan.2024.07.009","url":null,"abstract":"<p><p>Advances in cancer immunotherapy have transformed cancer care and realized unprecedented responses in many patients. The growing arsenal of novel therapeutics - including immune checkpoint inhibition (ICI), adoptive T cell therapies (ACTs), and cancer vaccines - reflects the success of cancer immunotherapy. The therapeutic benefits of these treatment modalities are generally attributed to the enhanced quantity and quality of antitumor CD8<sup>+</sup> T cell responses. Nevertheless, CD4<sup>+</sup> T cells are now recognized to play key roles in both the priming and effector phases of the antitumor immune response. In addition to providing T cell help through co-stimulation and cytokine production, CD4<sup>+</sup> T cells can also possess cytotoxicity either directly on MHC class II-expressing tumor cells or to other cells within the tumor microenvironment (TME). The presence of specific populations of CD4<sup>+</sup> T cells, and their intrinsic plasticity, within the TME can represent an important determinant of clinical response to immune checkpoint inhibitors, vaccines, and chimeric antigen receptor (CAR) T cell therapies. Understanding how the antitumor functions of specific CD4<sup>+</sup> T cell types are induced while limiting their protumorigenic attributes will enable more successful immunotherapies.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":"969-985"},"PeriodicalIF":14.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11464182/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142146404","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 : 2024-09-28DOI: 10.1016/j.trecan.2024.09.002
Afraah Cassim, Matthew D Dun, David Gallego-Ortega, Fatima Valdes-Mora
The enhancer of zeste inhibitory protein (EZHIP) is typically expressed during germ cell development and has been classified as a cancer-testis antigen (CTA) in various cancers. In 2020, 4% of diffuse midline gliomas (DMGs) were shown to aberrantly express EZHIP, mirroring the DMG hallmark histone H3 K27M (H3K27M) oncohistone mutation. Similar to H3K27M, EZHIP is a negative regulator of polycomb repressive complex 2 (PRC2), leading to global epigenomic remodeling. In this opinion, we explore the similarities and disparities between H3K27M- and EZHIP-DMGs with a focus on their shared functional hallmark of PRC2 inhibition, their genetic and epigenomic landscapes, plausible differences in the cell of origin, and therapeutic avenues. Upcoming research on EZHIP will help better understand its role in gliomagenesis and DMG therapy.
{"title":"EZHIP's role in diffuse midline glioma: echoes of oncohistones?","authors":"Afraah Cassim, Matthew D Dun, David Gallego-Ortega, Fatima Valdes-Mora","doi":"10.1016/j.trecan.2024.09.002","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.09.002","url":null,"abstract":"<p><p>The enhancer of zeste inhibitory protein (EZHIP) is typically expressed during germ cell development and has been classified as a cancer-testis antigen (CTA) in various cancers. In 2020, 4% of diffuse midline gliomas (DMGs) were shown to aberrantly express EZHIP, mirroring the DMG hallmark histone H3 K27M (H3K27M) oncohistone mutation. Similar to H3K27M, EZHIP is a negative regulator of polycomb repressive complex 2 (PRC2), leading to global epigenomic remodeling. In this opinion, we explore the similarities and disparities between H3K27M- and EZHIP-DMGs with a focus on their shared functional hallmark of PRC2 inhibition, their genetic and epigenomic landscapes, plausible differences in the cell of origin, and therapeutic avenues. Upcoming research on EZHIP will help better understand its role in gliomagenesis and DMG therapy.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2024-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142354699","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 : 2024-09-27DOI: 10.1016/j.trecan.2024.09.004
William G Nelson
Cancer researchers tend to be well-versed in communicating research and research results to scientific audiences. To maintain momentum and progress against cancer, they must acquire and nurture skills allowing for better engagement with the lay public.
{"title":"Cancer researchers as storytellers for the lay public.","authors":"William G Nelson","doi":"10.1016/j.trecan.2024.09.004","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.09.004","url":null,"abstract":"<p><p>Cancer researchers tend to be well-versed in communicating research and research results to scientific audiences. To maintain momentum and progress against cancer, they must acquire and nurture skills allowing for better engagement with the lay public.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142354697","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 : 2024-09-27DOI: 10.1016/j.trecan.2024.09.001
Bovannak S Chap, Nicolas Rayroux, Alizée J Grimm, Eleonora Ghisoni, Denarda Dangaj Laniti
Ovarian cancer (OC) represents ecosystems of highly diverse tumor microenvironments (TMEs). The presence of tumor-infiltrating lymphocytes (TILs) is linked to enhanced immune responses and long-term survival. In this review we present emerging evidence suggesting that cellular crosstalk tightly regulates the distribution of TILs within the TME, underscoring the need to better understand key cellular networks that promote or impede T cell infiltration in OC. We also capture the emergent methodologies and computational techniques that enable the dissection of cell-cell crosstalk. Finally, we present innovative ex vivo TME models that can be leveraged to map and perturb cellular communications to enhance T cell infiltration and immune reactivity.
卵巢癌(OC)代表着高度多样化的肿瘤微环境(TME)生态系统。肿瘤浸润淋巴细胞(TILs)的存在与增强的免疫反应和长期生存有关。在这篇综述中,我们介绍了新出现的证据,这些证据表明细胞间的串联密切调节着 TILs 在 TME 中的分布,强调了更好地了解促进或阻碍 T 细胞浸润 OC 的关键细胞网络的必要性。我们还捕捉了新出现的方法和计算技术,这些方法和技术有助于剖析细胞-细胞串联。最后,我们介绍了创新的体外 TME 模型,这些模型可用于绘制和扰乱细胞通讯,以增强 T 细胞浸润和免疫反应性。
{"title":"Crosstalk of T cells within the ovarian cancer microenvironment.","authors":"Bovannak S Chap, Nicolas Rayroux, Alizée J Grimm, Eleonora Ghisoni, Denarda Dangaj Laniti","doi":"10.1016/j.trecan.2024.09.001","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.09.001","url":null,"abstract":"<p><p>Ovarian cancer (OC) represents ecosystems of highly diverse tumor microenvironments (TMEs). The presence of tumor-infiltrating lymphocytes (TILs) is linked to enhanced immune responses and long-term survival. In this review we present emerging evidence suggesting that cellular crosstalk tightly regulates the distribution of TILs within the TME, underscoring the need to better understand key cellular networks that promote or impede T cell infiltration in OC. We also capture the emergent methodologies and computational techniques that enable the dissection of cell-cell crosstalk. Finally, we present innovative ex vivo TME models that can be leveraged to map and perturb cellular communications to enhance T cell infiltration and immune reactivity.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142354698","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 : 2024-09-25DOI: 10.1016/j.trecan.2024.09.003
Cesar Nava Gonzales, Mikias B Negussie, Saritha Krishna, Vardhaan S Ambati, Shawn L Hervey-Jumper
Tumor-associated epilepsy is the most common presenting symptom in patients diagnosed with diffuse gliomas. Recent evidence illustrates the requirement of synaptic activity to drive glioma proliferation and invasion. Class 1, 2, and 3 evidence is limited regarding the use of antiepileptic drugs (AEDs) as antitumor therapy in combination with chemotherapy. Furthermore, no central mechanism has emerged as the most targetable. The optimal timing of AED regimen remains unknown. Targeting aberrant neuronal activity is a promising avenue for glioma treatment. Clinical biomarkers may aid in identifying patients most likely to benefit from AEDs. Quality evidence is needed to guide treatment decisions.
{"title":"Malignant glioma remodeling of neuronal circuits: therapeutic opportunities and repurposing of antiepileptic drugs.","authors":"Cesar Nava Gonzales, Mikias B Negussie, Saritha Krishna, Vardhaan S Ambati, Shawn L Hervey-Jumper","doi":"10.1016/j.trecan.2024.09.003","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.09.003","url":null,"abstract":"<p><p>Tumor-associated epilepsy is the most common presenting symptom in patients diagnosed with diffuse gliomas. Recent evidence illustrates the requirement of synaptic activity to drive glioma proliferation and invasion. Class 1, 2, and 3 evidence is limited regarding the use of antiepileptic drugs (AEDs) as antitumor therapy in combination with chemotherapy. Furthermore, no central mechanism has emerged as the most targetable. The optimal timing of AED regimen remains unknown. Targeting aberrant neuronal activity is a promising avenue for glioma treatment. Clinical biomarkers may aid in identifying patients most likely to benefit from AEDs. Quality evidence is needed to guide treatment decisions.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":" ","pages":""},"PeriodicalIF":14.3,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142354700","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 : 2024-09-16DOI: 10.1016/j.trecan.2024.08.002
Halima Alnaqbi, Lisa M. Becker, Mira Mousa, Fatima Alshamsi, Sarah K. Azzam, Besa Emini Veseli, Lauren A. Hymel, Khalood Alhosani, Marwa Alhusain, Massimiliano Mazzone, Habiba Alsafar, Peter Carmeliet
Growing evidence highlights the importance of tumor endothelial cells (TECs) in the tumor microenvironment (TME) for promoting tumor growth and evading immune responses. Immunomodulatory endothelial cells (IMECs) represent a distinct plastic phenotype of ECs that exerts the ability to modulate immunity in health and disease. This review discusses our current understanding of IMECs in cancer biology, scrutinizing insights from single-cell reports to compare their characteristics and function dynamics across diverse tumor types, conditions, and species. We investigate possible implications of exploiting IMECs in the context of cancer treatment, particularly examining their influence on the efficacy of existing therapies and the potential to leverage them as targets in optimizing immunotherapeutic strategies.
{"title":"Immunomodulation by endothelial cells: prospects for cancer therapy","authors":"Halima Alnaqbi, Lisa M. Becker, Mira Mousa, Fatima Alshamsi, Sarah K. Azzam, Besa Emini Veseli, Lauren A. Hymel, Khalood Alhosani, Marwa Alhusain, Massimiliano Mazzone, Habiba Alsafar, Peter Carmeliet","doi":"10.1016/j.trecan.2024.08.002","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.08.002","url":null,"abstract":"<p>Growing evidence highlights the importance of tumor endothelial cells (TECs) in the tumor microenvironment (TME) for promoting tumor growth and evading immune responses. Immunomodulatory endothelial cells (IMECs) represent a distinct plastic phenotype of ECs that exerts the ability to modulate immunity in health and disease. This review discusses our current understanding of IMECs in cancer biology, scrutinizing insights from single-cell reports to compare their characteristics and function dynamics across diverse tumor types, conditions, and species. We investigate possible implications of exploiting IMECs in the context of cancer treatment, particularly examining their influence on the efficacy of existing therapies and the potential to leverage them as targets in optimizing immunotherapeutic strategies.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":"17 1","pages":""},"PeriodicalIF":18.4,"publicationDate":"2024-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142260216","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 : 2024-09-14DOI: 10.1016/j.trecan.2024.08.005
Benjamin N. Gantner, Flavio R. Palma, Madhura R. Pandkar, Marcelo J. Sakiyama, Daniel Arango, Gina M. DeNicola, Ana P. Gomes, Marcelo G. Bonini
Emerging evidence indicates that metabolism not only is a source of energy and biomaterials for cell division but also acts as a driver of cancer cell plasticity and treatment resistance. This is because metabolic changes lead to remodeling of chromatin and reprogramming of gene expression patterns, furthering tumor cell phenotypic transitions. Therefore, the crosstalk between metabolism and epigenetics seems to hold immense potential for the discovery of novel therapeutic targets for various aggressive tumors. Here, we highlight recent discoveries supporting the concept that the cooperation between metabolism and epigenetics enables cancer to overcome mounting treatment-induced pressures. We discuss how specific metabolites contribute to cancer cell resilience and provide perspective on how simultaneously targeting these key forces could produce synergistic therapeutic effects to improve treatment outcomes.
{"title":"Metabolism and epigenetics: drivers of tumor cell plasticity and treatment outcomes","authors":"Benjamin N. Gantner, Flavio R. Palma, Madhura R. Pandkar, Marcelo J. Sakiyama, Daniel Arango, Gina M. DeNicola, Ana P. Gomes, Marcelo G. Bonini","doi":"10.1016/j.trecan.2024.08.005","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.08.005","url":null,"abstract":"<p>Emerging evidence indicates that metabolism not only is a source of energy and biomaterials for cell division but also acts as a driver of cancer cell plasticity and treatment resistance. This is because metabolic changes lead to remodeling of chromatin and reprogramming of gene expression patterns, furthering tumor cell phenotypic transitions. Therefore, the crosstalk between metabolism and epigenetics seems to hold immense potential for the discovery of novel therapeutic targets for various aggressive tumors. Here, we highlight recent discoveries supporting the concept that the cooperation between metabolism and epigenetics enables cancer to overcome mounting treatment-induced pressures. We discuss how specific metabolites contribute to cancer cell resilience and provide perspective on how simultaneously targeting these key forces could produce synergistic therapeutic effects to improve treatment outcomes.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":"26 1","pages":""},"PeriodicalIF":18.4,"publicationDate":"2024-09-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142260218","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 : 2024-09-11DOI: 10.1016/j.trecan.2024.08.008
Nadieh Khalili, Francesco Ciompi
Recent advances in artificial intelligence (AI) have revolutionized computational pathology (CPath), particularly through deep learning (DL) and neural networks (NNs). In a recent study, Vorontsov et al. introduced Virchow, a new foundation model (FM) for CPath, which has shown promising results in cancer detection and biomarker prediction.
{"title":"Scaling data toward pan-cancer foundation models","authors":"Nadieh Khalili, Francesco Ciompi","doi":"10.1016/j.trecan.2024.08.008","DOIUrl":"https://doi.org/10.1016/j.trecan.2024.08.008","url":null,"abstract":"<p>Recent advances in artificial intelligence (AI) have revolutionized computational pathology (CPath), particularly through deep learning (DL) and neural networks (NNs). In a recent study, <span><span>Vorontsov <em>et al.</em></span><svg aria-label=\"Opens in new window\" focusable=\"false\" height=\"20\" viewbox=\"0 0 8 8\"><path d=\"M1.12949 2.1072V1H7V6.85795H5.89111V2.90281L0.784057 8L0 7.21635L5.11902 2.1072H1.12949Z\"></path></svg></span> introduced Virchow, a new foundation model (FM) for CPath, which has shown promising results in cancer detection and biomarker prediction.</p>","PeriodicalId":23336,"journal":{"name":"Trends in cancer","volume":"6 1","pages":""},"PeriodicalIF":18.4,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142206022","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}