{"title":"ETV7 limits the antiviral and antitumor efficacy of CD8<sup>+</sup> T cells by diverting their fate toward exhaustion.","authors":"Jie Cheng, Yifeng Xiao, Ting Peng, Zijian Zhang, You Qin, Yuqian Wang, Jiangzhou Shi, Jinxin Yan, Zihao Zhao, Liangtao Zheng, Zhijun He, Jianwei Wang, Zemin Zhang, Cheng Li, Haichuan Zhu, Peng Jiang","doi":"10.1038/s43018-024-00892-0","DOIUrl":"https://doi.org/10.1038/s43018-024-00892-0","url":null,"abstract":"<p><p>Terminal exhaustion is a critical barrier to antitumor immunity. By integrating and analyzing single-cell RNA-sequencing and single-cell assay for transposase-accessible chromatin with sequencing data, we found that ETS variant 7 (ETV7) is indispensable for determining CD8<sup>+</sup> T cell fate in tumors. ETV7 introduction drives T cell differentiation from memory to terminal exhaustion, limiting antiviral and antitumor efficacy in male mice. Mechanistically, ETV7 acts as a central transcriptional node by binding to specific memory genes and exhaustion genes and functionally skewing these transcriptional programs toward exhaustion. Clinically, ETV7 expression is negatively correlated with progression and responsiveness to immune checkpoint blockade in various human cancers. ETV7 depletion strongly enhances the antitumor efficacy of CD8<sup>+</sup> T cells and engineered chimeric antigen receptor T cells in solid tumors. Thus, these findings demonstrate a decisive role for ETV7 in driving CD8<sup>+</sup> T cell terminal exhaustion and reveal that ETV7 may be a promising target and biomarker for improving the efficacy of cancer immunotherapy.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142979203","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}
Nature cancerPub Date : 2025-01-13DOI: 10.1038/s43018-024-00898-8
Jackson Liang, Xiaosai Yao, Patrick Aouad, Bu-Er Wang, Lisa Crocker, Subhra Chaudhuri, Yuxin Liang, Spyros Darmanis, Jennifer Giltnane, Heather M Moore, Junko Aimi, Ching-Wei Chang, Mary R Gates, Jennifer Eng-Wong, Marc Hafner, Ciara Metcalfe
{"title":"ERα dysfunction caused by ESR1 mutations and therapeutic pressure promotes lineage plasticity in ER<sup>+</sup> breast cancer.","authors":"Jackson Liang, Xiaosai Yao, Patrick Aouad, Bu-Er Wang, Lisa Crocker, Subhra Chaudhuri, Yuxin Liang, Spyros Darmanis, Jennifer Giltnane, Heather M Moore, Junko Aimi, Ching-Wei Chang, Mary R Gates, Jennifer Eng-Wong, Marc Hafner, Ciara Metcalfe","doi":"10.1038/s43018-024-00898-8","DOIUrl":"https://doi.org/10.1038/s43018-024-00898-8","url":null,"abstract":"<p><p>Multiple next-generation molecules targeting estrogen receptor α (ERα) are being investigated in breast cancer clinical trials, encompassing thousands of women globally. Development of these molecules was partly motivated by the discovery of resistance-associated mutations in ESR1 (encodes ERα). Here, we studied the impact of ERα antagonist/degraders against Esr1 mutations expressed in mouse mammary glands. Inhibition of mutant ERα induced mixed-lineage cells, characterized by aberrant co-engagement of normally disparate master transcription factors. Lineage infidelity was also observed in Esr1-wild-type mice upon long-term estrogen deprivation. In ER<sup>+</sup> breast cancer biopsy specimens, heavily pretreated tumors with no ESR1 mutation detected (NMD) frequently exhibited mixed-lineage features. ESR1-mutant tumors generally retained luminal features and higher ERα activity and exhibited an anti-proliferative response to the ERα antagonist giredestrant. ESR1-mutant tumors acquired mixed-lineage features following treatment. Lineage heterogeneity in advanced ER<sup>+</sup> breast cancer may underpin the differential benefit of investigational ERα therapeutics observed in ESR1-mutant versus NMD contexts.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142979201","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}
Nature cancerPub Date : 2025-01-09DOI: 10.1038/s43018-024-00883-1
Dhruva Biswas, Yun-Hsin Liu, Javier Herrero, Yin Wu, David A Moore, Takahiro Karasaki, Kristiana Grigoriadis, Wei-Ting Lu, Selvaraju Veeriah, Cristina Naceur-Lombardelli, Neil Magno, Sophia Ward, Alexander M Frankell, Mark S Hill, Emma Colliver, Sophie de Carné Trécesson, Philip East, Aman Malhi, Daniel M Snell, Olga O'Neill, Daniel Leonce, Johanna Mattsson, Amanda Lindberg, Patrick Micke, Judit Moldvay, Zsolt Megyesfalvi, Balazs Dome, János Fillinger, Jerome Nicod, Julian Downward, Zoltan Szallasi, Allan Hackshaw, Mariam Jamal-Hanjani, Nnennaya Kanu, Nicolai J Birkbak, Charles Swanton
{"title":"Prospective validation of ORACLE, a clonal expression biomarker associated with survival of patients with lung adenocarcinoma.","authors":"Dhruva Biswas, Yun-Hsin Liu, Javier Herrero, Yin Wu, David A Moore, Takahiro Karasaki, Kristiana Grigoriadis, Wei-Ting Lu, Selvaraju Veeriah, Cristina Naceur-Lombardelli, Neil Magno, Sophia Ward, Alexander M Frankell, Mark S Hill, Emma Colliver, Sophie de Carné Trécesson, Philip East, Aman Malhi, Daniel M Snell, Olga O'Neill, Daniel Leonce, Johanna Mattsson, Amanda Lindberg, Patrick Micke, Judit Moldvay, Zsolt Megyesfalvi, Balazs Dome, János Fillinger, Jerome Nicod, Julian Downward, Zoltan Szallasi, Allan Hackshaw, Mariam Jamal-Hanjani, Nnennaya Kanu, Nicolai J Birkbak, Charles Swanton","doi":"10.1038/s43018-024-00883-1","DOIUrl":"https://doi.org/10.1038/s43018-024-00883-1","url":null,"abstract":"<p><p>Human tumors are diverse in their natural history and response to treatment, which in part results from genetic and transcriptomic heterogeneity. In clinical practice, single-site needle biopsies are used to sample this diversity, but cancer biomarkers may be confounded by spatiogenomic heterogeneity within individual tumors. Here we investigate clonally expressed genes as a solution to the sampling bias problem by analyzing multiregion whole-exome and RNA sequencing data for 450 tumor regions from 184 patients with lung adenocarcinoma in the TRACERx study. We prospectively validate the survival association of a clonal expression biomarker, Outcome Risk Associated Clonal Lung Expression (ORACLE), in combination with clinicopathological risk factors, and in stage I disease. We expand our mechanistic understanding, discovering that clonal transcriptional signals are detectable before tissue invasion, act as a molecular fingerprint for lethal metastatic clones and predict chemotherapy sensitivity. Lastly, we find that ORACLE summarizes the prognostic information encoded by genetic evolutionary measures, including chromosomal instability, as a concise 23-transcript assay.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952014","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}
Nature cancerPub Date : 2025-01-09DOI: 10.1038/s43018-024-00896-w
Tejas Jammihal, Renee Maria Saliby, Chris Labaki, Hanna Soulati, Juan Gallegos, Arnau Peris, Dustin McCurry, Chunlei Yu, Valisha Shah, Deepak Poduval, Talal El Zarif, Nourhan El Ahmar, Yasmin Nabil Laimon, Marc Eid, Aseman Bagheri Sheshdeh, Katherine M Krajewski, Florian A Büttner, Matthias Schwab, Daniel Heng, Rafael C Casellas, Kunal Rai, Niki M Zacharias Millward, Pavlos Msaouel, Jose Karam, Sabina Signoretti, Eliezer Van Allen, Toni K Choueiri, David A Braun, Sachet A Shukla
{"title":"Immunogenomic determinants of exceptional response to immune checkpoint inhibition in renal cell carcinoma.","authors":"Tejas Jammihal, Renee Maria Saliby, Chris Labaki, Hanna Soulati, Juan Gallegos, Arnau Peris, Dustin McCurry, Chunlei Yu, Valisha Shah, Deepak Poduval, Talal El Zarif, Nourhan El Ahmar, Yasmin Nabil Laimon, Marc Eid, Aseman Bagheri Sheshdeh, Katherine M Krajewski, Florian A Büttner, Matthias Schwab, Daniel Heng, Rafael C Casellas, Kunal Rai, Niki M Zacharias Millward, Pavlos Msaouel, Jose Karam, Sabina Signoretti, Eliezer Van Allen, Toni K Choueiri, David A Braun, Sachet A Shukla","doi":"10.1038/s43018-024-00896-w","DOIUrl":"https://doi.org/10.1038/s43018-024-00896-w","url":null,"abstract":"<p><p>Immune checkpoint inhibitors can lead to 'exceptional', durable responses in a subset of persons. However, the molecular basis of exceptional response (ER) to immunotherapy in metastatic clear cell renal cell carcinoma (mccRCC) has not been well characterized. Here we analyzed pretherapy genomic and transcriptomic data in treatment-naive persons with mccRCC treated with standard-of-care immunotherapies: (1) combination of programmed cell death protein and ligand 1 (PD1/PDL1) and cytotoxic T lymphocyte-associated protein 4 inhibitors (IO/IO) or (2) combination of PD1/PDL1 and vascular endothelial growth factor (VEGF) receptor inhibitors (IO/VEGF). In the IO/IO cohort, clonal neoantigen load was significantly higher in persons with ER. In the IO/VEGF cohort, ER participants displayed strong enrichment of B cell receptor signaling-related pathways, tertiary lymphoid structure (TLS) signatures and evidence of increased metabolic activity. Our results suggest that ER may be related to clonal neoantigen-driven cytotoxic T cell responses and TLS formation in tumor microenvironments. Therapeutic combinations that elicit both T cell-directed and B cell-directed antitumor immunity may be important to achieve exceptional benefit to IO-based treatment in ccRCC.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952008","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}
Nature cancerPub Date : 2025-01-09DOI: 10.1038/s43018-024-00881-3
Jason M Link, Jennifer R Eng, Carl Pelz, Kevin MacPherson-Hawthorne, Patrick J Worth, Shamaline Sivagnanam, Dove J Keith, Sydney Owen, Ellen M Langer, Alison Grossblatt-Wait, Gustavo Salgado-Garza, Allison L Creason, Sara Protzek, Julian Egger, Hannah Holly, Michael B Heskett, Koei Chin, Nell Kirchberger, Konjit Betre, Elmar Bucher, David Kilburn, Zhi Hu, Michael W Munks, Isabel A English, Motoyuki Tsuda, Jeremy Goecks, Emek Demir, Andrew C Adey, Adel Kardosh, Charles D Lopez, Brett C Sheppard, Alex Guimaraes, Brian Brinkerhoff, Terry K Morgan, Gordon B Mills, Lisa M Coussens, Jonathan R Brody, Rosalie C Sears
{"title":"Ongoing replication stress tolerance and clonal T cell responses distinguish liver and lung recurrence and outcomes in pancreatic cancer.","authors":"Jason M Link, Jennifer R Eng, Carl Pelz, Kevin MacPherson-Hawthorne, Patrick J Worth, Shamaline Sivagnanam, Dove J Keith, Sydney Owen, Ellen M Langer, Alison Grossblatt-Wait, Gustavo Salgado-Garza, Allison L Creason, Sara Protzek, Julian Egger, Hannah Holly, Michael B Heskett, Koei Chin, Nell Kirchberger, Konjit Betre, Elmar Bucher, David Kilburn, Zhi Hu, Michael W Munks, Isabel A English, Motoyuki Tsuda, Jeremy Goecks, Emek Demir, Andrew C Adey, Adel Kardosh, Charles D Lopez, Brett C Sheppard, Alex Guimaraes, Brian Brinkerhoff, Terry K Morgan, Gordon B Mills, Lisa M Coussens, Jonathan R Brody, Rosalie C Sears","doi":"10.1038/s43018-024-00881-3","DOIUrl":"https://doi.org/10.1038/s43018-024-00881-3","url":null,"abstract":"<p><p>Patients with metastatic pancreatic ductal adenocarcinoma survive longer if disease spreads to the lung but not the liver. Here we generated overlapping, multi-omic datasets to identify molecular and cellular features that distinguish patients whose disease develops liver metastasis (liver cohort) from those whose disease develops lung metastasis without liver metastases (lung cohort). Lung cohort patients survived longer than liver cohort patients, despite sharing the same tumor subtype. We developed a primary organotropism (pORG) gene set enriched in liver cohort versus lung cohort primary tumors. We identified ongoing replication stress response pathways in high pORG/liver cohort tumors, whereas low pORG/lung cohort tumors had greater densities of lymphocytes and shared T cell clonal responses. Our study demonstrates that liver-avid pancreatic ductal adenocarcinoma is associated with tolerance to ongoing replication stress, limited tumor immunity and less-favorable outcomes, whereas low replication stress, lung-avid/liver-averse tumors are associated with active tumor immunity that may account for favorable outcomes.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142952012","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}
Nature cancerPub Date : 2025-01-07DOI: 10.1038/s43018-024-00877-z
{"title":"Effects of CDKN2A loss on evolution of esophageal adenocarcinoma depend on context and time.","authors":"","doi":"10.1038/s43018-024-00877-z","DOIUrl":"https://doi.org/10.1038/s43018-024-00877-z","url":null,"abstract":"","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142951993","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}
Nature cancerPub Date : 2025-01-03DOI: 10.1038/s43018-024-00876-0
Piyali Ganguli, Celia C Basanta, Amelia Acha-Sagredo, Hrvoje Misetic, Maria Armero, Akram Mendez, Aeman Zahra, Ginny Devonshire, Gavin Kelly, Adam Freeman, Mary Green, Emma Nye, Anita Bichisecchi, Paola Bonfanti, Manuel Rodriguez-Justo, Jo Spencer, Rebecca C Fitzgerald, Francesca D Ciccarelli
{"title":"Context-dependent effects of CDKN2A and other 9p21 gene losses during the evolution of esophageal cancer.","authors":"Piyali Ganguli, Celia C Basanta, Amelia Acha-Sagredo, Hrvoje Misetic, Maria Armero, Akram Mendez, Aeman Zahra, Ginny Devonshire, Gavin Kelly, Adam Freeman, Mary Green, Emma Nye, Anita Bichisecchi, Paola Bonfanti, Manuel Rodriguez-Justo, Jo Spencer, Rebecca C Fitzgerald, Francesca D Ciccarelli","doi":"10.1038/s43018-024-00876-0","DOIUrl":"https://doi.org/10.1038/s43018-024-00876-0","url":null,"abstract":"<p><p>CDKN2A is a tumor suppressor located in chromosome 9p21 and frequently lost in Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC). How CDKN2A and other 9p21 gene co-deletions affect EAC evolution remains understudied. We explored the effects of 9p21 loss in EACs and cancer progressor and non-progressor BEs with matched genomic, transcriptomic and clinical data. Despite its cancer driver role, CDKN2A loss in BE prevents EAC initiation by counterselecting subsequent TP53 alterations. 9p21 gene co-deletions predict poor patient survival in EAC but not BE through context-dependent effects on cell cycle, oxidative phosphorylation and interferon response. Immune quantifications using bulk transcriptome, RNAscope and high-dimensional tissue imaging showed that IFNE loss reduces immune infiltration in BE, but not EAC. Mechanistically, CDKN2A loss suppresses the maintenance of squamous epithelium, contributing to a more aggressive phenotype. Our study demonstrates context-dependent roles of cancer genes during disease evolution, with consequences for cancer detection and patient management.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927561","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}
Nature cancerPub Date : 2025-01-03DOI: 10.1038/s43018-024-00882-2
Roberto Würth, Elisa Donato, Laura L Michel, Massimo Saini, Lisa Becker, Tasneem Cheytan, Daria Doncevic, Tobias Messmer, Ewgenija Gutjahr, Rebecca Weber, Corinna Klein, Hamed Alborzinia, Umut Yildiz, Vanessa Vogel, Mario Hlevnjak, Polina Kozyulina, Sarah-Jane Neuberth, Paul Schwerd-Kleine, Sevinç Jakab, Nicole Pfarr, Arlou Kristina Angeles, Astrid K Laut, Darja Karpova, Mattia Falcone, Olaf Hardt, Benjamin Theek, Celina V Wagner, Mirjam Becker, Sabine Wagner, Martina Haselmayr, Anita Schmitt, Carsten Müller-Tidow, Sabine Riethdorf, Klaus Pantel, Marc Zapatka, Holger Sültmann, Carl Herrmann, Verena Thewes, Peter Lichter, Andreas Schneeweiss, Martin R Sprick, Andreas Trumpp
{"title":"Circulating tumor cell plasticity determines breast cancer therapy resistance via neuregulin 1-HER3 signaling.","authors":"Roberto Würth, Elisa Donato, Laura L Michel, Massimo Saini, Lisa Becker, Tasneem Cheytan, Daria Doncevic, Tobias Messmer, Ewgenija Gutjahr, Rebecca Weber, Corinna Klein, Hamed Alborzinia, Umut Yildiz, Vanessa Vogel, Mario Hlevnjak, Polina Kozyulina, Sarah-Jane Neuberth, Paul Schwerd-Kleine, Sevinç Jakab, Nicole Pfarr, Arlou Kristina Angeles, Astrid K Laut, Darja Karpova, Mattia Falcone, Olaf Hardt, Benjamin Theek, Celina V Wagner, Mirjam Becker, Sabine Wagner, Martina Haselmayr, Anita Schmitt, Carsten Müller-Tidow, Sabine Riethdorf, Klaus Pantel, Marc Zapatka, Holger Sültmann, Carl Herrmann, Verena Thewes, Peter Lichter, Andreas Schneeweiss, Martin R Sprick, Andreas Trumpp","doi":"10.1038/s43018-024-00882-2","DOIUrl":"https://doi.org/10.1038/s43018-024-00882-2","url":null,"abstract":"<p><p>Circulating tumor cells (CTCs) drive metastasis, the leading cause of death in individuals with breast cancer. Due to their low abundance in the circulation, robust CTC expansion protocols are urgently needed to effectively study disease progression and therapy responses. Here we present the establishment of long-term CTC-derived organoids from female individuals with metastatic breast cancer. Multiomics analysis of CTC-derived organoids along with preclinical modeling with xenografts identified neuregulin 1 (NRG1)-ERBB2 receptor tyrosine kinase 3 (ERBB3/HER3) signaling as a key pathway required for CTC survival, growth and dissemination. Genome-wide CRISPR activation screens revealed that fibroblast growth factor receptor 1 (FGFR1) signaling serves a compensatory function to the NRG1-HER3 axis and rescues NRG1 deficiency in CTCs. Conversely, NRG1-HER3 activation induced resistance to FGFR1 inhibition, whereas combinatorial blockade impaired CTC growth. The dynamic interplay between NRG1-HER3 and FGFR1 signaling reveals the molecular basis of cancer cell plasticity and clinically relevant strategies to target it. Our CTC organoid platform enables the identification and validation of patient-specific vulnerabilities and represents an innovative tool for precision medicine.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-01-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142927543","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}
Nature cancerPub Date : 2025-01-02DOI: 10.1038/s43018-024-00880-4
Richa Shah, Nader Mounir Hanna, Ching Ee Loo, Michael David, Allini Mafra, Hanna Fink, Ethna McFerran, Montse Garcia, Robabeh Ghodssighassemabadi, Suryakanta Acharya, Jean Niyibaga, Oliver Langselius, Clara Frick, Nwamaka Lasebikan, Jerome Vignat, Julia Steinberg, Suzanne Hughes, Colleen Elizabeth Kircher, Catherine Lindsay Goldie, Sam Egger, Richard Sullivan, Ophira Ginsburg, Freddie Bray, Michael Caruana, Harriet Hui, André Michel Ilbawi, Karen Canfell, Isabelle Soerjomataram
{"title":"The global impact of the COVID-19 pandemic on delays and disruptions in cancer care services: a systematic review and meta-analysis.","authors":"Richa Shah, Nader Mounir Hanna, Ching Ee Loo, Michael David, Allini Mafra, Hanna Fink, Ethna McFerran, Montse Garcia, Robabeh Ghodssighassemabadi, Suryakanta Acharya, Jean Niyibaga, Oliver Langselius, Clara Frick, Nwamaka Lasebikan, Jerome Vignat, Julia Steinberg, Suzanne Hughes, Colleen Elizabeth Kircher, Catherine Lindsay Goldie, Sam Egger, Richard Sullivan, Ophira Ginsburg, Freddie Bray, Michael Caruana, Harriet Hui, André Michel Ilbawi, Karen Canfell, Isabelle Soerjomataram","doi":"10.1038/s43018-024-00880-4","DOIUrl":"https://doi.org/10.1038/s43018-024-00880-4","url":null,"abstract":"<p><p>The coronavirus disease 2019 pandemic substantially impacted the delivery of cancer services and programs. Here we reviewed and synthesized the global scale and impact of pandemic-related delays and disruptions on cancer services, including diagnosis, diagnostic procedures, screening, treatment and supportive and palliative care. Based on data from 245 articles in 46 countries, we observed declines in the number of cancer screening participation (39.0%), diagnoses (23.0%), diagnostic procedures (24.0%) and treatment (28.0%), ranging from a 15.0% decline for radiotherapy to a 35.0% decline for systemic treatment during the pandemic compared to during the prepandemic period. Medium-human development index (HDI) category countries experienced greater reductions than high- and very-high-HDI countries. Missing data from low-HDI countries emphasize the need for increased investments in cancer surveillance and research in these settings. PROSPERO registration: CRD42022301816.</p>","PeriodicalId":18885,"journal":{"name":"Nature cancer","volume":" ","pages":""},"PeriodicalIF":23.5,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142922109","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}
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