Pub Date : 2025-01-21DOI: 10.1158/2159-8290.cd-23-0543
Rahat Alam,Anna Reva,David G Edwards,Bree M Lege,Laura S Munoz-Arcos,Carolina Reduzzi,Swarnima Singh,Xiaoxin Hao,Yi-Hsuan Wu,Zeru Tian,Laura M Natalee,Gargi Damle,Deniz Demircioglu,Yixian Wang,Ling Wu,Elisabetta Molteni,Dan Hasson,Bora Lim,Zbigniew Gugala,Jerry E Chipuk,Julie E Lang,Joseph A Sparano,Chonghui Cheng,Massimo Cristofanilli,Han Xiao,Xiang H-F Zhang,Igor L Bado
Bone metastases can disseminate to secondary sites and promote breast cancer progression creating additional clinical challenges. The mechanisms contributing to secondary metastasis are barely understood. Here, we evaluate the prediction power of Her2-expressing (Her2E) circulating tumor cells (CTCs) after analyzing over 13,000 CTCs from a cohort of 137 metastatic breast cancer (MBC) patients with initial HR+/Her2- status and employ preclinical models of bone metastasis (BM) to validate the role of Her2E CTCs in multi-organ metastases. While Her2 expression was higher in patients with bone metastasis, experimental analyses revealed that Her2E CTCs derived from bone lesions were more dependent on Her2 activity and more susceptible to anti-Her2 therapy. Targeting the bone-mediated Her2 induction reduces CTC detection and abrogates secondary metastasis from bone. Overall, we elucidate that Her2E CTCs can serve as a non-invasive biomarker for BM formation with high therapeutic benefit for HR+ MBC patients.
{"title":"Bone-Induced Her2 Promotes Secondary Metastasis in HR+/Her2- Breast Cancer.","authors":"Rahat Alam,Anna Reva,David G Edwards,Bree M Lege,Laura S Munoz-Arcos,Carolina Reduzzi,Swarnima Singh,Xiaoxin Hao,Yi-Hsuan Wu,Zeru Tian,Laura M Natalee,Gargi Damle,Deniz Demircioglu,Yixian Wang,Ling Wu,Elisabetta Molteni,Dan Hasson,Bora Lim,Zbigniew Gugala,Jerry E Chipuk,Julie E Lang,Joseph A Sparano,Chonghui Cheng,Massimo Cristofanilli,Han Xiao,Xiang H-F Zhang,Igor L Bado","doi":"10.1158/2159-8290.cd-23-0543","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-23-0543","url":null,"abstract":"Bone metastases can disseminate to secondary sites and promote breast cancer progression creating additional clinical challenges. The mechanisms contributing to secondary metastasis are barely understood. Here, we evaluate the prediction power of Her2-expressing (Her2E) circulating tumor cells (CTCs) after analyzing over 13,000 CTCs from a cohort of 137 metastatic breast cancer (MBC) patients with initial HR+/Her2- status and employ preclinical models of bone metastasis (BM) to validate the role of Her2E CTCs in multi-organ metastases. While Her2 expression was higher in patients with bone metastasis, experimental analyses revealed that Her2E CTCs derived from bone lesions were more dependent on Her2 activity and more susceptible to anti-Her2 therapy. Targeting the bone-mediated Her2 induction reduces CTC detection and abrogates secondary metastasis from bone. Overall, we elucidate that Her2E CTCs can serve as a non-invasive biomarker for BM formation with high therapeutic benefit for HR+ MBC patients.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"32 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-01-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142991647","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 : 2025-01-17DOI: 10.1158/2159-8290.cd-24-0442
Anagh A. Sahasrabuddhe, Xiaofei Chen, Kaiyu Ma, Rui Wu, Huan-Chang Liang, Richa Kapoor, Rishi R. Chhipa, Ozlem Onder, Courtney McFetridge, John S. Van Arnam, Xiao Zhang, Jennifer J.D. Morrissette, Vinodh Pillai, Marilyn M. Li, Philippe Szankasi, Venkatesha Basrur, Kevin P. Conlon, Tobias D. Raabe, Nathanael G. Bailey, Cory M. Hogaboam, Robert Rottapel, Junhyong Kim, Cristina López, Matthias Schlesner, Reiner Siebert, Kostiantyn Dreval, Ryan D. Morin, Loredana Moro, Michele Pagano, Louis M. Staudt, Megan S. Lim, Kojo S.J. Elenitoba-Johnson
The role of ubiquitin-mediated degradation mechanisms in the pathogenesis of diffuse large B cell (DLBCL) and follicular lymphoma (FL) is not completely understood. We show that conditional deletion of the E3 ubiquitin ligase Fbxo45 in germinal center B-cells results in B-cell lymphomagenesis in homozygous (100%) and heterozygous (48%) mice. Mechanistically, FBXO45 targets the RHO guanine exchange factor ARHGEF2/GEF-H1 for ubiquitin-mediated degradation. Double genetic ablation of Fbxo45 and Arhgef2 ameliorated lymphoma formation. Transgenic knock-in mice harboring a GEF-H1 mutant unable to bind FBXO45 develop B-cell lymphomas with ~50% penetrance. Genome sequencing in human lymphomas identified mutually-exclusive FBXO45 copy number losses and ARHGEF2 gains, with combined frequencies ranging from 26.32% in FL to 45.12% in DLBCL. Notably, FBXO45 silencing enhances sensitivity to MEK1/2 inhibition. These results identify FBXO45 and ARHGEF2 as a novel tumor-suppressor and oncogene pair involved in the pathogenesis of B-cell lymphomas with significant implications for targeted therapies.
{"title":"The FBXO45-GEF-H1 axis controls germinal center formation and B-cell lymphomagenesis","authors":"Anagh A. Sahasrabuddhe, Xiaofei Chen, Kaiyu Ma, Rui Wu, Huan-Chang Liang, Richa Kapoor, Rishi R. Chhipa, Ozlem Onder, Courtney McFetridge, John S. Van Arnam, Xiao Zhang, Jennifer J.D. Morrissette, Vinodh Pillai, Marilyn M. Li, Philippe Szankasi, Venkatesha Basrur, Kevin P. Conlon, Tobias D. Raabe, Nathanael G. Bailey, Cory M. Hogaboam, Robert Rottapel, Junhyong Kim, Cristina López, Matthias Schlesner, Reiner Siebert, Kostiantyn Dreval, Ryan D. Morin, Loredana Moro, Michele Pagano, Louis M. Staudt, Megan S. Lim, Kojo S.J. Elenitoba-Johnson","doi":"10.1158/2159-8290.cd-24-0442","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-24-0442","url":null,"abstract":"The role of ubiquitin-mediated degradation mechanisms in the pathogenesis of diffuse large B cell (DLBCL) and follicular lymphoma (FL) is not completely understood. We show that conditional deletion of the E3 ubiquitin ligase Fbxo45 in germinal center B-cells results in B-cell lymphomagenesis in homozygous (100%) and heterozygous (48%) mice. Mechanistically, FBXO45 targets the RHO guanine exchange factor ARHGEF2/GEF-H1 for ubiquitin-mediated degradation. Double genetic ablation of Fbxo45 and Arhgef2 ameliorated lymphoma formation. Transgenic knock-in mice harboring a GEF-H1 mutant unable to bind FBXO45 develop B-cell lymphomas with ~50% penetrance. Genome sequencing in human lymphomas identified mutually-exclusive FBXO45 copy number losses and ARHGEF2 gains, with combined frequencies ranging from 26.32% in FL to 45.12% in DLBCL. Notably, FBXO45 silencing enhances sensitivity to MEK1/2 inhibition. These results identify FBXO45 and ARHGEF2 as a novel tumor-suppressor and oncogene pair involved in the pathogenesis of B-cell lymphomas with significant implications for targeted therapies.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"30 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-01-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142988897","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}
Identities of functional pSer/Thr.Pro protein substrates of the PIN1 prolyl isomerase and its effects on downstream signaling in bladder carcinogenesis remain largely unknown. Phenotypically, we found that PIN1 positively regulated bladder cancer cell proliferation, cell motility and urothelium clearance capacity in vitro and controlled tumor growth and potential metastasis in vivo. Mechanistically, we observed a negative enrichment of SREBP2-driven cholesterol metabolism pathways and a decrease in free/total cholesterol levels in PIN1-knockout bladder cancer cells. Moreover, we showed that PIN1 interacted with SREBP2 following its phosphorylation by the JNK MAP kinase at Ser455, which lies near the Site-2 cleavage site that generates the active, nuclear-form of SREBP2. Therapeutically, a combination of the sulfopin PIN1 covalent inhibitor and the simvastatin HMGCoA reductase inhibitor suppressed cell proliferation in vitro and tumor growth in vivo synergistically. Together, these findings emphasize that PIN1 can act as a driver and potential therapeutic target in bladder cancer.
{"title":"PIN1 prolyl isomerase promotes initiation and progression of bladder cancer through the SREBP2-mediated cholesterol biosynthesis pathway","authors":"Xue Wang, Derrick Lee, Haibo Xu, Yuan Sui, Jill Meisenhelder, Tony Hunter","doi":"10.1158/2159-8290.cd-24-0866","DOIUrl":"https://doi.org/10.1158/2159-8290.cd-24-0866","url":null,"abstract":"Identities of functional pSer/Thr.Pro protein substrates of the PIN1 prolyl isomerase and its effects on downstream signaling in bladder carcinogenesis remain largely unknown. Phenotypically, we found that PIN1 positively regulated bladder cancer cell proliferation, cell motility and urothelium clearance capacity in vitro and controlled tumor growth and potential metastasis in vivo. Mechanistically, we observed a negative enrichment of SREBP2-driven cholesterol metabolism pathways and a decrease in free/total cholesterol levels in PIN1-knockout bladder cancer cells. Moreover, we showed that PIN1 interacted with SREBP2 following its phosphorylation by the JNK MAP kinase at Ser455, which lies near the Site-2 cleavage site that generates the active, nuclear-form of SREBP2. Therapeutically, a combination of the sulfopin PIN1 covalent inhibitor and the simvastatin HMGCoA reductase inhibitor suppressed cell proliferation in vitro and tumor growth in vivo synergistically. Together, these findings emphasize that PIN1 can act as a driver and potential therapeutic target in bladder cancer.","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"60 1","pages":""},"PeriodicalIF":28.2,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142974775","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 : 2025-01-13DOI: 10.1158/2159-8290.CD-23-1117
John C Rose, Julia A Belk, Ivy Tsz-Lo Wong, Jens Luebeck, Hudson T Horn, Bence Daniel, Matthew G Jones, Kathryn E Yost, King L Hung, Kevin S Kolahi, Ellis J Curtis, Calvin J Kuo, Vineet Bafna, Paul S Mischel, Howard Y Chang
Significance: Our study harnesses a CRISPR-based method to examine ecDNA biogenesis, uncovering efficient circularization between double-strand breaks. ecDNAs and their corresponding chromosomal scars can form via nonhomologous end joining or microhomology-mediated end joining, but the ecDNA and scar formation processes are distinct. Based on our findings, we establish a mechanistic model of excisional ecDNA formation.
{"title":"Disparate Pathways for Extrachromosomal DNA Biogenesis and Genomic DNA Repair.","authors":"John C Rose, Julia A Belk, Ivy Tsz-Lo Wong, Jens Luebeck, Hudson T Horn, Bence Daniel, Matthew G Jones, Kathryn E Yost, King L Hung, Kevin S Kolahi, Ellis J Curtis, Calvin J Kuo, Vineet Bafna, Paul S Mischel, Howard Y Chang","doi":"10.1158/2159-8290.CD-23-1117","DOIUrl":"10.1158/2159-8290.CD-23-1117","url":null,"abstract":"<p><strong>Significance: </strong>Our study harnesses a CRISPR-based method to examine ecDNA biogenesis, uncovering efficient circularization between double-strand breaks. ecDNAs and their corresponding chromosomal scars can form via nonhomologous end joining or microhomology-mediated end joining, but the ecDNA and scar formation processes are distinct. Based on our findings, we establish a mechanistic model of excisional ecDNA formation.</p>","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":" ","pages":"69-82"},"PeriodicalIF":29.7,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11726015/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141896774","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 : 2025-01-13DOI: 10.1158/2159-8290.CD-23-0397
Paola D Vermeer, Anthony C Restaino, Jeffrey L Barr, Dan Yaniv, Moran Amit
The exponential growth of the cancer neuroscience field has shown that the host's immune, vascular, and nervous systems communicate with and influence each other in the tumor microenvironment, dictating the cancer malignant phenotype. Unraveling the nervous system's contributions toward this phenotype brings us closer to cancer cures. In this review, we summarize the peripheral nervous system's contributions to cancer. We highlight the effects of nerve recruitment and tumor innervation, the neuro-immune axis, glial cell activity, and neural regulation on cancer development and progression. We also discuss harnessing the neural control of peripheral cancers as a potential therapeutic approach in oncology. Significance: The continued and growing interest in cancer neuroscience by the scientific and medical communities reflects the rapidly accumulating interdisciplinary understanding of the nervous system's modulation of immune, vascular, and cancer cells' functions in malignancies. Understanding these regulatory functions can identify targets for intervention that may already be clinically available for other indications. This potential brings great excitement and hope for patients with cancer worldwide.
{"title":"Nerves at Play: The Peripheral Nervous System in Extracranial Malignancies.","authors":"Paola D Vermeer, Anthony C Restaino, Jeffrey L Barr, Dan Yaniv, Moran Amit","doi":"10.1158/2159-8290.CD-23-0397","DOIUrl":"https://doi.org/10.1158/2159-8290.CD-23-0397","url":null,"abstract":"<p><p>The exponential growth of the cancer neuroscience field has shown that the host's immune, vascular, and nervous systems communicate with and influence each other in the tumor microenvironment, dictating the cancer malignant phenotype. Unraveling the nervous system's contributions toward this phenotype brings us closer to cancer cures. In this review, we summarize the peripheral nervous system's contributions to cancer. We highlight the effects of nerve recruitment and tumor innervation, the neuro-immune axis, glial cell activity, and neural regulation on cancer development and progression. We also discuss harnessing the neural control of peripheral cancers as a potential therapeutic approach in oncology. Significance: The continued and growing interest in cancer neuroscience by the scientific and medical communities reflects the rapidly accumulating interdisciplinary understanding of the nervous system's modulation of immune, vascular, and cancer cells' functions in malignancies. Understanding these regulatory functions can identify targets for intervention that may already be clinically available for other indications. This potential brings great excitement and hope for patients with cancer worldwide.</p>","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"15 1","pages":"52-68"},"PeriodicalIF":29.7,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969747","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 : 2025-01-13DOI: 10.1158/2159-8290.CD-24-1201
Proteeti Bhattacharjee, Esther H Lips, Elinor J Sawyer, E Shelley Hwang, Alastair M Thompson, Jelle Wesseling
As we cannot reliably distinguish indolent, low-risk ductal carcinoma in situ (DCIS) from potentially progressive, high-risk DCIS, all women with DCIS diagnosis undergo intensive treatment without any benefit. The PREvent ductal Carcinoma In Situ Invasive Overtreatment Now team was established to unravel DCIS biology and develop new multidisciplinary approaches for accurate risk stratification to tackle the global problem of DCIS overdiagnosis and overtreatment. See related article by Bressan et al., p. 16 See related article by Stratton et al., p. 22 See related article by Goodwin et al., p. 34.
{"title":"Conquering Overtreatment of DCIS: Lessons from PRECISION.","authors":"Proteeti Bhattacharjee, Esther H Lips, Elinor J Sawyer, E Shelley Hwang, Alastair M Thompson, Jelle Wesseling","doi":"10.1158/2159-8290.CD-24-1201","DOIUrl":"https://doi.org/10.1158/2159-8290.CD-24-1201","url":null,"abstract":"<p><p>As we cannot reliably distinguish indolent, low-risk ductal carcinoma in situ (DCIS) from potentially progressive, high-risk DCIS, all women with DCIS diagnosis undergo intensive treatment without any benefit. The PREvent ductal Carcinoma In Situ Invasive Overtreatment Now team was established to unravel DCIS biology and develop new multidisciplinary approaches for accurate risk stratification to tackle the global problem of DCIS overdiagnosis and overtreatment. See related article by Bressan et al., p. 16 See related article by Stratton et al., p. 22 See related article by Goodwin et al., p. 34.</p>","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"15 1","pages":"28-33"},"PeriodicalIF":29.7,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969745","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 : 2025-01-13DOI: 10.1158/2159-8290.CD-24-0287
Hiroki Kobayashi, Tadashi Iida, Yosuke Ochiai, Ermanno Malagola, Xiaofei Zhi, Ruth A White, Jin Qian, Feijing Wu, Quin T Waterbury, Ruhong Tu, Biyun Zheng, Jonathan S LaBella, Leah B Zamechek, Atsushi Ogura, Susan L Woods, Daniel L Worthley, Atsushi Enomoto, Timothy C Wang
Significance: Our work demonstrates that the bidirectional interplay between sympathetic nerves and NGF-expressing CAFs drives colorectal tumorigenesis. This study also offers novel mechanistic insights into catecholamine action in colorectal cancer. Inhibiting the neuro-mesenchymal interaction by TRK blockade could be a potential strategy for treating colorectal cancer.
{"title":"Neuro-Mesenchymal Interaction Mediated by a β2-Adrenergic Nerve Growth Factor Feedforward Loop Promotes Colorectal Cancer Progression.","authors":"Hiroki Kobayashi, Tadashi Iida, Yosuke Ochiai, Ermanno Malagola, Xiaofei Zhi, Ruth A White, Jin Qian, Feijing Wu, Quin T Waterbury, Ruhong Tu, Biyun Zheng, Jonathan S LaBella, Leah B Zamechek, Atsushi Ogura, Susan L Woods, Daniel L Worthley, Atsushi Enomoto, Timothy C Wang","doi":"10.1158/2159-8290.CD-24-0287","DOIUrl":"10.1158/2159-8290.CD-24-0287","url":null,"abstract":"<p><strong>Significance: </strong>Our work demonstrates that the bidirectional interplay between sympathetic nerves and NGF-expressing CAFs drives colorectal tumorigenesis. This study also offers novel mechanistic insights into catecholamine action in colorectal cancer. Inhibiting the neuro-mesenchymal interaction by TRK blockade could be a potential strategy for treating colorectal cancer.</p>","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":" ","pages":"202-226"},"PeriodicalIF":29.7,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11729495/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141975087","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 : 2025-01-13DOI: 10.1158/2159-8290.CD-24-1686
Dario Bressan, Nicholas Walton, Gregory J Hannon
The Imaging and Molecular Annotation of Xenografts and Tumors Cancer Grand Challenges team was set up with the objective of developing the "next generation" of pathology and cancer research by using a combination of single-cell and spatial omics tools to produce 3D molecularly annotated maps of tumors. Its activities overlapped, and in some cases catalyzed, a spatial revolution in biology that saw new technologies being deployed to investigate the roles of tumor heterogeneity and of the tumor micro-environment. See related article by Stratton et al., p. 22 See related article by Bhattacharjee et al., p. 28 See related article by Goodwin et al., p. 34.
{"title":"Cancer Research in the Age of Spatial Omics: Lessons from IMAXT.","authors":"Dario Bressan, Nicholas Walton, Gregory J Hannon","doi":"10.1158/2159-8290.CD-24-1686","DOIUrl":"https://doi.org/10.1158/2159-8290.CD-24-1686","url":null,"abstract":"<p><p>The Imaging and Molecular Annotation of Xenografts and Tumors Cancer Grand Challenges team was set up with the objective of developing the \"next generation\" of pathology and cancer research by using a combination of single-cell and spatial omics tools to produce 3D molecularly annotated maps of tumors. Its activities overlapped, and in some cases catalyzed, a spatial revolution in biology that saw new technologies being deployed to investigate the roles of tumor heterogeneity and of the tumor micro-environment. See related article by Stratton et al., p. 22 See related article by Bhattacharjee et al., p. 28 See related article by Goodwin et al., p. 34.</p>","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"15 1","pages":"16-21"},"PeriodicalIF":29.7,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969744","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 : 2025-01-13DOI: 10.1158/2159-8290.CD-24-1776
Linghua Wang, Mingyao Li, Tae Hyun Hwang
{"title":"Correction: The 3D Revolution in Cancer Discovery.","authors":"Linghua Wang, Mingyao Li, Tae Hyun Hwang","doi":"10.1158/2159-8290.CD-24-1776","DOIUrl":"https://doi.org/10.1158/2159-8290.CD-24-1776","url":null,"abstract":"","PeriodicalId":9430,"journal":{"name":"Cancer discovery","volume":"15 1","pages":"245"},"PeriodicalIF":29.7,"publicationDate":"2025-01-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142969746","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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