Pub Date : 2026-01-29DOI: 10.1016/j.ccell.2026.01.002
Justin Jee, Travis Zack
{"title":"AI for cancer treatment information: Can academia stay in the game?","authors":"Justin Jee, Travis Zack","doi":"10.1016/j.ccell.2026.01.002","DOIUrl":"https://doi.org/10.1016/j.ccell.2026.01.002","url":null,"abstract":"","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"8 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146072066","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 : 2026-01-29DOI: 10.1016/j.ccell.2026.01.001
Jakob M. Riedl, Hiroyuki Matsubara, Reid McNeil, Parasvi S. Patel, Ferran Fece de la Cruz, Doga C. Gulhan, Ryan B. Corcoran
Alterations in KRAS, NRAS, and HRAS occur in roughly 20% of patients with cancer, making RAS one of the most intensively studied oncogenic targets. The discovery of mutant-selective KRASG12C inhibitors has provided a proof-of-concept for RAS-directed therapies, heralding a new era in the treatment of RAS-driven cancers. Yet, the efficacy of first-generation KRASG12C inhibitors is limited by the rapid emergence of resistance. Novel classes of (K)RAS inhibitors with distinct mechanisms of action and broader target coverage hold promise to overcome resistance and extend the benefits of RAS-targeted therapies to a wider patient population. In this review, we summarize clinical evidence for KRASG12C inhibitors across tumor types and delineate key mechanisms of resistance. We further discuss the rapidly evolving landscape of next-generation (K)RAS inhibitors, with particular emphasis on their target selectivity, mechanisms of action, preliminary clinical efficacy, and the therapeutic opportunities and challenges inherent to each class.
{"title":"Emerging landscape of KRAS inhibitors in cancer treatment","authors":"Jakob M. Riedl, Hiroyuki Matsubara, Reid McNeil, Parasvi S. Patel, Ferran Fece de la Cruz, Doga C. Gulhan, Ryan B. Corcoran","doi":"10.1016/j.ccell.2026.01.001","DOIUrl":"https://doi.org/10.1016/j.ccell.2026.01.001","url":null,"abstract":"Alterations in <em>KRAS</em>, <em>NRAS</em>, and <em>HRAS</em> occur in roughly 20% of patients with cancer, making RAS one of the most intensively studied oncogenic targets. The discovery of mutant-selective KRAS<sup>G12C</sup> inhibitors has provided a proof-of-concept for RAS-directed therapies, heralding a new era in the treatment of RAS-driven cancers. Yet, the efficacy of first-generation KRAS<sup>G12C</sup> inhibitors is limited by the rapid emergence of resistance. Novel classes of (K)RAS inhibitors with distinct mechanisms of action and broader target coverage hold promise to overcome resistance and extend the benefits of RAS-targeted therapies to a wider patient population. In this review, we summarize clinical evidence for KRAS<sup>G12C</sup> inhibitors across tumor types and delineate key mechanisms of resistance. We further discuss the rapidly evolving landscape of next-generation (K)RAS inhibitors, with particular emphasis on their target selectivity, mechanisms of action, preliminary clinical efficacy, and the therapeutic opportunities and challenges inherent to each class.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"54 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146070575","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 : 2026-01-22DOI: 10.1016/j.ccell.2025.11.009
Gal Yagel, Dana Rimini, Michelle von Locquenghien, Roberto Avellino, Oren Barboy, Paulina Chalan, Gaya Granot, Ken Xie, Shir Shlomi-Loubaton, Fadi Sheban, Kfir Mazuz, Eyal David, Pascale Zwicky, Ido Amit
Chimeric antigen receptor (CAR) T cell therapy has shown remarkable success in hematologic malignancies and autoimmune diseases but remains limited in solid tumors due to antigen heterogeneity, escape, and an immunosuppressive tumor microenvironment (TME) dominated by tumor-associated macrophages (TAMs). We developed a macrophage-directed CAR T strategy targeting TREM2+ immunosuppressive TAMs, achieving potent in vitro activity and robust antitumor efficacy in vivo. To enhance intratumoral activity, we incorporated synthetic CAR-responsive biosensors containing NFAT, IRF, and AP1 motifs that enable localized IL-12 secretion upon activation. In an immunocompetent human TREM2 transgenic murine model, IL-12-armored hTREM2 CAR T cells remodel the TME and tumor-draining lymph nodes, depleting TREM2+ TAMs, enhancing T and natural killer (NK) cell infiltration and activation, and inducing tumor regression without systemic toxicity. This study highlights the potential for developing universal and efficacious CAR T cell therapies targeting tumor-associated macrophages for the treatment of solid tumors.
{"title":"Tumor-antigen-independent targeting of solid tumors by armored macrophage-directed anti-TREM2 CAR T cells","authors":"Gal Yagel, Dana Rimini, Michelle von Locquenghien, Roberto Avellino, Oren Barboy, Paulina Chalan, Gaya Granot, Ken Xie, Shir Shlomi-Loubaton, Fadi Sheban, Kfir Mazuz, Eyal David, Pascale Zwicky, Ido Amit","doi":"10.1016/j.ccell.2025.11.009","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.11.009","url":null,"abstract":"Chimeric antigen receptor (CAR) T cell therapy has shown remarkable success in hematologic malignancies and autoimmune diseases but remains limited in solid tumors due to antigen heterogeneity, escape, and an immunosuppressive tumor microenvironment (TME) dominated by tumor-associated macrophages (TAMs). We developed a macrophage-directed CAR T strategy targeting TREM2<sup>+</sup> immunosuppressive TAMs, achieving potent <em>in vitro</em> activity and robust antitumor efficacy <em>in vivo</em>. To enhance intratumoral activity, we incorporated synthetic CAR-responsive biosensors containing NFAT, IRF, and AP1 motifs that enable localized IL-12 secretion upon activation. In an immunocompetent human TREM2 transgenic murine model, IL-12-armored hTREM2 CAR T cells remodel the TME and tumor-draining lymph nodes, depleting TREM2<sup>+</sup> TAMs, enhancing T and natural killer (NK) cell infiltration and activation, and inducing tumor regression without systemic toxicity. This study highlights the potential for developing universal and efficacious CAR T cell therapies targeting tumor-associated macrophages for the treatment of solid tumors.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"16 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022168","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 : 2026-01-22DOI: 10.1016/j.ccell.2025.12.021
Jaime Mateus-Tique, Ashwitha Lakshmi, Bhavya Singh, Rhea Iyer, Alfonso R. Sánchez-Paulete, Chiara Falcomatà, Matthew Lin, Gvantsa Pantsulaia, Alexander Tepper, Trung Nguyen, Angelo Amabile, Gurkan Mollaoglu, Luisanna Pia, Divya Chhamalwan, Jessica Le Berichel, Hunter Potak, Marco Colonna, Alessia Baccarini, Joshua Brody, Miriam Merad, Brian D. Brown
{"title":"Armored macrophage-targeted CAR-T cells reset and reprogram the tumor microenvironment and control metastatic cancer growth","authors":"Jaime Mateus-Tique, Ashwitha Lakshmi, Bhavya Singh, Rhea Iyer, Alfonso R. Sánchez-Paulete, Chiara Falcomatà, Matthew Lin, Gvantsa Pantsulaia, Alexander Tepper, Trung Nguyen, Angelo Amabile, Gurkan Mollaoglu, Luisanna Pia, Divya Chhamalwan, Jessica Le Berichel, Hunter Potak, Marco Colonna, Alessia Baccarini, Joshua Brody, Miriam Merad, Brian D. Brown","doi":"10.1016/j.ccell.2025.12.021","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.12.021","url":null,"abstract":"","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"3 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146033186","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 : 2026-01-22DOI: 10.1016/j.ccell.2025.12.019
Triantafyllia Karakousi, Vanessa Cristaldi, Maria Luiza Lopes de Oliveira, Ines Delclaux, Naomi R. Besson, Luiz Henrique Geraldo, Tania J. González-Robles, Devyon R. McDonnough, Daniel Martinez-Krams, Gabrielle da Silva, Alec P. Breazeale, Joel Encarnacion-Rosado, Joanna Pozniak, Shi Qiu, Irineu Illa Bochaca, Medard E. Kaiza, Hye Mi Kim, Tullia C. Bruno, Boris Reizis, Ata S. Moshiri, Amanda W. Lund
Lymphatic vessels activate anti-tumor immune surveillance and support metastasis. Whether there are distinct lymphatic phenotypes that govern immunity and metastasis remains unclear. Here we reveal that cytotoxic immunity normalizes lymphatic function and uncouples immune and metastatic potential. We demonstrate that intratumoral lymphatic vessel density negatively correlates with cytotoxic immunity and that IFNγ reprograms the intratumoral lymphatic state. Lymphatic deletion of Ifngr1 expanded the intratumoral lymphatic network and drove the emergence of a tip-like state that promotes lymph node metastasis but not dendritic cell migration or response to immune checkpoint blockade (ICB). Mechanistically, IFNγ restrains proliferation and cell state programs through inhibition of mitochondrial respiration. Lymphatic-specific inhibition of mitochondrial complex III restrained the intratumoral tip-like state, blocked metastasis, and enhanced the response to ICB. Our data reveal that IFNγ induces a metabolic and phenotypic switch in tumor-associated lymphatic vessels that blocks regional metastasis and reinforces immune surveillance.
{"title":"IFNγ-dependent metabolic reprogramming restrains an immature, pro-metastatic lymphatic state in melanoma","authors":"Triantafyllia Karakousi, Vanessa Cristaldi, Maria Luiza Lopes de Oliveira, Ines Delclaux, Naomi R. Besson, Luiz Henrique Geraldo, Tania J. González-Robles, Devyon R. McDonnough, Daniel Martinez-Krams, Gabrielle da Silva, Alec P. Breazeale, Joel Encarnacion-Rosado, Joanna Pozniak, Shi Qiu, Irineu Illa Bochaca, Medard E. Kaiza, Hye Mi Kim, Tullia C. Bruno, Boris Reizis, Ata S. Moshiri, Amanda W. Lund","doi":"10.1016/j.ccell.2025.12.019","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.12.019","url":null,"abstract":"Lymphatic vessels activate anti-tumor immune surveillance and support metastasis. Whether there are distinct lymphatic phenotypes that govern immunity and metastasis remains unclear. Here we reveal that cytotoxic immunity normalizes lymphatic function and uncouples immune and metastatic potential. We demonstrate that intratumoral lymphatic vessel density negatively correlates with cytotoxic immunity and that IFNγ reprograms the intratumoral lymphatic state. Lymphatic deletion of <em>Ifngr1</em> expanded the intratumoral lymphatic network and drove the emergence of a tip-like state that promotes lymph node metastasis but not dendritic cell migration or response to immune checkpoint blockade (ICB). Mechanistically, IFNγ restrains proliferation and cell state programs through inhibition of mitochondrial respiration. Lymphatic-specific inhibition of mitochondrial complex III restrained the intratumoral tip-like state, blocked metastasis, and enhanced the response to ICB. Our data reveal that IFNγ induces a metabolic and phenotypic switch in tumor-associated lymphatic vessels that blocks regional metastasis and reinforces immune surveillance.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"31 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146022165","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 : 2026-01-22DOI: 10.1016/j.ccell.2026.01.011
Peiwen Fei, Wenge Wang, Seok-hyun Kim, Shulin Wang, Timothy F. Burns, Joanna K. Sax, Monica Buzzai, David T. Dicker, W. Gillies McKenna, Eric J. Bernhard, Wafik S. El-Deiry
{"title":"Bnip3L is induced by p53 under hypoxia, and its knockdown promotes tumor growth","authors":"Peiwen Fei, Wenge Wang, Seok-hyun Kim, Shulin Wang, Timothy F. Burns, Joanna K. Sax, Monica Buzzai, David T. Dicker, W. Gillies McKenna, Eric J. Bernhard, Wafik S. El-Deiry","doi":"10.1016/j.ccell.2026.01.011","DOIUrl":"https://doi.org/10.1016/j.ccell.2026.01.011","url":null,"abstract":"","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"31 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146033187","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 : 2026-01-22DOI: 10.1016/j.ccell.2025.12.020
Raphaël Collot, Cristian Ruiz-Moreno, Celina Honhoff, Thijs J.M. van den Broek, Amber K.L. Wezenaar, Daan J. Kloosterman, Hendrikus C.R. Ariese, Hannah Johnson, Britt M.T. Vervoort, Amal Jeiroshi, Jens Bunt, Ravian L. van Ineveld, Emma Bokobza, Heggert G. Rebel, Brigit M. te Pas, Femke C.A. Ringnalda, Marc van de Wetering, Pierre A. Robe, Marcel Kool, Jennifer R. Cochran, Anne C. Rios
Diffuse midline glioma (DMG) is an aggressive pediatric brain tumor with no curative treatment, and lacks a comprehensive understanding of immune-tumor cell interactions within their spatial context. Our multi-omics approach, integrating single-nuclei RNA sequencing, spatial transcriptomics, and high-dimensional imaging, utilizes patient samples and an experimental murine DMG model to unveil two spatially distinct regions. MES-patterns are defined by mesenchymal (MES) tumor cells and blood-derived immune cells, whereas AOO-patterns are enriched with astrocyte (AC)-, oligodendrocyte (OC)-, and oligodendrocyte precursor cell (OPC)-like cancer populations, alongside homeostatic-like microglia. The less-studied immune checkpoint, IGSF11, is primarily expressed by AOO-associated cancer cells, while its receptor VISTA is detected mainly in homeostatic microglia. Targeting IGSF11-VISTA results in tumor reduction and survival benefit, mediated by brain-resident microglia and independent of T cell infiltration. This positions IGSF11-VISTA as a promising immune checkpoint treatment axis to harness the local brain immune response against DMG.
{"title":"IGSF11-VISTA is a critical and targetable immune checkpoint axis in diffuse midline glioma","authors":"Raphaël Collot, Cristian Ruiz-Moreno, Celina Honhoff, Thijs J.M. van den Broek, Amber K.L. Wezenaar, Daan J. Kloosterman, Hendrikus C.R. Ariese, Hannah Johnson, Britt M.T. Vervoort, Amal Jeiroshi, Jens Bunt, Ravian L. van Ineveld, Emma Bokobza, Heggert G. Rebel, Brigit M. te Pas, Femke C.A. Ringnalda, Marc van de Wetering, Pierre A. Robe, Marcel Kool, Jennifer R. Cochran, Anne C. Rios","doi":"10.1016/j.ccell.2025.12.020","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.12.020","url":null,"abstract":"Diffuse midline glioma (DMG) is an aggressive pediatric brain tumor with no curative treatment, and lacks a comprehensive understanding of immune-tumor cell interactions within their spatial context. Our multi-omics approach, integrating single-nuclei RNA sequencing, spatial transcriptomics, and high-dimensional imaging, utilizes patient samples and an experimental murine DMG model to unveil two spatially distinct regions. MES-patterns are defined by mesenchymal (MES) tumor cells and blood-derived immune cells, whereas AOO-patterns are enriched with astrocyte (AC)-, oligodendrocyte (OC)-, and oligodendrocyte precursor cell (OPC)-like cancer populations, alongside homeostatic-like microglia. The less-studied immune checkpoint, IGSF11, is primarily expressed by AOO-associated cancer cells, while its receptor VISTA is detected mainly in homeostatic microglia. Targeting IGSF11-VISTA results in tumor reduction and survival benefit, mediated by brain-resident microglia and independent of T cell infiltration. This positions IGSF11-VISTA as a promising immune checkpoint treatment axis to harness the local brain immune response against DMG.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"119 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2026-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146021991","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 : 2026-01-12DOI: 10.1016/j.ccell.2025.12.010
Kenny Kwok Hei Yu, Zaki Abou-Mrad, Kristof Törkenczy, Isabell Schulze, Jennifer Gantchev, Gerard Baquer, Kelsey Hopland, Evan D. Bander, Umberto Tosi, Cameron Brennan, Nelson S. Moss, Pierre-Jacques Hamard, Richard Koche, Caleb Lareau, Nathalie Y.R. Agar, Taha Merghoub, Viviane Tabar
Primary de novo high grade gliomas, such as glioblastoma and lower grade gliomas both converge on a common aggressive phenotype, and the basis for this progression is unknown. Glioma associated macrophages (GAM) have been strongly implicated in supporting tumor growth, however, robust isolation of functional subpopulations has been elusive. We hypothesize that functional populations of GAMs can be resolved through gene regulatory network (GRN) inference and show that a subpopulation of human GAMs, defined by a GRN centered around the activator protein-1 transcription factor FOSL2 is preferentially enriched in high grade gliomas. We nominate ANXA1 and HMOX1 as surrogate cell surface markers for a subpopulation we term malignancy associated GAMs (mGAMs) which possess distinct pro-tumorigenic properties, share partial ontogeny with peripheral blood monocytes, and are enriched in newly transformed regions of glioma. mGAMs potentially play a pivotal role in glioma progression and represent a plausible therapeutic target.
{"title":"Characterization of a pathogenic subpopulation of human glioma associated macrophages linked to glioma progression","authors":"Kenny Kwok Hei Yu, Zaki Abou-Mrad, Kristof Törkenczy, Isabell Schulze, Jennifer Gantchev, Gerard Baquer, Kelsey Hopland, Evan D. Bander, Umberto Tosi, Cameron Brennan, Nelson S. Moss, Pierre-Jacques Hamard, Richard Koche, Caleb Lareau, Nathalie Y.R. Agar, Taha Merghoub, Viviane Tabar","doi":"10.1016/j.ccell.2025.12.010","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.12.010","url":null,"abstract":"Primary <em>de novo</em> high grade gliomas, such as glioblastoma and lower grade gliomas both converge on a common aggressive phenotype, and the basis for this progression is unknown. Glioma associated macrophages (GAM) have been strongly implicated in supporting tumor growth, however, robust isolation of functional subpopulations has been elusive. We hypothesize that functional populations of GAMs can be resolved through gene regulatory network (GRN) inference and show that a subpopulation of human GAMs, defined by a GRN centered around the activator protein-1 transcription factor <em>FOSL2</em> is preferentially enriched in high grade gliomas. We nominate ANXA1 and HMOX1 as surrogate cell surface markers for a subpopulation we term malignancy associated GAMs (mGAMs) which possess distinct pro-tumorigenic properties, share partial ontogeny with peripheral blood monocytes, and are enriched in newly transformed regions of glioma. mGAMs potentially play a pivotal role in glioma progression and represent a plausible therapeutic target.","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"83 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145961693","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 : 2026-01-12DOI: 10.1016/j.ccell.2025.12.003
Valentin Marteau, Niloofar Nemati, Kristina Handler, Deeksha Raju, Alexander Kirchmair, Dietmar Rieder, Erika Kvalem Soto, Georgios Fotakis, Glenn De Lange, Sandro Carollo, Nina Boeck, Alessia Rossi, Sophia Daum, Alexandra Scheiber, Arno Amann, Andreas Seeber, Elisabeth Gasser, Steffen Ormanns, Michael Günther, Agnieszka Martowicz, Zuzana Loncova, Giorgia Lamberti, Anne Krogsdam, Michela Carlet, Lena Horvath, Marie Theres Eling, Hassan Fazilaty, Tomas Valenta, Gregor Sturm, Sieghart Sopper, Andreas Pircher, Patrizia Stoitzner, Peter J. Wild, Patrick Welker, Pascal J. May, Paul Ziegler, Markus Tschurtschenthaler, Daniel Neureiter, Florian Huemer, Richard Greil, Lukas Weiss, Marieke Ijsselsteijn, Noel F.C.C. de Miranda, Dominik Wolf, Isabelle C. Arnold, Stefan Salcher, Zlatko Trajanoski
{"title":"Single-cell integration and multi-modal profiling reveals phenotypes and spatial organization of neutrophils in colorectal cancer","authors":"Valentin Marteau, Niloofar Nemati, Kristina Handler, Deeksha Raju, Alexander Kirchmair, Dietmar Rieder, Erika Kvalem Soto, Georgios Fotakis, Glenn De Lange, Sandro Carollo, Nina Boeck, Alessia Rossi, Sophia Daum, Alexandra Scheiber, Arno Amann, Andreas Seeber, Elisabeth Gasser, Steffen Ormanns, Michael Günther, Agnieszka Martowicz, Zuzana Loncova, Giorgia Lamberti, Anne Krogsdam, Michela Carlet, Lena Horvath, Marie Theres Eling, Hassan Fazilaty, Tomas Valenta, Gregor Sturm, Sieghart Sopper, Andreas Pircher, Patrizia Stoitzner, Peter J. Wild, Patrick Welker, Pascal J. May, Paul Ziegler, Markus Tschurtschenthaler, Daniel Neureiter, Florian Huemer, Richard Greil, Lukas Weiss, Marieke Ijsselsteijn, Noel F.C.C. de Miranda, Dominik Wolf, Isabelle C. Arnold, Stefan Salcher, Zlatko Trajanoski","doi":"10.1016/j.ccell.2025.12.003","DOIUrl":"https://doi.org/10.1016/j.ccell.2025.12.003","url":null,"abstract":"","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":"84 1","pages":""},"PeriodicalIF":50.3,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145962521","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 : 2026-01-12Epub Date: 2025-12-31DOI: 10.1016/j.ccell.2025.12.007
Vito Amodio, Giorgio Patelli, Alberto Bardelli
In this issue of Cancer Cell, Zhang et al. show that dual KRAS-EGFR inhibition induces a reversible Paneth-like transition in colorectal cancer, sustaining mitogen-activated protein kinase (MAPK) reactivation through a SMAD1-FGFR3 axis. This reinforces emerging evidence that lineage remodeling underlies early adaptive escape from targeted therapy and carries potential clinical relevance.
{"title":"Adaptive plasticity in targeted therapy.","authors":"Vito Amodio, Giorgio Patelli, Alberto Bardelli","doi":"10.1016/j.ccell.2025.12.007","DOIUrl":"10.1016/j.ccell.2025.12.007","url":null,"abstract":"<p><p>In this issue of Cancer Cell, Zhang et al. show that dual KRAS-EGFR inhibition induces a reversible Paneth-like transition in colorectal cancer, sustaining mitogen-activated protein kinase (MAPK) reactivation through a SMAD1-FGFR3 axis. This reinforces emerging evidence that lineage remodeling underlies early adaptive escape from targeted therapy and carries potential clinical relevance.</p>","PeriodicalId":9670,"journal":{"name":"Cancer Cell","volume":" ","pages":"15-17"},"PeriodicalIF":44.5,"publicationDate":"2026-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145888711","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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