Carretero

@ugr.es

Profesor ayudante Doctor. Departamento de bioquímica, biología molecular 3 e inmunología
Universidad de Granada

Carretero


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https://researchid.co/rafaelcarretero

RESEARCH, TEACHING, or OTHER INTERESTS

Immunology, Oncology, Biotechnology, Applied Microbiology and Biotechnology
28

Scopus Publications

2167

Scholar Citations

19

Scholar h-index

26

Scholar i10-index

Scopus Publications

  • Activated ATF6α is a hepatic tumour driver restricting immunosurveillance
    Xin Li, Cynthia Lebeaupin, Aikaterini Kadianaki, Clementine Druelle-Cedano, Niklas Vesper, Charlotte Rennert, Júlia Huguet-Pradell, Borja Gomez Ramos, Chaofan Fan, Robert Stefan Piecyk, Laimdota Zizmare, Pierluigi Ramadori, Luqing Li, Lukas Frick, Menjie Qiu, Cangang Zhang, Luiza Martins Nascentes Melo, Vikas Prakash Ranvir, Peng Shen, Johannes Hanselmann, Jan Kosla, Mirian Fernández-Vaquero, Mihael Vucur, Praveen Baskaran, Xuanwen Bao, Olivia I. Coleman, Yingyue Tang, Miray Cetin, Zhouji Chen, Insook Jang, Stefania Del Prete, Mohammad Rahbari, Peng Zhang, Timothy V. Pham, Yushan Hou, Aihua Sun, Li Gu, Laura C. Kim, Ulrike Rothermel, Danijela Heide, Adnan Ali, Suchira Gallage, Nana Talvard-Balland, Marta Piqué-Gili, Albert Gris-Oliver, Alessio Bevilacqua, Lisa Schlicker, Alec Duffey, Kristian Unger, Marta Szydlowska, Jenny Hetzer, Duncan T. Odom, Tim Machauer, Daniele Bucci, Pooja Sant, Jun-Hoe Lee, Jonas Rösler, Sven W. Meckelmann, Johannes Schreck, Sue Murray, M. Celeste Simon, Sven Nahnsen, Almut Schulze, Ping-Chih Ho, Manfred Jugold, Kai Breuhahn, Jan-Philipp Mallm, Peter Schirmacher, Susanne Roth, Nuh Rahbari, Darjus F. Tschaharganeh, Stephanie Roessler, Benjamin Goeppert, Bertram Bengsch, Geoffroy Andrieux, Melanie Boerries, Nisar P. Malek, Marco Prinz, Achim Weber, Robert Zeiser, Pablo Tamayo, Peter Bronsert, Konrad Kurowski, Robert Thimme, Detian Yuan, Rafael Carretero, Tom Luedde, Roser Pinyol, Felix J. Hartmann, Michael Karin, Alpaslan Tasdogan, Christoph Trautwein, Moritz Mall, Maike Hofmann, Josep M. Llovet, Dirk Haller, Randal J. Kaufman, Mathias Heikenwälder
    Nature, 2026
    Hepatocellular carcinoma (HCC) is the fastest growing cause of cancer-related mortality and there are limited therapies 1 . Although endoplasmic reticulum (ER) stress and the unfolded protein response (UPR) are implicated in HCC, the involvement of the UPR transducer ATF6α remains unclear 2 . Here we demonstrate the function of ATF6α as an ER-stress-inducing tumour driver and metabolic master regulator restricting cancer immunosurveillance for HCC, in contrast to its well-characterized role as an adaptive response to ER stress 3 . ATF6α activation in human HCC is significantly correlated with an aggressive tumour phenotype, characterized by reduced patient survival, enhanced tumour progression and local immunosuppression. Hepatocyte-specific ATF6α activation in mice induced progressive hepatitis with ER stress, immunosuppression and hepatocyte proliferation. Concomitantly, activated ATF6α increased glycolysis and directly repressed the gluconeogenic enzyme FBP1 by binding to gene regulatory elements. Restoring FBP1 expression limited ATF6α-activation-related pathologies. Prolonged ATF6α activation in hepatocytes triggered hepatocarcinogenesis, intratumoural T cell infiltration and nutrient-deprived immune exhaustion. Immune checkpoint blockade (ICB) 4 restored immunosurveillance and reduced HCC. Consistently, patients with HCC who achieved a complete response to immunotherapy displayed significantly increased ATF6α activation compared with those with a weaker response. Targeting Atf6 through germline ablation, hepatocyte-specific ablation or therapeutic hepatocyte delivery of antisense oligonucleotides dampened HCC in preclinical liver cancer models. Thus, prolonged ATF6α activation drives ER stress, leading to glycolysis-dependent immunosuppression in liver cancer and sensitizing to ICB. Our findings suggest that persistently activated ATF6α is a tumour driver, a potential stratification marker for ICB response and a therapeutic target for HCC.
  • Discovery of BAY-405: An Azaindole-Based MAP4K1 Inhibitor for the Enhancement of T-Cell Immunity against Cancer
    Jeffrey Mowat, Rafael Carretero, Gabriele Leder, Nuria Aiguabella Font, Roland Neuhaus, Sandra Berndt, Judith Günther, Anders Friberg, Martina Schäfer, Hans Briem, Marian Raschke, Hideki Miyatake Ondozabal, Bernd Buchmann, Ulf Boemer, Bertolt Kreft, Ingo V. Hartung, Rienk Offringa
    Journal of Medicinal Chemistry, 2024
    High Resolution Image Download MS PowerPoint Slide Mitogen-activated protein kinase kinase kinase kinase 1 (MAP4K1) is a serine/threonine kinase that acts as an immune checkpoint downstream of T-cell receptor stimulation. MAP4K1 activity is enhanced by prostaglandin E2 (PGE2) and transforming growth factor beta (TGFβ), immune modulators commonly present in the tumor microenvironment. Therefore, its pharmacological inhibition is an attractive immuno-oncology concept for inducing therapeutic T-cell responses in cancer patients. Here, we describe the systematic optimization of azaindole-based lead compound 1, resulting in the discovery of potent and selective MAP4K1 inhibitor 38 (BAY-405) that displays nanomolar potency in biochemical and cellular assays as well as in vivo exposure after oral dosing. BAY-405 enhances T-cell immunity and overcomes the suppressive effect of PGE2 and TGFβ. Treatment of tumor-bearing mice shows T-cell-dependent antitumor efficacy. MAP4K1 inhibition in conjunction with PD-L1 blockade results in a superior antitumor impact, illustrating the complementarity of the single agent treatments.
  • Pericyte phenotype switching alleviates immunosuppression and sensitizes vascularized tumors to immunotherapy in preclinical models
    Zhi-Jie Li, Bo He, Alice Domenichini, Jiulia Satiaputra, Kira H. Wood, Devina D. Lakhiani, Abate A. Bashaw, Lisa M. Nilsson, Ji Li, Edward R. Bastow, Anna Johansson-Percival, Elena Denisenko, Alistair R.R. Forrest, Suraj Sakaram, Rafael Carretero, Günter J. Hämmerling, Jonas A. Nilsson, Gabriel Y.F. Lee, Ruth Ganss
    Journal of Clinical Investigation, 2024
    T cell-based immunotherapies are a promising therapeutic approach for multiple malignancies, but their efficacy is limited by tumor hypoxia arising from dysfunctional blood vessels. Here, we report that cell-intrinsic properties of a single vascular component, namely the pericyte, contribute to the control of tumor oxygenation, macrophage polarization, vessel inflammation, and T cell infiltration. Switching pericyte phenotype from a synthetic to a differentiated state reverses immune suppression and sensitizes tumors to adoptive T cell therapy, leading to regression of melanoma in mice. In melanoma patients, improved survival is correlated with enhanced pericyte maturity. Importantly, pericyte plasticity is regulated by signaling pathways converging on Rho kinase activity, with pericyte maturity being inducible by selective low-dose therapeutics that suppress pericyte MEK, AKT, or notch signaling. We also show that low-dose targeted anticancer therapy can durably change the tumor microenvironment without inducing adaptive resistance, creating a highly translatable pathway for redosing anticancer targeted therapies in combination with immunotherapy to improve outcome.
  • The Alliance Between the German Cancer Research Center and Bayer: A Retrospective of an Innovative Collaboration Model
    A. Zuccotti, R. Carretero, H. Hess-Stumpp
    Handbook of Experimental Pharmacology, 2024
  • Secretogranin II influences the assembly and function of MHC class I in melanoma
    Tamara Steinfass, Juliane Poelchen, Qian Sun, Giovanni Mastrogiulio, Daniel Novak, Marlene Vierthaler, Sandra Pardo, Aniello Federico, Laura Hüser, Thomas Hielscher, Rafael Carretero, Rienk Offringa, Peter Altevogt, Viktor Umansky, Jochen Utikal
    Experimental Hematology and Oncology, 2023
    Melanoma is the deadliest form of skin cancer showing rising incidence over the past years. New insights into the mechanisms of melanoma progression contributed to the development of novel treatment options, such as immunotherapies. However, acquiring resistance to treatment poses a big problem to therapy success. Therefore, understanding the mechanisms underlying resistance could improve therapy efficacy. Correlating expression levels in tissue samples of primary melanoma and metastases revealed that secretogranin 2 (SCG2) is highly expressed in advanced melanoma patients with poor overall survival (OS) rates. By conducting transcriptional analysis between SCG2-overexpressing (OE) and control melanoma cells, we detected a downregulation of components of the antigen presenting machinery (APM), which is important for the assembly of the MHC class I complex. Flow cytometry analysis revealed a downregulation of surface MHC class I expression on melanoma cells that showed resistance towards the cytotoxic activity of melanoma-specific T cells. IFNγ treatment partially reversed these effects. Based on our findings, we suggest that SCG2 might stimulate mechanisms of immune evasion and therefore be associated with resistance to checkpoint blockade and adoptive immunotherapy.
  • Targeting the aryl hydrocarbon receptor (AhR) with BAY 2416964: A selective small molecule inhibitor for cancer immunotherapy
    Christina Kober, Julian Roewe, Norbert Schmees, Lars Roese, Ulrike Roehn, Benjamin Bader, Detlef Stoeckigt, Florian Prinz, Mátyás Gorjánácz, Helge Gottfried Roider, Catherine Olesch, Gabriele Leder, Horst Irlbacher, Ralf Lesche, Julien Lefranc, Mine Oezcan-Wahlbrink, Ankita Sati Batra, Nirmeen Elmadany, Rafael Carretero, Katharina Sahm, Iris Oezen, Frederik Cichon, Daniel Baumann, Ahmed Sadik, Christiane A Opitz, Hilmar Weinmann, Ingo V Hartung, Bertolt Kreft, Rienk Offringa, Michael Platten, Ilona Gutcher
    Journal for Immunotherapy of Cancer, 2023
    Background The metabolism of tryptophan to kynurenines (KYN) by indoleamine-2,3-dioxygenase or tryptophan-2,3-dioxygenase is a key pathway of constitutive and adaptive tumor immune resistance. The immunosuppressive effects of KYN in the tumor microenvironment are predominantly mediated by the aryl hydrocarbon receptor (AhR), a cytosolic transcription factor that broadly suppresses immune cell function. Inhibition of AhR thus offers an antitumor therapy opportunity via restoration of immune system functions. Methods The expression of AhR was evaluated in tissue microarrays of head and neck squamous cell carcinoma (HNSCC), non-small cell lung cancer (NSCLC) and colorectal cancer (CRC). A structure class of inhibitors that block AhR activation by exogenous and endogenous ligands was identified, and further optimized, using a cellular screening cascade. The antagonistic properties of the selected AhR inhibitor candidate BAY 2416964 were determined using transactivation assays. Nuclear translocation, target engagement and the effect of BAY 2416964 on agonist-induced AhR activation were assessed in human and mouse cancer cells. The immunostimulatory properties on gene and cytokine expression were examined in human immune cell subsets. The in vivo efficacy of BAY 2416964 was tested in the syngeneic ovalbumin-expressing B16F10 melanoma model in mice. Coculture of human H1299 NSCLC cells, primary peripheral blood mononuclear cells and fibroblasts mimicking the human stromal-tumor microenvironment was used to assess the effects of AhR inhibition on human immune cells. Furthermore, tumor spheroids cocultured with tumor antigen-specific MART-1 T cells were used to study the antigen-specific cytotoxic T cell responses. The data were analyzed statistically using linear models. Results AhR expression was observed in tumor cells and tumor-infiltrating immune cells in HNSCC, NSCLC and CRC. BAY 2416964 potently and selectively inhibited AhR activation induced by either exogenous or endogenous AhR ligands. In vitro, BAY 2416964 restored immune cell function in human and mouse cells, and furthermore enhanced antigen-specific cytotoxic T cell responses and killing of tumor spheroids. In vivo, oral application with BAY 2416964 was well tolerated, induced a proinflammatory tumor microenvironment, and demonstrated antitumor efficacy in a syngeneic cancer model in mice. Conclusions These findings identify AhR inhibition as a novel therapeutic approach to overcome immune resistance in various types of cancers.
  • Rgs16 promotes antitumor CD8+ T cell exhaustion
    Nina Weisshaar, Jingxia Wu, Yanan Ming, Alaa Madi, Agnes Hotz-Wagenblatt, Sicong Ma, Alessa Mieg, Marvin Hering, Ferdinand Zettl, Kerstin Mohr, Tilo Schlimbach, Nora Ten Bosch, Franziska Hertel, Lisann Müller, Hannah Byren, Mona Wang, Helena Borgers, Mareike Munz, Lukas Schmitt, Franciscus van der Hoeven, Ulrich Kloz, Rafael Carretero, Nikolai Schleußner, Rene-Filip Jackstadt, Ilse Hofmann, Guoliang Cui
    Science Immunology, 2022
    T cells become functionally exhausted in tumors, limiting T cell–based immunotherapies. Although several transcription factors regulating the exhausted T (T ex ) cell differentiation are known, comparatively little is known about the regulators of T ex cell survival. Here, we reported that the regulator of G protein signaling 16 (Rgs-16) suppressed T ex cell survival in tumors. By performing lineage tracing using reporter mice in which mCherry marked Rgs16-expressing cells, we identified that Rgs16 + CD8 + tumor-infiltrating lymphocytes (TILs) were terminally differentiated, expressed low levels of T cell factor 1 (Tcf1), and underwent apoptosis as early as 6 days after the onset of Rgs16 expression. Rgs16 deficiency inhibited CD8 + T cell apoptosis and promoted antitumor effector functions of CD8 + T cells. Furthermore, Rgs16 deficiency synergized with programmed cell death protein 1 (PD-1) blockade to enhance antitumor CD8 + T cell responses. Proteomics revealed that Rgs16 interacted with the scaffold protein IQGAP1, suppressed the recruitment of Ras and B-Raf, and inhibited Erk1 activation. Rgs16 deficiency enhanced antitumor CD8 + TIL survival in an Erk1-dependent manner. Loss of function of Erk1 decreased antitumor functions of Rgs16 -deficient CD8 + T cells. RGS16 mRNA expression levels in CD8 + TILs of patients with melanoma negatively correlated with genes associated with T cell stemness, such as SELL , TCF7 , and IL7R , and predicted low responses to PD-1 blockade. This study uncovers Rgs16 as an inhibitor of T ex cell survival in tumors and has implications for improving T cell–based immunotherapies.
  • T cell-mediated elimination of cancer cells by blocking CEACAM6–CEACAM1 interaction
    Jessica Pinkert, Hans-Henning Boehm, Mark Trautwein, Wolf-Dietrich Doecke, Florian Wessel, Yingzi Ge, Eva Maria Gutierrez, Rafael Carretero, Christoph Freiberg, Uwe Gritzan, Merlin Luetke-Eversloh, Sven Golfier, Oliver Von Ahsen, Valentina Volpin, Antonio Sorrentino, Anchana Rathinasamy, Maria Xydia, Robert Lohmayer, Julian Sax, Ayse Nur-Menevse, Abir Hussein, Slava Stamova, Georg Beckmann, Julian Marius Glueck, Dorian Schoenfeld, Joerg Weiske, Dieter Zopf, Rienk Offringa, Bertolt Kreft, Philipp Beckhove, Joerg Willuda
    Oncoimmunology, 2022
    efficacy of BAY 1834942 correlated with the degree of CEACAM6 expression on cancer cells, suggesting potential in guiding patient selection. BAY 1834942 was equally or more efficacious compared to blockade of PD-L1, and at least an additive efficacy was observed in combination with anti-PD-1 or anti-TIM-3 antibodies, suggesting an efficacy independent of the PD-1/PD-L1 axis. In summary, CEACAM6 blockade by BAY 1834942 reactivates the antitumor response of T cells. This warrants clinical evaluation.
  • Basophils promote tumor rejection via chemotaxis and infiltration of CD8+ T cells
    Ibrahim M. Sektioglu, Rafael Carretero, Nadja Bulbuc, Tobias Bald, Thomas Tüting, Alexander Y. Rudensky, Günter J. Hämmerling
    Cancer Research, 2017
    Elevated numbers of regulatory T cells (Treg) in patient tumors are known to inhibit efficient antitumor T-cell responses. To study the mechanisms controlling tumor rejection, we assessed different mouse models for Treg depletion. In Foxp3DTR knock-in mice, about 99% Treg depletion was achieved, resulting in complete rejection of transplanted HCmel12 melanomas in a CD8+ T-cell–dependent way. In contrast, about 90% Treg depletion obtained in BAC transgenic Foxp3.LuciDTR4 mice failed to induce complete rejection of HCmel12 melanomas, demonstrating that residual Tregs were able to control CD8+ T-cell responses against the tumor. Ninety-nine percent of Treg depletion provoked drastic changes in the tumor microenvironment, such as strong infiltration of CD8+ T cells and basophils. Intratumoral basophils enhanced CD8+ T-cell infiltration via production of chemokines CCL3 and CCL4; antibody-based blocking of these chemokines inhibited CD8+ T-cell infiltration. Therapeutic induction of basophilia by IL3/anti-IL3 antibody complexes, combined with transfer of CD8+ T cells, resulted in enhanced T-cell infiltration and tumor rejection. Our study identifies a critical role basophils play in tumor rejection and that this role can be exploited for therapeutic intervention. Cancer Res; 77(2); 291–302. ©2016 AACR.
  • Macrophage-derived nitric oxide initiates T-cell diapedesis and tumor rejection
    Ibrahim M. Sektioglu, Rafael Carretero, Noemi Bender, Christian Bogdan, Natalio Garbi, Viktor Umansky, Ludmila Umansky, Katharina Urban, Magnus von Knebel-Döberitz, Veena Somasundaram, David Wink, Philipp Beckhove, Günter J. Hämmerling
    Oncoimmunology, 2016
    In tumor biology, nitric oxide (NO) is generally regarded as an immunosuppressive molecule that impedes T-cell functions and activation of endothelial cells. Contrasting with this view, we here describe a critical role for NO derived from inducible nitric oxide (iNOS)-expressing tumor macrophages in T-cell infiltration and tumor rejection as shown by iNOS gene deletion, inhibition of iNOS, or NO donors. Specifically, macrophage-derived NO was found to induce on tumor vessels adhesion molecules that were required for T-cell extravasation. Experiments with human endothelial cells revealed a bimodal dose-dependent effect of NO. High doses of NO donors were indeed suppressive but lower, more physiological concentrations, induced adhesion molecules in an NFkB-dependent pathway and preferentially activated transcription of genes involved in lymphocyte diapedesis. iNOS+ macrophages in tumors appear to generate precisely the amount of NO that promotes endothelial activation and T-cell infiltration. These results will be valuable for the development of strategies designed to overcome the paucity of T-cell infiltration into tumors that is a major obstacle in clinical cancer immunotherapy.
  • Erratum : Corrigendum: Eosinophils orchestrate cancer rejection by normalizing tumor vessels and enhancing infiltration of CD8 + T cells (Nature Immunology)
    Rafael Carretero, Ibrahim M Sektioglu, Natalio Garbi, Oscar C Salgado, Philipp Beckhove, Günter J Hämmerling
    Nature Immunology, 2016
  • Eosinophils orchestrate cancer rejection by normalizing tumor vessels and enhancing infiltration of CD8 + T cells
    Rafael Carretero, Ibrahim M Sektioglu, Natalio Garbi, Oscar C Salgado, Philipp Beckhove, Günter J Hämmerling
    Nature Immunology, 2015
  • Antibody therapy to human L1CAM in a transgenic mouse model blocks local tumor growth but induces EMT
    Kai Doberstein, Patrick N. Harter, Uwe Haberkorn, Niko P. Bretz, Bernd Arnold, Rafael Carretero, Gerhard Moldenhauer, Michel Mittelbronn, Peter Altevogt
    International Journal of Cancer, 2015
  • Radiotherapy combined with TLR7/8 activation induces strong immune responses against gastrointestinal tumors
    Sebastian Schölch, Conrad Rauber, Alexandra Tietz, Nuh N. Rahbari, Ulrich Bork, Thomas Schmidt, Christoph Kahlert, Uwe Haberkorn, Mark A. Tomai, Kenneth E. Lipson, Rafael Carretero, Jürgen Weitz, Moritz Koch, Peter E. Huber
    Oncotarget, 2015
  • Involvement of HLA class i molecules in the immune escape of urologic tumors
    R. Carretero, H. Gil-Julio, F. Vázquez-Alonso, F. Garrido, J. Castiñeiras, J.M. Cózar
    Actas Urologicas Espanolas, 2014
  • A transcriptome-proteome integrated network identifies endoplasmic reticulum thiol oxidoreductase (ERp57) as a hub that mediates bone metastasis
    Naiara Santana-Codina, Rafael Carretero, Rebeca Sanz-Pamplona, Teresa Cabrera, Emre Guney, Baldo Oliva, Philippe Clezardin, Omar E. Olarte, Pablo Loza-Alvarez, Andrés Méndez-Lucas, Jose Carlos Perales, Angels Sierra
    Molecular and Cellular Proteomics, 2013
  • VEGF polymorphisms are not associated with an increased risk of developing renal cell carcinoma in Spanish population
    Pablo Sáenz-López, Fernando Vazquez, Jose Manuel Cozar, Rafael Carretero, Federico Garrido, Francisco Ruiz-Cabello
    Human Immunology, 2013
  • Correlates between host and viral transcriptional program associated with different oncolytic vaccinia virus isolates
    Jennifer Reinboth, Maria L. Ascierto, Nanhai G. Chen, Qian Zhang, Yong A. Yu, Richard J. Aguilar, Rafael Carretero, Andrea Worschech, Yingdong Zhao, Ena Wang, Francesco M. Marincola, Aladar A. Szalay
    Human Gene Therapy Methods, 2012
  • Regression of melanoma metastases after immunotherapy is associated with activation of antigen presentation and interferon-mediated rejection genes
    Rafael Carretero, Ena Wang, Ana I. Rodriguez, Jennifer Reinboth, Maria L. Ascierto, Alyson M. Engle, Hui Liu, Francisco M. Camacho, Francesco M. Marincola, Federico Garrido, Teresa Cabrera
    International Journal of Cancer, 2012
  • Association between C13ORF31, NOD2, RIPK2 and TLR10 polymorphisms and urothelial bladder cancer
    Macarena Guirado, Hernani Gil, Pablo Saenz-Lopez, Jennifer Reinboth, Federico Garrido, José Manuel Cozar, Francisco Ruiz-Cabello, Rafael Carretero
    Human Immunology, 2012
  • Bacillus Calmette-Guerin immunotherapy of bladder cancer induces selection of human leukocyte antigen class I-deficient tumor cells
    Rafael Carretero, Teresa Cabrera, Hernani Gil, Pablo Saenz‐Lopez, Isabel Maleno, Natalia Aptsiauri, Jose M. Cozar, Federico Garrido
    International Journal of Cancer, 2011
  • Impact of interleukin-18 polymorphisms-607 and -137 on clinical characteristics of renal cell carcinoma patients
    Pablo Sáenz-López, Rafael Carretero, Fernando Vazquez, Javier Martin, Elena Sánchez, Miguel Tallada, Federico Garrido, José Manuel Cózar, Francisco Ruiz-Cabello
    Human Immunology, 2010
  • Changes in activatory and inhibitory natural killer (NK) receptors may induce progression to multiple myeloma: Implications for tumor evasion of T and NK cells
    Mónica Bernal, Pilar Garrido, Pilar Jiménez, Rafael Carretero, Manuel Almagro, Pilar López, Pilar Navarro, Federico Garrido, Francisco Ruiz-Cabello
    Human Immunology, 2009
  • Polymorphisms in inflammatory response genes in metastatic renal cancer
    Pablo Sáenz López, Fernando Vázquez Alonso, José M. Romero, Rafael Carretero, Miguel Tallada Buñuel, Francisco Ruiz Cabello, José Manuel Cózar Olmo
    Actas Urologicas Espanolas, 2009
  • A polymorphism in the interleukin-10 promoter affects the course of disease in patients with clear-cell renal carcinoma
    José María Romero, Pablo Sáenz-López, José Manuel Cózar, Rafael Carretero, Julia Canton, Fernando Vazquez, Angel Concha, Miguel Tallada, Federico Garrido, Francisco Ruiz-Cabello
    Human Immunology, 2009
  • Genetic polymorphisms of RANTES, IL1-A, MCP-1 and TNF-A genes in patients with prostate cancer
    Pablo Sáenz-López, Rafael Carretero, José Manuel Cózar, José Maria Romero, Julia Canton, José Ramón Vilchez, Miguel Tallada, Federico Garrido, Francisco Ruiz-Cabello
    BMC Cancer, 2008
  • Regressing and progressing metastatic lesions: Resistance to immunotherapy is predetermined by irreversible HLA class I antigen alterations
    Natalia Aptsiauri, Rafael Carretero, Angel Garcia-Lora, Luis M. Real, Teresa Cabrera, Federico Garrido
    Cancer Immunology Immunotherapy, 2008
  • Analysis of HLA class I expression in progressing and regressing metastatic melanoma lesions after immunotherapy
    Rafael Carretero, José M. Romero, Francisco Ruiz-Cabello, Isabel Maleno, Felix Rodriguez, Francisco M. Camacho, Luis M. Real, Federico Garrido, Teresa Cabrera
    Immunogenetics, 2008

RECENT SCHOLAR PUBLICATIONS

  • 2-heteroaryl-3-oxo-2, 3-dihydropyridazine-4-carboxamides for the treatment of cancer
    I GUTCHER, U Röhn, N Schmees, L Zorn, L Röse, B Bader, C KOBER, ...
    US Patent App. 19/402,587 , 2026
    2026
  • Activated ATF6α is a hepatic tumour driver restricting immunosurveillance
    X Li, C Lebeaupin, A Kadianaki, C Druelle-Cedano, N Vesper, C Rennert, ...
    Nature, 1-12 , 2026
    2026
    Citations: 5
  • 2-heteroaryl-3-oxo-2, 3-dihydropyridazine-4-carboxamides for the treatment of cancer
    I GUTCHER, U Röhn, N Schmees, L Zorn, L Röse, B Bader, C KOBER, ...
    US Patent 12,522,594 , 2026
    2026
    Citations: 3
  • Employing RNA editing to engineer personalized tumor-specific neoantigens (editopes)
    R Pecori, B Casati, R Merdler-Rabinowicz, N Landesman, K Sanghvi, ...
    bioRxiv, 2023.03. 16.532918 , 2025
    2025
  • P2RY2 is a purinergic immune checkpoint linking extracellular ATP to immune evasion and adaptive resistance to immunotherapy
    Z Hu, H Matsuo, S Du, C Berzain Battioni, L Jassowicz, R Carretero, ...
    bioRxiv, 2025.10. 09.681049 , 2025
    2025
    Citations: 3
  • Anti-cecam6 antibodies with reduced side-effects
    M Trautwein, J Willuda, WD Döcke, P Buchmann, R CARRETERO, ...
    US Patent App. 18/688,693 , 2024
    2024
  • Discovery of BAY-405: An azaindole-based MAP4K1 inhibitor for the enhancement of T-cell immunity against cancer
    J Mowat, R Carretero, G Leder, N Aiguabella Font, R Neuhaus, S Berndt, ...
    Journal of Medicinal Chemistry 67 (19), 17429-17453 , 2024
    2024
    Citations: 16
  • Pericyte phenotype switching alleviates immunosuppression and sensitizes vascularized tumors to immunotherapy in preclinical models
    ZJ Li, B He, A Domenichini, J Satiaputra, KH Wood, DD Lakhiani, ...
    The Journal of Clinical Investigation 134 (18) , 2024
    2024
    Citations: 18
  • The Alliance Between the German Cancer Research Center and Bayer: A Retrospective of an Innovative Collaboration Model
    A Zuccotti, R Carretero, H Hess-Stumpp
    Public-Private-Partnerships in Drug Research and Development, 83-95 , 2024
    2024
  • Map4k1 inhibitors
    U Lücking, JS MOWAT, L Zorn, L Wortmann, S Müller, G Leder, S Berndt, ...
    US Patent App. 18/275,978 , 2024
    2024
    Citations: 1
  • Targeting the aryl hydrocarbon receptor (AhR) with BAY 2416964: a selective small molecule inhibitor for cancer immunotherapy
    C Kober, J Roewe, N Schmees, L Roese, U Roehn, B Bader, D Stoeckigt, ...
    Journal for Immunotherapy of Cancer 11 (11), e007495 , 2023
    2023
    Citations: 93
  • 2-heteroaryl-3-oxo-2, 3-dihydropyridazine-4-carboxamides for the treatment of cancer
    I GUTCHER, N Schmees, L Röse, B Bader, C KOBER, R CARRETERO, ...
    US Patent 11,795,164 , 2023
    2023
    Citations: 3
  • Secretogranin II influences the assembly and function of MHC class I in melanoma
    T Steinfass, J Poelchen, Q Sun, G Mastrogiulio, D Novak, M Vierthaler, ...
    Experimental hematology & oncology 12 (1), 29 , 2023
    2023
    Citations: 15
  • 3-oxo-6-heteroaryl-2-phenyl-2, 3-dihydropyridazine-4-carboxamides
    I GUTCHER, U Röhn, L Zorn, L Röse, B Bader, C KOBER, ...
    US Patent 11,591,311 , 2023
    2023
    Citations: 1
  • Secretogranin II influences the assembly and function of MHC class I in melanoma
    M Vierthaler, S Pardo, A Federico, L Hüser, T Hielscher, R Carretero, ...
    2023
  • T cell-mediated elimination of cancer cells by blocking CEACAM6–CEACAM1 interaction
    J Pinkert, HH Boehm, M Trautwein, WD Doecke, F Wessel, Y Ge, ...
    Oncoimmunology 11 (1), 2008110 , 2022
    2022
    Citations: 48
  • Sulphur substituted 3-oxo-2, 3-dihydropyridazine-4-carboxamides
    L Zorn, U Röhn, I GUTCHER, L Röse, B Bader, C KOBER, ...
    US Patent 11,459,312 , 2022
    2022
    Citations: 3
  • Substituted pyrrolopyridine-derivatives
    JS MOWAT, B Buchmann, NA FONT, G Leder, R CARRETERO, ...
    US Patent 11,427,578 , 2022
    2022
  • Rgs16 promotes antitumor CD8 + T cell exhaustion
    N Weisshaar, J Wu, Y Ming, A Madi, A Hotz-Wagenblatt, S Ma, A Mieg, ...
    Science immunology 7 (71), eabh1873 , 2022
    2022
    Citations: 64
  • Substituted pyrrolopyridine-derivatives
    JS MOWAT, B Buchmann, NA FONT, R Neuhaus, G Leder, ...
    US Patent App. 17/312,776 , 2022
    2022

MOST CITED SCHOLAR PUBLICATIONS

  • Eosinophils orchestrate cancer rejection by normalizing tumor vessels and enhancing infiltration of CD8 + T cells
    R Carretero, IM Sektioglu, N Garbi, OC Salgado, P Beckhove, ...
    Nature immunology 16 (6), 609-617 , 2015
    2015
    Citations: 587
  • Analysis of HLA class I expression in progressing and regressing metastatic melanoma lesions after immunotherapy
    R Carretero, JM Romero, F Ruiz-Cabello, I Maleno, F Rodriguez, ...
    Immunogenetics 60 (8), 439-447 , 2008
    2008
    Citations: 183
  • Basophils promote tumor rejection via chemotaxis and infiltration of CD8+ T cells
    IM Sektioglu, R Carretero, N Bulbuc, T Bald, T Tüting, AY Rudensky, ...
    Cancer research 77 (2), 291-302 , 2017
    2017
    Citations: 131
  • Regression of melanoma metastases after immunotherapy is associated with activation of antigen presentation and interferon‐mediated rejection genes
    R Carretero, E Wang, AI Rodriguez, J Reinboth, ML Ascierto, AM Engle, ...
    International journal of cancer 131 (2), 387-395 , 2012
    2012
    Citations: 116
  • Targeting the aryl hydrocarbon receptor (AhR) with BAY 2416964: a selective small molecule inhibitor for cancer immunotherapy
    C Kober, J Roewe, N Schmees, L Roese, U Roehn, B Bader, D Stoeckigt, ...
    Journal for Immunotherapy of Cancer 11 (11), e007495 , 2023
    2023
    Citations: 93
  • Genetic polymorphisms of RANTES, IL1-A, MCP-1 and TNF-A genes in patients with prostate cancer
    P Sáenz-López, R Carretero, JM Cózar, JM Romero, J Canton, JR Vilchez, ...
    BMC cancer 8 (1), 382 , 2008
    2008
    Citations: 92
  • Association between C13ORF31, NOD2, RIPK2 and TLR10 polymorphisms and urothelial bladder cancer
    M Guirado, H Gil, P Saenz-Lopez, J Reinboth, F Garrido, JM Cozar, ...
    Human immunology 73 (6), 668-672 , 2012
    2012
    Citations: 91
  • Regressing and progressing metastatic lesions: resistance to immunotherapy is predetermined by irreversible HLA class I antigen alterations
    N Aptsiauri, R Carretero, A Garcia-Lora, LM Real, T Cabrera, F Garrido
    Cancer Immunology, Immunotherapy 57 (11), 1727-1733 , 2008
    2008
    Citations: 89
  • Changes in activatory and inhibitory natural killer (NK) receptors may induce progression to multiple myeloma: implications for tumor evasion of T and NK cells
    M Bernal, P Garrido, P Jiménez, R Carretero, M Almagro, P López, ...
    Human Immunology 70 (10), 854-857 , 2009
    2009
    Citations: 80
  • Radiotherapy combined with TLR7/8 activation induces strong immune responses against gastrointestinal tumors
    S Schölch, C Rauber, A Tietz, NN Rahbari, U Bork, T Schmidt, C Kahlert, ...
    Oncotarget 6 (7), 4663 , 2014
    2014
    Citations: 77
  • Bacillus Calmette‐Guerin immunotherapy of bladder cancer induces selection of human leukocyte antigen class I‐deficient tumor cells
    R Carretero, T Cabrera, H Gil, P Saenz‐Lopez, I Maleno, N Aptsiauri, ...
    International journal of cancer 129 (4), 839-846 , 2011
    2011
    Citations: 70
  • Macrophage-derived nitric oxide initiates T-cell diapedesis and tumor rejection
    IM Sektioglu, R Carretero, N Bender, C Bogdan, N Garbi, V Umansky, ...
    Oncoimmunology 5 (10), e1204506 , 2016
    2016
    Citations: 66
  • Rgs16 promotes antitumor CD8 + T cell exhaustion
    N Weisshaar, J Wu, Y Ming, A Madi, A Hotz-Wagenblatt, S Ma, A Mieg, ...
    Science immunology 7 (71), eabh1873 , 2022
    2022
    Citations: 64
  • Antibody therapy to human L1CAM in a transgenic mouse model blocks local tumor growth but induces EMT
    K Doberstein, PN Harter, U Haberkorn, NP Bretz, B Arnold, R Carretero, ...
    International journal of cancer 136 (5), E326-E339 , 2015
    2015
    Citations: 60
  • A transcriptome-proteome integrated network identifies endoplasmic reticulum thiol oxidoreductase (ERp57) as a hub that mediates bone metastasis
    N Santana-Codina, R Carretero, R Sanz-Pamplona, T Cabrera, E Guney, ...
    Molecular & Cellular Proteomics 12 (8), 2111-2125 , 2013
    2013
    Citations: 55
  • T cell-mediated elimination of cancer cells by blocking CEACAM6–CEACAM1 interaction
    J Pinkert, HH Boehm, M Trautwein, WD Doecke, F Wessel, Y Ge, ...
    Oncoimmunology 11 (1), 2008110 , 2022
    2022
    Citations: 48
  • VEGF polymorphisms are not associated with an increased risk of developing renal cell carcinoma in Spanish population
    P Sáenz-López, F Vazquez, JM Cozar, R Carretero, F Garrido, ...
    Human immunology 74 (1), 98-103 , 2013
    2013
    Citations: 46
  • Impact of interleukin-18 polymorphisms-607 and-137 on clinical characteristics of renal cell carcinoma patients
    P Sáenz-López, R Carretero, F Vazquez, J Martin, E Sánchez, M Tallada, ...
    Human immunology 71 (3), 309-313 , 2010
    2010
    Citations: 37
  • A polymorphism in the interleukin-10 promoter affects the course of disease in patients with clear-cell renal carcinoma
    JM Romero, P Sáenz-López, JM Cózar, R Carretero, J Canton, F Vazquez, ...
    Human immunology 70 (1), 60-64 , 2009
    2009
    Citations: 23
  • Pericyte phenotype switching alleviates immunosuppression and sensitizes vascularized tumors to immunotherapy in preclinical models
    ZJ Li, B He, A Domenichini, J Satiaputra, KH Wood, DD Lakhiani, ...
    The Journal of Clinical Investigation 134 (18) , 2024
    2024
    Citations: 18