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  1. Article ; Online: Metabolic shift underlies tumor progression and immune evasion in S-nitrosoglutathione reductase-deficient cancer.

    Mena-Osuna, Rafael / Mantrana, Ana / Guil-Luna, Silvia / Sánchez-Montero, María Teresa / Navarrete-Sirvent, Carmen / Morales-Ruiz, Teresa / Rivas-Crespo, Aurora / Toledano-Fonseca, Marta / García-Ortíz, María Victoria / García-Jurado, Gema / Gómez-España, María Auxiliadora / González-Fernández, Rafael / Villar, Carlos / Medina-Fernández, Francisco Javier / Villalba, José Manuel / Aranda, Enrique / Rodríguez-Ariza, Antonio

    The Journal of pathology

    2023  Volume 260, Issue 3, Page(s) 261–275

    Abstract: S-nitrosoglutathione reductase (GSNOR) is a denitrosylase enzyme that has been suggested to play a tumor suppressor role, although the mechanisms responsible are still largely unclear. In this study, we show that GSNOR deficiency in tumors is associated ... ...

    Abstract S-nitrosoglutathione reductase (GSNOR) is a denitrosylase enzyme that has been suggested to play a tumor suppressor role, although the mechanisms responsible are still largely unclear. In this study, we show that GSNOR deficiency in tumors is associated with poor prognostic histopathological features and poor survival in patients with colorectal cancer (CRC). GSNOR-low tumors were characterized by an immunosuppressive microenvironment with exclusion of cytotoxic CD8
    MeSH term(s) Mice ; Animals ; Humans ; Oxidoreductases ; CD8-Positive T-Lymphocytes ; Immune Evasion ; Proteomics ; Neoplasms ; Tumor Microenvironment
    Chemical Substances Oxidoreductases (EC 1.-) ; formaldehyde dehydrogenase, glutathione-independent (EC 1.2.1.46)
    Language English
    Publishing date 2023-04-05
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3119-7
    ISSN 1096-9896 ; 0022-3417
    ISSN (online) 1096-9896
    ISSN 0022-3417
    DOI 10.1002/path.6080
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.12: Show issues Location:
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    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Clinical significance of glycogen synthase kinase 3 (GSK-3) expression and tumor budding grade in colorectal cancer: Implications for targeted therapy.

    Guil-Luna, Silvia / Rivas-Crespo, Aurora / Navarrete-Sirvent, Carmen / Mantrana, Ana / Pera, Alejandra / Mena-Osuna, Rafael / Toledano-Fonseca, Marta / García-Ortíz, María Victoria / Villar, Carlos / Sánchez-Montero, Maria Teresa / Krueger, Janna / Medina-Fernández, Francisco Javier / De La Haba-Rodríguez, Juan / Gómez-España, Auxiliadora / Aranda, Enrique / Rudd, Christopher E / Rodríguez-Ariza, Antonio

    Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

    2023  Volume 167, Page(s) 115592

    Abstract: Introduction: Glycogen synthase kinase 3 (GSK-3) has been proposed as a novel cancer target due to its regulating role in both tumor and immune cells. However, the connection between GSK-3 and immunoevasive contexture, including tumor budding (TB) has ... ...

    Abstract Introduction: Glycogen synthase kinase 3 (GSK-3) has been proposed as a novel cancer target due to its regulating role in both tumor and immune cells. However, the connection between GSK-3 and immunoevasive contexture, including tumor budding (TB) has not been previously examined.
    Methods: we investigated the expression levels of total GSK-3 as well as its isoforms (GSK-3β and GSK-3α) and examined their potential correlation with TB grade and the programmed cell death-ligand 1 (PD-L1) in colorectal cancer (CRC) tumor samples. Additionally, we compared the efficacy of GSK-3-inhibition with PD-1/PD-L1 blockade in humanized patient-derived (PDXs) xenografts models of high-grade TB CRC.
    Results: we show that high-grade (BD3) TB CRC is associated with elevated expression levels of total GSK-3, specifically the GSK-3β isoform, along with increased expression of PD-L1 in tumor cells. Moreover, we define an improved risk stratification of CRC patients based on the presence of GSK-3
    Conclusions: our study provides compelling evidence for the clinical significance of GSK-3 expression and TB grade in risk stratification of CRC patients. Moreover, our findings strongly support GSK-3 inhibition as an effective therapy specifically targeting high-grade TB in CRC.
    MeSH term(s) Humans ; CD8-Positive T-Lymphocytes ; Glycogen Synthase Kinase 3 ; Glycogen Synthase Kinase 3 beta ; B7-H1 Antigen ; Programmed Cell Death 1 Receptor ; Clinical Relevance ; Colorectal Neoplasms/pathology
    Chemical Substances Glycogen Synthase Kinase 3 (EC 2.7.11.26) ; Glycogen Synthase Kinase 3 beta (EC 2.7.11.1) ; B7-H1 Antigen ; Programmed Cell Death 1 Receptor
    Language English
    Publishing date 2023-09-29
    Publishing country France
    Document type Journal Article
    ZDB-ID 392415-4
    ISSN 1950-6007 ; 0753-3322 ; 0300-0893
    ISSN (online) 1950-6007
    ISSN 0753-3322 ; 0300-0893
    DOI 10.1016/j.biopha.2023.115592
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ud II Zs.198: Show issues Location:
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    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  3. Article: Association of Tumor Budding With Immune Evasion Pathways in Primary Colorectal Cancer and Patient-Derived Xenografts.

    Guil-Luna, Silvia / Mena, Rafael / Navarrete-Sirvent, Carmen / López-Sánchez, Laura María / Khouadri, Karima / Toledano-Fonseca, Marta / Mantrana, Ana / Guler, Ipek / Villar, Carlos / Díaz, Cesar / Medina-Fernández, Francisco Javier / De la Haba-Rodríguez, Juan Rafael / Aranda, Enrique / Rodríguez-Ariza, Antonio

    Frontiers in medicine

    2020  Volume 7, Page(s) 264

    Abstract: Tumor budding has been found to be of prognostic significance for several cancers, including colorectal cancer (CRC). Additionally, the molecular classification of CRC has led to the identification of different immune microenvironments linked to distinct ...

    Abstract Tumor budding has been found to be of prognostic significance for several cancers, including colorectal cancer (CRC). Additionally, the molecular classification of CRC has led to the identification of different immune microenvironments linked to distinct prognosis and therapeutic response. However, the association between tumor budding and the different molecular subtypes of CRC and distinct immune profiles have not been fully elucidated. This study focused, firstly, on the validation of derived xenograft models (PDXs) for the evaluation of tumor budding and their human counterparts and, secondly, on the association between tumor budding and the immune tumor microenvironment by the analysis of gene expression signatures of immune checkpoints, Toll-like receptors (TLRs), and chemokine families. Clinical CRC samples with different grades of tumor budding and their corresponding PDXs were included in this study. Tumor budding grade was reliably reproduced in early passages of PDXs, and high-grade tumor budding was intimately related with a poor-prognosis CMS4 mesenchymal subtype. In addition, an upregulation of negative regulatory immune checkpoints (PDL1, TIM-3, NOX2, and IDO1), TLRs (TLR1, TLR3, TLR4, and TLR6), and chemokine receptors and ligands (CXCR2, CXCR4, CXCL1, CXCL2, CXCL6, and CXCL9) was detected in high-grade tumor budding in both human samples and their corresponding xenografts. Our data support a close link between high-grade tumor budding in CRC and a distinctive immune-suppressive microenvironment promoting tumor invasion, which may have a determinant role in the poor prognosis of the CMS4 mesenchymal subtype. In addition, our study demonstrates that PDX models may constitute a robust preclinical platform for the development of novel therapies directed against tumor budding in CRC.
    Keywords covid19
    Language English
    Publishing date 2020-07-03
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2775999-4
    ISSN 2296-858X
    ISSN 2296-858X
    DOI 10.3389/fmed.2020.00264
    Database MEDical Literature Analysis and Retrieval System OnLINE

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