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  1. Article ; Online: T

    Agalioti, Theodora / Cortesi, Filippo / Gagliani, Nicola

    Current opinion in immunology

    2023  Volume 83, Page(s) 102333

    Abstract: At mucosal barriers, the T helper 17 ( ... ...

    Abstract At mucosal barriers, the T helper 17 (T
    MeSH term(s) Humans ; Cell Plasticity ; Neoplasms/metabolism ; Adaptation, Physiological ; Th17 Cells
    Language English
    Publishing date 2023-05-10
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 1035767-1
    ISSN 1879-0372 ; 0952-7915
    ISSN (online) 1879-0372
    ISSN 0952-7915
    DOI 10.1016/j.coi.2023.102333
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: T

    Agalioti, Theodora / Villablanca, Eduardo J / Huber, Samuel / Gagliani, Nicola

    Journal of autoimmunity

    2018  Volume 87, Page(s) 50–60

    Abstract: Upon interaction with dendritic cells (DCs), naïve CD4 T cells differentiate into distinct subsets and orchestrate the development of a physiological immune response. When uncontrolled by cellular and molecular mechanisms, CD4 T cells can also lead to ... ...

    Abstract Upon interaction with dendritic cells (DCs), naïve CD4 T cells differentiate into distinct subsets and orchestrate the development of a physiological immune response. When uncontrolled by cellular and molecular mechanisms, CD4 T cells can also lead to immune mediated inflammatory diseases (IMIDs). Initially, these distinct CD4 T-cell subsets were defined according to the expression of a limited number of cytokines. Later it was revealed that CD4 T cells can acquire much more complex functional phenotypes than previously thought. Experimental data showed that the CD4 T-cell subset T
    MeSH term(s) Animals ; Cell Plasticity ; Cell Transdifferentiation ; Dendritic Cells/immunology ; Humans ; Immune System Diseases/immunology ; Immune System Diseases/therapy ; Immunotherapy/methods ; Inflammation/immunology ; Inflammation/therapy ; Lymphocyte Depletion ; Th17 Cells/immunology
    Language English
    Publishing date 2018-01-19
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 639452-8
    ISSN 1095-9157 ; 0896-8411
    ISSN (online) 1095-9157
    ISSN 0896-8411
    DOI 10.1016/j.jaut.2017.12.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Pleural involvement in lung cancer.

    Agalioti, Theodora / Giannou, Anastasios D / Stathopoulos, Georgios T

    Journal of thoracic disease

    2015  Volume 7, Issue 6, Page(s) 1021–1030

    Abstract: The pleural space, a sterile secluded environment in the thoracic cavity, represents an attractive metastatic site for various cancers of lung, breast and gastrointestinal origins. Whereas lung and breast adenocarcinomas could invade the pleural space ... ...

    Abstract The pleural space, a sterile secluded environment in the thoracic cavity, represents an attractive metastatic site for various cancers of lung, breast and gastrointestinal origins. Whereas lung and breast adenocarcinomas could invade the pleural space because of their anatomic proximity, "distant" cancers like ovarian or gastrointestinal tract adenocarcinomas may employ more active mechanisms to the same end. A pleural metastasis is often accompanied by a malignant pleural effusion (MPE), an unfavorable complication that severely restricts the quality of life and expectancy of the cancer patient. MPE is the net "product" of three different processes, namely inflammation, enhanced angiogenesis and vascular leakage. Current efforts are focusing on the identification of cancer cell autocrine (specific mutation spectra and biochemical pathways) and paracrine (cytokine and chemokine signals) characteristics as well as host features (immunological or other) that underlie the MPE phenotype. Herein we examine the pleural histology, cytology and molecular characteristics that make the pleural cavity an attractive metastasis destination for lung adenocarcinoma. Mesothelial and tumor features that may account for the tumor's ability to invade the pleural space are highlighted. Finally, possible therapeutic interventions specifically targeting MPE are discussed.
    Language English
    Publishing date 2015-07-06
    Publishing country China
    Document type Journal Article ; Review
    ZDB-ID 2573571-8
    ISSN 2077-6624 ; 2072-1439
    ISSN (online) 2077-6624
    ISSN 2072-1439
    DOI 10.3978/j.issn.2072-1439.2015.04.23
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Dnmt3a1 upregulates transcription of distinct genes and targets chromosomal gene clusters for epigenetic silencing in mouse embryonic stem cells.

    Kotini, Andriana G / Mpakali, Anastasia / Agalioti, Theodora

    Molecular and cellular biology

    2011  Volume 31, Issue 7, Page(s) 1577–1592

    Abstract: Dnmt3a1 and Dnmt3a2 are two de novo DNA methyltransferases expressed in mouse embryonic stem cells (mESCs). They differ in that a 219-amino-acid (aa) amino (N)-terminal noncatalytic domain is present only in Dnmt3a1. Here, we examined the unique ... ...

    Abstract Dnmt3a1 and Dnmt3a2 are two de novo DNA methyltransferases expressed in mouse embryonic stem cells (mESCs). They differ in that a 219-amino-acid (aa) amino (N)-terminal noncatalytic domain is present only in Dnmt3a1. Here, we examined the unique functions of Dnmt3a1 in mESCs by targeting the coding sequence of the Dnmt3a1 N-terminal domain tagged with enhanced green fluorescent protein (GFP) for insertion into the mouse Rosa26 locus. Using these targeted cells (GFP-3a1Nter), we showed that Dnmt3a1 was efficiently recruited to the silenced Oct3/4 and activated Vtn (vitronectin) gene promoters via its unique N-terminal domain. This recruitment affected the two genes in contrasting ways, compromising Oct3/4 gene promoter DNA methylation to prevent consolidation of the silent state while significantly reducing Vtn transcription. We used this negative effect of the Dnmt3a1 N-terminal domain to investigate the extent of transcriptional regulation by Dnmt3a1 in mESCs by using microarrays. A small group of all-trans retinoic acid (tRA)-inducible genes had lower transcript levels in GFP-3a1Nter cells than in wild-type mESCs. Intriguingly, this group included genes that are important for fetal nutrition, placenta development, and metabolic functions and is enriched for a distinct set of imprinted genes. We also identified a larger group of genes that showed higher transcript levels in the GFP-3a1Nter-expressing cells than in wild-type mESCs, including pluripotency factors and key regulators of primordial germ cell differentiation. Thus, Dnmt3a1 in mESCs functions primarily as a negative and to a lesser extent as a positive regulator of transcription. Our findings suggest that Dnmt3a1 positively affects transcription of specific genes at the promoter level and targets chromosomal domains to epigenetically silence gene clusters in mESCs.
    MeSH term(s) Animals ; Chromosomes, Mammalian/genetics ; DNA (Cytosine-5-)-Methyltransferases/chemistry ; DNA (Cytosine-5-)-Methyltransferases/metabolism ; DNA Modification Methylases/chemistry ; DNA Modification Methylases/metabolism ; DNA, Complementary/genetics ; Embryonic Stem Cells/drug effects ; Embryonic Stem Cells/metabolism ; Gene Silencing/drug effects ; Genetic Loci/genetics ; Green Fluorescent Proteins/metabolism ; Homeodomain Proteins/metabolism ; Mice ; Multigene Family/genetics ; Nanog Homeobox Protein ; Octamer Transcription Factor-3/metabolism ; Oligonucleotide Array Sequence Analysis ; Promoter Regions, Genetic/genetics ; Protein Binding/drug effects ; Protein Structure, Tertiary ; Proteins/genetics ; Proteins/metabolism ; RNA, Untranslated ; Transcription, Genetic/drug effects ; Transcriptional Activation/drug effects ; Transcriptional Activation/genetics ; Tretinoin/pharmacology ; Up-Regulation/drug effects ; Up-Regulation/genetics ; Vitronectin/genetics
    Chemical Substances DNA, Complementary ; Gt(ROSA)26Sor non-coding RNA, mouse ; Homeodomain Proteins ; Nanog Homeobox Protein ; Nanog protein, mouse ; Octamer Transcription Factor-3 ; Pou5f1 protein, mouse ; Proteins ; RNA, Untranslated ; Vitronectin ; enhanced green fluorescent protein ; Green Fluorescent Proteins (147336-22-9) ; Tretinoin (5688UTC01R) ; DNA Modification Methylases (EC 2.1.1.-) ; Dnmt3a1 protein, mouse (EC 2.1.1.-) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; DNA methyltransferase 3A (EC 2.1.1.37)
    Language English
    Publishing date 2011-01-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 779397-2
    ISSN 1098-5549 ; 0270-7306
    ISSN (online) 1098-5549
    ISSN 0270-7306
    DOI 10.1128/MCB.01093-10
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Multicytokine-producing CD4+ T cells characterize the livers of patients with NASH.

    Woestemeier, Anna / Scognamiglio, Pasquale / Zhao, Yu / Wagner, Jonas / Muscate, Franziska / Casar, Christian / Siracusa, Francesco / Cortesi, Filippo / Agalioti, Theodora / Müller, Simone / Sagebiel, Adrian / Konczalla, Leonie / Wahib, Ramez / Karstens, Karl-Frederick / Giannou, Anastasios D / Duprée, Anna / Wolter, Stefan / Wong, Milagros N / Mühlig, Anne K /
    Bielecka, Agata A / Bansal, Vikas / Zhang, Tianran / Mann, Oliver / Puelles, Victor G / Huber, Tobias B / Lohse, Ansgar W / Izbicki, Jakob R / Palm, Noah W / Bonn, Stefan / Huber, Samuel / Gagliani, Nicola

    JCI insight

    2023  Volume 8, Issue 1

    Abstract: A role of CD4+ T cells during the progression from nonalcoholic fatty liver disease (NAFLD) to nonalcoholic steatohepatitis (NASH) has been suggested, but which polarization state of these cells characterizes this progression and the development of ... ...

    Abstract A role of CD4+ T cells during the progression from nonalcoholic fatty liver disease (NAFLD) to nonalcoholic steatohepatitis (NASH) has been suggested, but which polarization state of these cells characterizes this progression and the development of fibrosis remain unclear. In addition, a gut-liver axis has been suggested to play a role in NASH, but the role of CD4+ T cells in this axis has just begun to be investigated. Combining single-cell RNA sequencing and multiple-parameter flow cytometry, we provide the first cell atlas to our knowledge focused on liver-infiltrating CD4+ T cells in patients with NAFLD and NASH, showing that NASH is characterized by a population of multicytokine-producing CD4+ T cells. Among these cells, only those with a Th17 polarization state were enriched in patients with advanced fibrosis. In parallel, we observed that Bacteroides appeared to be enriched in the intestine of NASH patients and to correlate with the frequency of multicytokine-producing CD4+ T cells. In short, we deliver a CD4+ T cell atlas of NAFLD and NASH, providing the rationale to target CD4+ T cells with a Th17 polarization state to block fibrosis development. Finally, our data offer an early indication to test whether multicytokine-producing CD4+ T cells are part of the gut-liver axis characterizing NASH.
    MeSH term(s) Humans ; Non-alcoholic Fatty Liver Disease ; CD4-Positive T-Lymphocytes ; Fibrosis
    Language English
    Publishing date 2023-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.153831
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Short-term dietary changes can result in mucosal and systemic immune depression.

    Siracusa, Francesco / Schaltenberg, Nicola / Kumar, Yogesh / Lesker, Till R / Steglich, Babett / Liwinski, Timur / Cortesi, Filippo / Frommann, Laura / Diercks, Björn-Phillip / Bönisch, Friedericke / Fischer, Alexander W / Scognamiglio, Pasquale / Pauly, Mira J / Casar, Christian / Cohen, Yotam / Pelczar, Penelope / Agalioti, Theodora / Delfs, Flemming / Worthmann, Anna /
    Wahib, Ramez / Jagemann, Bettina / Mittrücker, Hans-Willi / Kretz, Oliver / Guse, Andreas H / Izbicki, Jakob R / Lassen, Kara G / Strowig, Till / Schweizer, Michaela / Villablanca, Eduardo J / Elinav, Eran / Huber, Samuel / Heeren, Joerg / Gagliani, Nicola

    Nature immunology

    2023  Volume 24, Issue 9, Page(s) 1473–1486

    Abstract: Omnivorous animals, including mice and humans, tend to prefer energy-dense nutrients rich in fat over plant-based diets, especially for short periods of time, but the health consequences of this short-term consumption of energy-dense nutrients are ... ...

    Abstract Omnivorous animals, including mice and humans, tend to prefer energy-dense nutrients rich in fat over plant-based diets, especially for short periods of time, but the health consequences of this short-term consumption of energy-dense nutrients are unclear. Here, we show that short-term reiterative switching to 'feast diets', mimicking our social eating behavior, breaches the potential buffering effect of the intestinal microbiota and reorganizes the immunological architecture of mucosa-associated lymphoid tissues. The first dietary switch was sufficient to induce transient mucosal immune depression and suppress systemic immunity, leading to higher susceptibility to Salmonella enterica serovar Typhimurium and Listeria monocytogenes infections. The ability to respond to antigenic challenges with a model antigen was also impaired. These observations could be explained by a reduction of CD4
    MeSH term(s) Humans ; Mice ; Animals ; Mucous Membrane ; Salmonella typhimurium ; T-Lymphocytes ; Immunity, Mucosal
    Language English
    Publishing date 2023-08-14
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-023-01587-x
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  7. Article ; Online: IL-10 dampens antitumor immunity and promotes liver metastasis via PD-L1 induction.

    Shiri, Ahmad Mustafa / Zhang, Tao / Bedke, Tanja / Zazara, Dimitra E / Zhao, Lilan / Lücke, Jöran / Sabihi, Morsal / Fazio, Antonella / Zhang, Siwen / Tauriello, Daniele V F / Batlle, Eduard / Steglich, Babett / Kempski, Jan / Agalioti, Theodora / Nawrocki, Mikołaj / Xu, Yang / Riecken, Kristoffer / Liebold, Imke / Brockmann, Leonie /
    Konczalla, Leonie / Bosurgi, Lidia / Mercanoglu, Baris / Seeger, Philipp / Küsters, Natalie / Lykoudis, Panagis M / Heumann, Asmus / Arck, Petra C / Fehse, Boris / Busch, Philipp / Grotelüschen, Rainer / Mann, Oliver / Izbicki, Jakob R / Hackert, Thilo / Flavell, Richard A / Gagliani, Nicola / Giannou, Anastasios D / Huber, Samuel

    Journal of hepatology

    2023  Volume 80, Issue 4, Page(s) 634–644

    Abstract: Background & aims: The liver is one of the organs most commonly affected by metastasis. The presence of liver metastases has been reported to be responsible for an immunosuppressive microenvironment and diminished immunotherapy efficacy. Herein, we ... ...

    Abstract Background & aims: The liver is one of the organs most commonly affected by metastasis. The presence of liver metastases has been reported to be responsible for an immunosuppressive microenvironment and diminished immunotherapy efficacy. Herein, we aimed to investigate the role of IL-10 in liver metastasis and to determine how its modulation could affect the efficacy of immunotherapy in vivo.
    Methods: To induce spontaneous or forced liver metastasis in mice, murine cancer cells (MC38) or colon tumor organoids were injected into the cecum or the spleen, respectively. Mice with complete and cell type-specific deletion of IL-10 and IL-10 receptor alpha were used to identify the source and the target of IL-10 during metastasis formation. Programmed death ligand 1 (PD-L1)-deficient mice were used to test the role of this checkpoint. Flow cytometry was applied to characterize the regulation of PD-L1 by IL-10.
    Results: We found that Il10-deficient mice and mice treated with IL-10 receptor alpha antibodies were protected against liver metastasis formation. Furthermore, by using IL-10 reporter mice, we demonstrated that Foxp3+ regulatory T cells (Tregs) were the major cellular source of IL-10 in liver metastatic sites. Accordingly, deletion of IL-10 in Tregs, but not in myeloid cells, led to reduced liver metastasis. Mechanistically, IL-10 acted on Tregs in an autocrine manner, thereby further amplifying IL-10 production. Furthermore, IL-10 acted on myeloid cells, i.e. monocytes, and induced the upregulation of the immune checkpoint protein PD-L1. Finally, the PD-L1/PD-1 axis attenuated CD8-dependent cytotoxicity against metastatic lesions.
    Conclusions: Treg-derived IL-10 upregulates PD-L1 expression in monocytes, which in turn reduces CD8+ T-cell infiltration and related antitumor immunity in the context of colorectal cancer-derived liver metastases. These findings provide the basis for future monitoring and targeting of IL-10 in colorectal cancer-derived liver metastases.
    Impact and implications: Liver metastasis diminishes the effectiveness of immunotherapy and increases the mortality rate in patients with colorectal cancer. We investigated the role of IL-10 in liver metastasis formation and assessed its impact on the effectiveness of immunotherapy. Our data show that IL-10 is a pro-metastatic factor involved in liver metastasis formation and that it acts as a regulator of PD-L1. This provides the basis for future monitoring and targeting of IL-10 in colorectal cancer-derived liver metastasis.
    MeSH term(s) Animals ; Humans ; Mice ; B7-H1 Antigen/genetics ; B7-H1 Antigen/metabolism ; CD8-Positive T-Lymphocytes ; Cell Line, Tumor ; Colorectal Neoplasms ; Interleukin-10 ; Liver Neoplasms/pathology ; Receptors, Interleukin-10 ; Tumor Microenvironment
    Chemical Substances B7-H1 Antigen ; Interleukin-10 (130068-27-8) ; Receptors, Interleukin-10 ; Cd274 protein, mouse ; IL10 protein, mouse
    Language English
    Publishing date 2023-12-30
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 605953-3
    ISSN 1600-0641 ; 0168-8278
    ISSN (online) 1600-0641
    ISSN 0168-8278
    DOI 10.1016/j.jhep.2023.12.015
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  8. Article ; Online: The induction and function of the anti-inflammatory fate of T

    Xu, Hao / Agalioti, Theodora / Zhao, Jun / Steglich, Babett / Wahib, Ramez / Vesely, Maria Carolina Amezcua / Bielecki, Piotr / Bailis, Will / Jackson, Ruaidhri / Perez, Daniel / Izbicki, Jakob / Licona-Limón, Paula / Kaartinen, Vesa / Geginat, Jens / Esplugues, Enric / Tolosa, Eva / Huber, Samuel / Flavell, Richard A / Gagliani, Nicola

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 3334

    Abstract: ... ...

    Abstract T
    MeSH term(s) Animals ; Cell Plasticity/immunology ; Disease Resistance/genetics ; Disease Resistance/immunology ; HEK293 Cells ; Homeostasis/immunology ; Humans ; Inflammation/immunology ; Interleukin-10/genetics ; Interleukin-10/immunology ; Interleukin-10/metabolism ; Interleukin-17/genetics ; Interleukin-17/immunology ; Interleukin-17/metabolism ; Intestines/immunology ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Staphylococcal Infections/immunology ; Staphylococcal Infections/microbiology ; Staphylococcus aureus/immunology ; Staphylococcus aureus/physiology ; Th17 Cells/immunology ; Th17 Cells/metabolism ; Transforming Growth Factor beta/immunology ; Transforming Growth Factor beta/metabolism
    Chemical Substances Interleukin-17 ; Transforming Growth Factor beta ; Interleukin-10 (130068-27-8)
    Language English
    Publishing date 2020-07-03
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-17097-5
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  9. Article: Tumor-derived osteopontin isoforms cooperate with TRP53 and CCL2 to promote lung metastasis.

    Giopanou, Ioanna / Lilis, Ioannis / Papaleonidopoulos, Vassilios / Agalioti, Theodora / Kanellakis, Nikolaos I / Spiropoulou, Nikolitsa / Spella, Magda / Stathopoulos, Georgios T

    Oncoimmunology

    2016  Volume 6, Issue 1, Page(s) e1256528

    Abstract: The lungs are ubiquitous receptacles of metastases originating from various bodily tumors. Although osteopontin (SPP1) has been associated with tumor dissemination, the role of its isoforms in lung-directed metastasis is incompletely understood. We ... ...

    Abstract The lungs are ubiquitous receptacles of metastases originating from various bodily tumors. Although osteopontin (SPP1) has been associated with tumor dissemination, the role of its isoforms in lung-directed metastasis is incompletely understood. We employed syngeneic mouse models of spontaneous and induced lung-targeted metastasis in
    Language English
    Publishing date 2016-11-18
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2645309-5
    ISSN 2162-402X ; 2162-4011
    ISSN (online) 2162-402X
    ISSN 2162-4011
    DOI 10.1080/2162402X.2016.1256528
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  10. Article ; Online: Tobacco chemical-induced mouse lung adenocarcinoma cell lines pin the prolactin orthologue proliferin as a lung tumour promoter.

    Kanellakis, Nikolaos I / Giannou, Anastasios D / Pepe, Mario A A / Agalioti, Theodora / Zazara, Dimitra E / Giopanou, Ioanna / Psallidas, Ioannis / Spella, Magda / Marazioti, Antonia / Arendt, Kristina A M / Lamort, Anne Sophie / Champeris Tsaniras, Spyridon / Taraviras, Stavros / Papadaki, Helen / Lilis, Ioannis / Stathopoulos, Georgios T

    Carcinogenesis

    2019  Volume 40, Issue 11, Page(s) 1352–1362

    Abstract: Lung adenocarcinoma (LADC) is the leading cause of cancer death worldwide. Nevertheless, syngeneic mouse models of the disease are sparse, and cell lines suitable for transplantable and immunocompetent mouse models of LADC remain unmet needs. We ... ...

    Abstract Lung adenocarcinoma (LADC) is the leading cause of cancer death worldwide. Nevertheless, syngeneic mouse models of the disease are sparse, and cell lines suitable for transplantable and immunocompetent mouse models of LADC remain unmet needs. We established multiple mouse LADC cell lines by repeatedly exposing two mouse strains (FVB, Balb/c) to the tobacco carcinogens urethane or diethylnitrosamine and by culturing out the resulting lung tumours for prolonged periods of time. Characterization of the resulting cell lines (n = 7) showed that they were immortal and phenotypically stable in vitro, and oncogenic, metastatic and lethal in vivo. The primary tumours that gave rise to the cell lines, as well as secondary tumours generated by transplantation of the cell lines, displayed typical LADC features, such as glandular architecture and mucin and thyroid transcription factor 1 expression. Moreover, these cells exhibited marked molecular similarity with human smokers' LADC, including carcinogen-specific Kras point mutations (KrasQ61R in urethane- and KrasQ61H in diethylnitrosamine-triggered cell lines) and Trp53 deletions and displayed stemness features. Interestingly, all cell lines overexpressed proliferin, a murine prolactin orthologue, which functioned as a lung tumour promoter. Furthermore, prolactin was overexpressed and portended poor prognosis in human LADC. In conclusion, we report the first LADC cell lines derived from mice exposed to tobacco carcinogens. These cells closely resemble human LADC and provide a valuable tool for the functional investigation of the pathobiology of the disease.
    MeSH term(s) Adenocarcinoma of Lung/chemically induced ; Adenocarcinoma of Lung/genetics ; Adenocarcinoma of Lung/metabolism ; Animals ; Carcinogenesis ; Carcinogens ; Cell Line, Tumor ; Diethylnitrosamine/toxicity ; Disease Models, Animal ; Gene Expression Regulation, Neoplastic ; Genes, ras/genetics ; Lung Neoplasms/chemically induced ; Lung Neoplasms/genetics ; Lung Neoplasms/metabolism ; Mice ; Mutation ; Prolactin/genetics ; Thyroid Nuclear Factor 1/genetics ; Nicotiana/toxicity ; Tumor Suppressor Protein p53/genetics ; Urethane/toxicity
    Chemical Substances Carcinogens ; Prl2c2 protein, mouse ; Thyroid Nuclear Factor 1 ; Tumor Suppressor Protein p53 ; Urethane (3IN71E75Z5) ; Diethylnitrosamine (3IQ78TTX1A) ; Prolactin (9002-62-4)
    Language English
    Publishing date 2019-03-02
    Publishing country England
    Document type Journal Article
    ZDB-ID 603134-1
    ISSN 1460-2180 ; 0143-3334
    ISSN (online) 1460-2180
    ISSN 0143-3334
    DOI 10.1093/carcin/bgz047
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