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  1. Article ; Online: SARS-CoV-2 accessory proteins involvement in inflammatory and profibrotic processes through IL11 signaling.

    López-Ayllón, Blanca D / de Lucas-Rius, Ana / Mendoza-García, Laura / García-García, Tránsito / Fernández-Rodríguez, Raúl / Suárez-Cárdenas, José M / Santos, Fátima Milhano / Corrales, Fernando / Redondo, Natalia / Pedrucci, Federica / Zaldívar-López, Sara / Jiménez-Marín, Ángeles / Garrido, Juan J / Montoya, María

    Frontiers in immunology

    2023  Volume 14, Page(s) 1220306

    Abstract: SARS-CoV-2, the cause of the COVID-19 pandemic, possesses eleven accessory proteins encoded in its genome. Their roles during infection are still not completely understood. In this study, transcriptomics analysis revealed that ... ...

    Abstract SARS-CoV-2, the cause of the COVID-19 pandemic, possesses eleven accessory proteins encoded in its genome. Their roles during infection are still not completely understood. In this study, transcriptomics analysis revealed that both
    MeSH term(s) Humans ; COVID-19 ; Interleukin-11 ; SARS-CoV-2/genetics ; Viral Proteins/genetics ; Idiopathic Pulmonary Fibrosis
    Chemical Substances Interleukin-11 ; Viral Proteins
    Language English
    Publishing date 2023-07-20
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1220306
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Metabolic and mitochondria alterations induced by SARS-CoV-2 accessory proteins ORF3a, ORF9b, ORF9c and ORF10

    Lopez-Ayllon, Blanca D. / Marin, Silvia / Farinas Fernandez, Marcos / Garcia-Garcia, Transito / Fernandez-Rodriguez, Raul / de Lucas-Rius, Ana / Redondo, Natalia / Mendoza-Garcia, Laura / Foguet, Carles / Grigas, Jouzas / Calvet, Alba / Villalba, Jose Manuel / Rodriguez Gomez, Maria Josefa / Megias, Diego / Mandracchia, Biagio / Luque, Daniel / Lozano, Juan Jose / Calvo, Cristina / Thomson, Timothy M. /
    Garrido, Juan Jose / Cascante, Marta / Montoya, Maria

    bioRxiv

    Abstract: Antiviral signaling, immune response and cell metabolism in human body are dysregulated by SARS-CoV-2, the causative agent of the COVID-19. Here, we show that SARS-CoV-2 accessory proteins ORF3a, ORF9b, ORF9c and ORF10 induce a significant mitochondrial ... ...

    Abstract Antiviral signaling, immune response and cell metabolism in human body are dysregulated by SARS-CoV-2, the causative agent of the COVID-19. Here, we show that SARS-CoV-2 accessory proteins ORF3a, ORF9b, ORF9c and ORF10 induce a significant mitochondrial and metabolic reprogramming in A549 lung epithelial cells. While all four ORFs caused mitochondrial fragmentation and altered mitochondrial function, only ORF3a and ORF9c induced a marked structural alteration in mitochondrial cristae. ORF9b, ORF9c and ORF10 induced largely overlapping transcriptomes. In contrast, ORF3a induced a distinct transcriptome, including the downregulation of numerous genes for proteins with critical mitochondrial functions and morphology. Genome-Scale Metabolic Models predicted common and private metabolic flux reprogramming, notably a depressed amino acid metabolism, and an enhanced metabolism of specific lipids distinctly induced by ORF3a. These findings reveal metabolic dependencies and vulnerabilities prompted by SARS-CoV-2 accessory proteins that may be exploited to identify new targets for intervention.
    Keywords covid19
    Language English
    Publishing date 2023-09-26
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2023.09.26.559506
    Database COVID19

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  3. Article ; Online: A role for cancer stem cells in drug resistance and metastasis in non-small-cell lung cancer.

    Perona, Rosario / López-Ayllón, Blanca D / de Castro Carpeño, Javier / Belda-Iniesta, Cristóbal

    Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico

    2011  Volume 13, Issue 5, Page(s) 289–293

    Abstract: The cancer stem cell (CSC) theory is currently a very important field in cancer research. This theory states that tumours are organised in a hierarchical manner with a subpopulation of limited number called CSCs with the ability to self-renew and undergo ...

    Abstract The cancer stem cell (CSC) theory is currently a very important field in cancer research. This theory states that tumours are organised in a hierarchical manner with a subpopulation of limited number called CSCs with the ability to self-renew and undergo asymmetrical divisions, giving rise to a differentiated progeny that represents most of the tumour populations. CSCs are metastatic and chemoresistant, two features that very likely contribute to the poor response of locally advanced lung cancer. CSCs have been identified in non-small-cell lung cancer cell lines as well as those from patient primary samples. A correlation has been found in terms of chemoresistance and bad prognosis in patient-derived samples enriched with CSCs, indicating that these cells are an important target for future therapy combinations. Therefore, understanding the biology and exploring cell markers and signalling pathways specific for CSCs of lung cancer may help in achieving progress in the treatment of the disease.
    MeSH term(s) AC133 Antigen ; Aldehyde Dehydrogenase/metabolism ; Antigens, CD/biosynthesis ; Antigens, CD34/biosynthesis ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Differentiation ; Drug Resistance, Neoplasm ; Glycoproteins/biosynthesis ; Humans ; Hyaluronan Receptors/biosynthesis ; Lung Neoplasms/drug therapy ; Lung Neoplasms/pathology ; Medical Oncology/methods ; Neoplasm Metastasis ; Neoplastic Stem Cells/cytology ; Peptides ; Signal Transduction ; Transcription Factors/metabolism ; Treatment Outcome
    Chemical Substances AC133 Antigen ; Antigens, CD ; Antigens, CD34 ; Glycoproteins ; Hyaluronan Receptors ; Peptides ; Transcription Factors ; Aldehyde Dehydrogenase (EC 1.2.1.3)
    Language English
    Publishing date 2011-05-19
    Publishing country Italy
    Document type Journal Article ; Review
    ZDB-ID 2397359-6
    ISSN 1699-3055 ; 1699-048X
    ISSN (online) 1699-3055
    ISSN 1699-048X
    DOI 10.1007/s12094-011-0656-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6644: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Biomarkers of erlotinib response in non-small cell lung cancer tumors that do not harbor the more common epidermal growth factor receptor mutations.

    López-Ayllón, Blanca D / de Castro-Carpeño, Javier / Rodriguez, Carlos / Pernía, Olga / Ibañez de Cáceres, Inmaculada / Belda-Iniesta, Cristobal / Perona, Rosario / Sastre, Leandro

    International journal of clinical and experimental pathology

    2015  Volume 8, Issue 3, Page(s) 2888–2898

    Abstract: Non-small cell lung cancer (NSCLC) represents approximately 85% of all lung cancers, which are the leading cause of cancer-related deaths in the world. Tyrosine kinase inhibitors such as erlotinib represent one therapeutic options presently recommended ... ...

    Abstract Non-small cell lung cancer (NSCLC) represents approximately 85% of all lung cancers, which are the leading cause of cancer-related deaths in the world. Tyrosine kinase inhibitors such as erlotinib represent one therapeutic options presently recommended for tumors produced by activating mutations in the gene coding of epidermal growth factor receptor (EGFR). The aim of this study is the identification of possible biomarkers for tumor sensitivity to erlotinib in the absence of the main EGFR mutations. The erlotinib sensitivity of cells isolated from 41 untreated NSCLC patients was determined and compared with the presence of the more frequent EGFR mutations. Several patients had tumor cells highly sensitive to erlitinib in the absence of the EGFR mutations analyzed. The gene expression profile of 3 erlotinib-sensitive tumors was compared with that of 4 resistant tumors by DNA microarray hybridization. Sixteen genes were expressed at significantly higher levels in the resistant tumors than in the sensitive tumors. The possible correlation between erlotinib sensitivity and the expression of these genes was further analyzed using the data for the NSCLC, breast cancer and colon cancer cell lines of the NCI60 collection. The expression of these genes was correlated with the overall survival of 5 patients treated with erlotinib, according to The Cancer Genome Atlas (TCGA) database. Overlapping groups of 7, 5 and 3 genes, including UGT1A6, TRIB3, MET, MMP7, COL17A1, LCN2 and PTPRZ1, whose expression correlated with erlotinib activity was identified. In particular, low MET expression levels showed the strongest correlation.
    MeSH term(s) Adult ; Aged ; Aged, 80 and over ; Antineoplastic Agents/therapeutic use ; Biomarkers, Tumor/analysis ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/genetics ; Drug Resistance, Neoplasm/genetics ; Erlotinib Hydrochloride/therapeutic use ; Female ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Male ; Middle Aged ; Mutation ; Oligonucleotide Array Sequence Analysis ; Receptor, Epidermal Growth Factor/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; Transcriptome
    Chemical Substances Antineoplastic Agents ; Biomarkers, Tumor ; Erlotinib Hydrochloride (DA87705X9K) ; EGFR protein, human (EC 2.7.10.1) ; Receptor, Epidermal Growth Factor (EC 2.7.10.1)
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2418306-4
    ISSN 1936-2625 ; 1936-2625
    ISSN (online) 1936-2625
    ISSN 1936-2625
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  5. Article ; Online: Cancer stem cells and cisplatin-resistant cells isolated from non-small-lung cancer cell lines constitute related cell populations.

    Lopez-Ayllon, Blanca D / Moncho-Amor, Veronica / Abarrategi, Ander / Ibañez de Cáceres, Inmaculada / Castro-Carpeño, Javier / Belda-Iniesta, Cristobal / Perona, Rosario / Sastre, Leandro

    Cancer medicine

    2014  Volume 3, Issue 5, Page(s) 1099–1111

    Abstract: Lung cancer is the top cause of cancer-related deceases. One of the reasons is the development of resistance to the chemotherapy treatment. In particular, cancer stem cells (CSCs), can escape treatment and regenerate the bulk of the tumor. In this ... ...

    Abstract Lung cancer is the top cause of cancer-related deceases. One of the reasons is the development of resistance to the chemotherapy treatment. In particular, cancer stem cells (CSCs), can escape treatment and regenerate the bulk of the tumor. In this article, we describe a comparison between cancer cells resistant to cisplatin and CSCs, both derived from the non-small-cell lung cancer cell lines H460 and A549. Cisplatin-resistant cells were obtained after a single treatment with the drug. CSCs were isolated by culture in defined media, under nonadherent conditions. The isolated CSCs were clonogenic, could be differentiated into adherent cells and were less sensitive to cisplatin than the original cells. Cisplatin resistant and CSCs were able to generate primary tumors and to metastasize when injected into immunodeficient Nu/Nu mice, although they formed smaller tumors with a larger latency than untreated cells. Notably, under appropriated proportions, CSCs synergized with differentiated cells to form larger tumors. CSCs also showed increased capacity to induce angiogenesis in Nu/Nu mice. Conversely, H460 cisplatin-resistant cells showed increased tendency to develop bone metastasis. Gene expression analysis showed that several genes involved in tumor development and metastasis (EGR1, COX2, MALAT1, AKAP12, ADM) were similarly induced in CSC and cisplatin-resistant H460 cells, in agreement with a close similarity between these two cell populations. Cells with the characteristic growth properties of CSCs were also isolated from surgical samples of 18 out of 44 lung cancer patients. A significant correlation (P = 0.028) was found between the absence of CSCs and cisplatin sensitivity.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Carcinoma, Non-Small-Cell Lung/genetics ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; Cisplatin/pharmacology ; Disease Models, Animal ; Drug Resistance, Neoplasm ; Female ; Gene Expression Profiling ; Heterografts ; Humans ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mice ; Neoplasm Invasiveness ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Neovascularization, Pathologic ; Tumor Stem Cell Assay
    Chemical Substances Antineoplastic Agents ; Cisplatin (Q20Q21Q62J)
    Language English
    Publishing date 2014-06-25
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2659751-2
    ISSN 2045-7634 ; 2045-7634
    ISSN (online) 2045-7634
    ISSN 2045-7634
    DOI 10.1002/cam4.291
    Database MEDical Literature Analysis and Retrieval System OnLINE

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