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  1. Book ; Thesis: P53-induced miR-30e acts as a tumor and metastasis suppressor miRNA in colorectal cancer

    Laudato, Sara

    2016  

    Author's details vorgelegt von Sara Laudato
    Language English
    Size VII, 136 Blätter, Illustrationen, Diagramme
    Publishing place Heidelberg
    Publishing country Germany
    Document type Book ; Thesis
    Thesis / German Habilitation thesis Dissertation, Ruprecht-Karls-Universität Heidelberg, 2016
    HBZ-ID HT019294348
    Database Catalogue ZB MED Medicine, Health

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    2017 E 634 order for loan Magazin

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  2. Article ; Online: Clonal Evolution and Epithelial Plasticity in the Emergence of AR-Independent Prostate Carcinoma.

    Laudato, Sara / Aparicio, Ana / Giancotti, Filippo G

    Trends in cancer

    2019  Volume 5, Issue 7, Page(s) 440–455

    Abstract: In spite of an initial clinical response to androgen deprivation therapy (ADT), the majority of prostate cancer patients eventually develop castration-resistant prostate cancer (CRPC). Recent studies have highlighted the role of epithelial plasticity, ... ...

    Abstract In spite of an initial clinical response to androgen deprivation therapy (ADT), the majority of prostate cancer patients eventually develop castration-resistant prostate cancer (CRPC). Recent studies have highlighted the role of epithelial plasticity, including transdifferentiation and epithelial-to-mesenchymal transition (EMT), in the development of AR pathway-negative CRPC, a form of the disease that has increased in incidence after the introduction of potent AR inhibitors. In this review, we will discuss the switches between different cell fates that occur in response to AR blockade or acquisition of specific oncogenic mutations, such as those in TP53 and RB1, during the evolution to CRPC. We highlight the urgent need to dissect the mechanistic underpinnings of these transitions and identify novel vulnerabilities that can be targeted therapeutically.
    MeSH term(s) Antineoplastic Agents, Hormonal/pharmacology ; Antineoplastic Agents, Hormonal/therapeutic use ; Cell Plasticity ; Clonal Evolution ; Drug Resistance, Neoplasm/genetics ; Epithelial-Mesenchymal Transition/genetics ; Epithelium/metabolism ; Epithelium/pathology ; Humans ; Male ; Neoplastic Stem Cells/metabolism ; Neoplastic Stem Cells/pathology ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/etiology ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Receptors, Androgen/metabolism
    Chemical Substances Antineoplastic Agents, Hormonal ; Receptors, Androgen
    Language English
    Publishing date 2019-06-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2852626-0
    ISSN 2405-8025 ; 2405-8033 ; 2405-8033
    ISSN (online) 2405-8025 ; 2405-8033
    ISSN 2405-8033
    DOI 10.1016/j.trecan.2019.05.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: SARS-CoV-2 Exploits Sexually Dimorphic and Adaptive IFN and TNFa Signaling to Gain Entry into Alveolar Epithelium

    Giancotti, Filippo / Wang, Yan / Gurrapu, Sreeharsha / Chen, Hong / Laudato, Sara / Caggiano, Emily / Jiang, Yan / Ling, Hsiang-Hsi

    bioRxiv

    Abstract: Infection of the alveolar epithelium constitutes a bottleneck in the progression of COVID-19 to SARS presumably due to the paucity of viral entry receptors in alveolar epithelial type 1 and 2 cells. We have found that the male alveolar epithelial cells ... ...

    Abstract Infection of the alveolar epithelium constitutes a bottleneck in the progression of COVID-19 to SARS presumably due to the paucity of viral entry receptors in alveolar epithelial type 1 and 2 cells. We have found that the male alveolar epithelial cells express twice as many ACE2 and TMPRSS2 entry receptors as the female ones. Intriguingly, IFN and TNF-α signaling are preferentially active in male alveolar cells and induce binding of the cognate transcription factors to the promoters and lung-active enhancers of ACE2 and TMPRSS2. Cotreatment with IFN-I and III dramatically increases expression of the receptors and viral entry in alveolar epithelial cells. TNFα and IFN-II, typically overproduced during the cytokine storm, similarly collaborate to induce these events. Whereas JAK inhibitors suppress viral entry induced by IFN-I/III, simultaneous inhibition of IKK/NF-κB is necessary to block viral entry induced by TNFα and IFN II. In addition to explaining the increased incidence of SARS in males, these findings indicate that SARS-Cov-2 hijacks epithelial immune signaling to promote infection of the alveolar epithelium and suggest that JAK inhibitors, singly and in combination with NF-KB inhibitors, may exhibit efficacy in preventing or treating COVID-19 SARS.
    Keywords covid19
    Language English
    Publishing date 2021-07-23
    Publisher Cold Spring Harbor Laboratory
    Document type Article ; Online
    DOI 10.1101/2021.07.23.453505
    Database COVID19

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  4. Article ; Online: Mesenchymal and stem-like prostate cancer linked to therapy-induced lineage plasticity and metastasis.

    Han, Hyunho / Wang, Yan / Curto, Josue / Gurrapu, Sreeharsha / Laudato, Sara / Rumandla, Alekya / Chakraborty, Goutam / Wang, Xiaobo / Chen, Hong / Jiang, Yan / Kumar, Dhiraj / Caggiano, Emily G / Capogiri, Monica / Zhang, Boyu / Ji, Yan / Maity, Sankar N / Hu, Min / Bai, Shanshan / Aparicio, Ana M /
    Efstathiou, Eleni / Logothetis, Christopher J / Navin, Nicholas / Navone, Nora M / Chen, Yu / Giancotti, Filippo G

    Cell reports

    2022  Volume 39, Issue 1, Page(s) 110595

    Abstract: Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) ...

    Abstract Bioinformatic analysis of 94 patient-derived xenografts (PDXs), cell lines, and organoids (PCOs) identifies three intrinsic transcriptional subtypes of metastatic castration-resistant prostate cancer: androgen receptor (AR) pathway + prostate cancer (PC) (ARPC), mesenchymal and stem-like PC (MSPC), and neuroendocrine PC (NEPC). A sizable proportion of castration-resistant and metastatic stage PC (M-CRPC) cases are admixtures of ARPC and MSPC. Analysis of clinical datasets and mechanistic studies indicates that MSPC arises from ARPC as a consequence of therapy-induced lineage plasticity. AR blockade with enzalutamide induces (1) transcriptional silencing of TP53 and hence dedifferentiation to a hybrid epithelial and mesenchymal and stem-like state and (2) inhibition of BMP signaling, which promotes resistance to AR inhibition. Enzalutamide-tolerant LNCaP cells re-enter the cell cycle in response to neuregulin and generate metastasis in mice. Combined inhibition of HER2/3 and AR or mTORC1 exhibits efficacy in models of ARPC and MSPC or MSPC, respectively. These results define MSPC, trace its origin to therapy-induced lineage plasticity, and reveal its sensitivity to HER2/3 inhibition.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Benzamides ; Carcinoma, Neuroendocrine ; Cell Line, Tumor ; Cell Plasticity/drug effects ; Cell Plasticity/physiology ; Drug Resistance, Neoplasm ; Humans ; Male ; Mice ; Neoplastic Stem Cells/drug effects ; Neoplastic Stem Cells/metabolism ; Nitriles ; Phenylthiohydantoin ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/metabolism ; Receptors, Androgen/drug effects ; Receptors, Androgen/metabolism ; Signal Transduction ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/physiology
    Chemical Substances Antineoplastic Agents ; Benzamides ; Nitriles ; Receptors, Androgen ; Phenylthiohydantoin (2010-15-3) ; enzalutamide (93T0T9GKNU)
    Language English
    Publishing date 2022-04-03
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.110595
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: P53-induced miR-30e-5p inhibits colorectal cancer invasion and metastasis by targeting ITGA6 and ITGB1.

    Laudato, Sara / Patil, Nitin / Abba, Mohammed L / Leupold, Joerg H / Benner, Axel / Gaiser, Timo / Marx, Alexander / Allgayer, Heike

    International journal of cancer

    2017  Volume 141, Issue 9, Page(s) 1879–1890

    Abstract: The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential ... ...

    Abstract The tumor suppressor P53 is a critical regulator of normal cellular homeostasis whose function is either distorted or lost in several cancer types including colorectal cancer (CRC). A small group of microRNAs have come to be recognized as essential mediators of P53 function. In a genome-wide systematic approach, we explored miRNAs that are substantially altered by P53 loss and found miR-30e to be the most significantly deregulated miRNA in P53-knockout human CRC cells. We identified miR-30e-5p to be a novel direct transcriptional target of P53 with gain and loss of function experiments revealing miR-30e-5p to be a significant regulator of tumor cell migration, invasion and in vivo metastasis mediated in part by integrins alpha-6 and beta-1 as novel targets. MiR-30e-5p also significantly reduced tumor cell proliferation by causing G1/S cell cycle arrest, which was achieved by inducing P21 and P27 expression. Finally, we found miR-30e-5p to be lost in resected CRC tumors as compared to normal colon tissues. Taken together, miR-30e-5p is a novel effector of P53-induced suppression of migration, invasion and metastasis.
    MeSH term(s) Adaptor Proteins, Signal Transducing ; Animals ; Cell Cycle Checkpoints/genetics ; Cell Line, Tumor ; Cell Proliferation/genetics ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Cyclin-Dependent Kinase Inhibitor p21/genetics ; Cyclin-Dependent Kinase Inhibitor p27/genetics ; Gene Expression Regulation, Neoplastic ; HCT116 Cells ; Humans ; Integrin alpha6/genetics ; Intracellular Signaling Peptides and Proteins/genetics ; Membrane Proteins/genetics ; Mice ; MicroRNAs/genetics ; Neoplasm Invasiveness/genetics ; Neoplasm Invasiveness/pathology ; Neoplasm Metastasis ; Tumor Suppressor Protein p53/genetics ; Xenograft Model Antitumor Assays
    Chemical Substances Adaptor Proteins, Signal Transducing ; CDKN1A protein, human ; Cyclin-Dependent Kinase Inhibitor p21 ; ITGA6 protein, human ; ITGB1BP1 protein, human ; Integrin alpha6 ; Intracellular Signaling Peptides and Proteins ; MIRN30b microRNA, human ; Membrane Proteins ; MicroRNAs ; TP53 protein, human ; Tumor Suppressor Protein p53 ; Cyclin-Dependent Kinase Inhibitor p27 (147604-94-2)
    Language English
    Publishing date 2017-07-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.30854
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 478: Show issues Location:
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    Zs.MO 576: Show issues

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  6. Article ; Online: Erratum: DNMT and HDAC inhibitors induce cryptic transcription start sites encoded in long terminal repeats.

    Brocks, David / Schmidt, Christopher R / Daskalakis, Michael / Jang, Hyo Sik / Shah, Nakul M / Li, Daofeng / Li, Jing / Zhang, Bo / Hou, Yiran / Laudato, Sara / Lipka, Daniel B / Schott, Johanna / Bierhoff, Holger / Assenov, Yassen / Helf, Monika / Ressnerova, Alzbeta / Islam, Md Saiful / Lindroth, Anders M / Haas, Simon /
    Essers, Marieke / Imbusch, Charles D / Brors, Benedikt / Oehme, Ina / Witt, Olaf / Lübbert, Michael / Mallm, Jan-Philipp / Rippe, Karsten / Will, Rainer / Weichenhan, Dieter / Stoecklin, Georg / Gerhäuser, Clarissa / Oakes, Christopher C / Wang, Ting / Plass, Christoph

    Nature genetics

    2017  Volume 49, Issue 11, Page(s) 1661

    Abstract: This corrects the article DOI: 10.1038/ng.3889. ...

    Abstract This corrects the article DOI: 10.1038/ng.3889.
    Language English
    Publishing date 2017-10-23
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/ng1117-1661c
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    Zs.A 3613: Show issues Location:
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  7. Article ; Online: DNMT and HDAC inhibitors induce cryptic transcription start sites encoded in long terminal repeats.

    Brocks, David / Schmidt, Christopher R / Daskalakis, Michael / Jang, Hyo Sik / Shah, Nakul M / Li, Daofeng / Li, Jing / Zhang, Bo / Hou, Yiran / Laudato, Sara / Lipka, Daniel B / Schott, Johanna / Bierhoff, Holger / Assenov, Yassen / Helf, Monika / Ressnerova, Alzbeta / Islam, Md Saiful / Lindroth, Anders M / Haas, Simon /
    Essers, Marieke / Imbusch, Charles D / Brors, Benedikt / Oehme, Ina / Witt, Olaf / Lübbert, Michael / Mallm, Jan-Philipp / Rippe, Karsten / Will, Rainer / Weichenhan, Dieter / Stoecklin, Georg / Gerhäuser, Clarissa / Oakes, Christopher C / Wang, Ting / Plass, Christoph

    Nature genetics

    2017  Volume 49, Issue 7, Page(s) 1052–1060

    Abstract: Several mechanisms of action have been proposed for DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi), primarily based on candidate-gene approaches. However, less is known about their genome-wide transcriptional and epigenomic ... ...

    Abstract Several mechanisms of action have been proposed for DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi), primarily based on candidate-gene approaches. However, less is known about their genome-wide transcriptional and epigenomic consequences. By mapping global transcription start site (TSS) and chromatin dynamics, we observed the cryptic transcription of thousands of treatment-induced non-annotated TSSs (TINATs) following DNMTi and HDACi treatment. The resulting transcripts frequently splice into protein-coding exons and encode truncated or chimeric ORFs translated into products with predicted abnormal or immunogenic functions. TINAT transcription after DNMTi treatment coincided with DNA hypomethylation and gain of classical promoter histone marks, while HDACi specifically induced a subset of TINATs in association with H2AK9ac, H3K14ac, and H3K23ac. Despite this mechanistic difference, both inhibitors convergently induced transcription from identical sites, as we found TINATs to be encoded in solitary long terminal repeats of the ERV9/LTR12 family, which are epigenetically repressed in virtually all normal cells.
    MeSH term(s) Alternative Splicing/genetics ; Animals ; Benzimidazoles/pharmacology ; Cell Line, Tumor ; DNA (Cytosine-5-)-Methyltransferase 1 ; DNA (Cytosine-5-)-Methyltransferases/antagonists & inhibitors ; DNA (Cytosine-5-)-Methyltransferases/physiology ; DNA Methylation ; Death-Associated Protein Kinases/antagonists & inhibitors ; Death-Associated Protein Kinases/genetics ; Epigenetic Repression ; Exons/genetics ; Female ; Gene Expression Profiling ; Gene Silencing ; Histone Code ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Hydroxamic Acids/pharmacology ; Introns/genetics ; Mice ; Mice, Nude ; RNA Interference ; Recombinant Fusion Proteins/genetics ; Recombinant Fusion Proteins/metabolism ; Terminal Repeat Sequences/genetics ; Transcription Initiation Site/drug effects
    Chemical Substances Benzimidazoles ; Histone Deacetylase Inhibitors ; Hydroxamic Acids ; Recombinant Fusion Proteins ; SB939 compound ; vorinostat (58IFB293JI) ; DNA (Cytosine-5-)-Methyltransferase 1 (EC 2.1.1.37) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37) ; DAPK1 protein, human (EC 2.7.11.1) ; Death-Associated Protein Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2017-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1108734-1
    ISSN 1546-1718 ; 1061-4036
    ISSN (online) 1546-1718
    ISSN 1061-4036
    DOI 10.1038/ng.3889
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