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  1. Book: Lung cancer metastasis

    Keshamouni, Venkateshwar G.

    novel biological mechanisms and impact on clinical practice

    2009  

    Author's details Venkateshwar Keshamouni ... ed
    Language English
    Size XIII, 409 S. : Ill., 24 cm
    Publisher Springer
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT016104843
    ISBN 978-1-441-90771-4 ; 1-441-90771-8 ; 9781441907721 ; 1441907726
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2009 A 5227 order for loan Magazin

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  2. Article ; Online: Excavation of FOSL1 in the Ruins of KRAS-Driven Lung Cancer.

    Keshamouni, Venkateshwar G

    American journal of respiratory cell and molecular biology

    2018  Volume 58, Issue 5, Page(s) 551–552

    MeSH term(s) Amphiregulin ; Cell Survival ; Humans ; Lung Neoplasms ; Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins p21(ras)
    Chemical Substances Amphiregulin ; KRAS protein, human ; Proto-Oncogene Proteins c-fos ; Proto-Oncogene Proteins p21(ras) (EC 3.6.5.2)
    Language English
    Publishing date 2018-04-23
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2017-0369ED
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Immunological Consequences of Epithelial-Mesenchymal Transition in Tumor Progression.

    Chockley, Peter J / Keshamouni, Venkateshwar G

    Journal of immunology (Baltimore, Md. : 1950)

    2016  Volume 197, Issue 3, Page(s) 691–698

    Abstract: Microenvironments that tumor cells encounter are different during the stages of cancer progression-primary tumor, metastasis, and at the metastatic site. This suggests potential differences in immune surveillance of primary tumor and metastasis. ... ...

    Abstract Microenvironments that tumor cells encounter are different during the stages of cancer progression-primary tumor, metastasis, and at the metastatic site. This suggests potential differences in immune surveillance of primary tumor and metastasis. Epithelial-mesenchymal transition (EMT) is a key reversible process in which cancer cells transition into highly motile and invasive cells for dissemination. Only a tiny proportion successfully metastasize, supporting the notion of metastasis-specific immune surveillance. EMT involves extensive molecular reprogramming of cells conferring many clinically relevant features to cancer cells and affects tumor cell interactions within the tumor microenvironment. We review the impact of tumor immune infiltrates on tumor cell EMT and the consequences of EMT in shaping the immune microenvironment of tumors. The usefulness of EMT as a model to investigate metastasis-specific immune surveillance mechanisms are also explored. Finally, we discuss potential implications of EMT for tumor immunogenicity, as well as current immunotherapies and future strategies.
    MeSH term(s) Animals ; Disease Progression ; Epithelial-Mesenchymal Transition/immunology ; Humans ; Lymphocytes, Tumor-Infiltrating/immunology ; Neoplasms/immunology ; Neoplasms/pathology ; Tumor Escape/immunology ; Tumor Microenvironment/immunology
    Language English
    Publishing date 2016-08-01
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1600458
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  4. Article ; Online: Human α1 type IV collagen NC1 domain exhibits distinct antiangiogenic activity mediated by α1β1 integrin.

    Sudhakar, Akulapalli / Nyberg, Pia / Keshamouni, Venkateshwar G / Mannam, Arjuna P / Li, Jian / Sugimoto, Hikaru / Cosgrove, Dominic / Kalluri, Raghu

    The Journal of clinical investigation

    2020  Volume 130, Issue 1, Page(s) 552

    Language English
    Publishing date 2020-02-06
    Publishing country United States
    Document type Journal Article ; Retraction of Publication
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI135305
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  5. Article: Breaking the tolerance for tumor: Targeting negative regulators of TLR signaling.

    Standiford, Theodore J / Keshamouni, Venkateshwar G

    Oncoimmunology

    2012  Volume 1, Issue 3, Page(s) 340–345

    Abstract: Tumors arise and progress in immunocompetent hosts presumably by activating tolerance mechanisms critical for normal homeostasis. Host immune cells can mount anti-tumor responses by activation of Toll-like receptors (TLRs). However, emerging data ... ...

    Abstract Tumors arise and progress in immunocompetent hosts presumably by activating tolerance mechanisms critical for normal homeostasis. Host immune cells can mount anti-tumor responses by activation of Toll-like receptors (TLRs). However, emerging data suggests that molecules that negatively regulate TLRs are exploited by tumors to induce tolerance and mitigate the host immunosurveillance. Targeting these negative regulators can be a potential new immunotherapeutic strategy.
    Language English
    Publishing date 2012-01-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2645309-5
    ISSN 2162-402X ; 2162-4011
    ISSN (online) 2162-402X
    ISSN 2162-4011
    DOI 10.4161/onci.18434
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Polyarginine and its analogues inhibit p53 mutant aggregation and cancer cell proliferation in vitro.

    Chen, Zhaolin / Chen, Jun / Keshamouni, Venkateshwar G / Kanapathipillai, Mathumai

    Biochemical and biophysical research communications

    2017  Volume 489, Issue 2, Page(s) 130–134

    Abstract: Arginine, a cationic amino acid is known to stabilize proteins under harsh conditions. It is widely used to stabilize protein aggregation, and to correct protein folding during protein production. Hence it would be a good therapeutic candidate for ... ...

    Abstract Arginine, a cationic amino acid is known to stabilize proteins under harsh conditions. It is widely used to stabilize protein aggregation, and to correct protein folding during protein production. Hence it would be a good therapeutic candidate for treating protein aggregation related diseases. Recent reports suggest, that the aggregation of tumor suppressor protein p53 is one of the leading causes of tumor progression. When mutated, p53 protein aggregates, loses its function leading to unwanted cell growth and ultimately results in tumor. Here in this study we focus on the inhibitory effects of polyarginine and its analogues polyornithine, canavanine, and citrulline on the inhibition of p53 mutant peptide aggregation, and p53 mutant cancer cell proliferation inhibition in vitro. Biochemical assays and cell toxicity studies were used to characterize the study. The results show that polyarginine, and polyornithine, in micromolar concentrations, significantly inhibits p53 conserved peptide aggregation, and the cell proliferation of p53 mutant cancer cells. Hence they could be promising candidates for treating p53 mutant/misfolded protein aggregation associated cancer.
    MeSH term(s) Antineoplastic Agents/administration & dosage ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Dose-Response Relationship, Drug ; Drug Screening Assays, Antitumor ; High-Throughput Screening Assays ; Humans ; Mutation ; Neoplasms/genetics ; Neoplasms/pathology ; Peptides/administration & dosage ; Peptides/chemistry ; Peptides/pharmacology ; Protein Aggregates/drug effects ; Protein Aggregation, Pathological/drug therapy ; Protein Aggregation, Pathological/pathology ; Protein Aggregation, Pathological/prevention & control ; Structure-Activity Relationship ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Antineoplastic Agents ; Peptides ; Protein Aggregates ; Tumor Suppressor Protein p53 ; polyarginine (25212-18-4)
    Language English
    Publishing date 2017-07-22
    Publishing country United States
    Document type Journal Article
    ZDB-ID 205723-2
    ISSN 1090-2104 ; 0006-291X ; 0006-291X
    ISSN (online) 1090-2104 ; 0006-291X
    ISSN 0006-291X
    DOI 10.1016/j.bbrc.2017.05.111
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Epithelial-mesenchymal transition leads to NK cell-mediated metastasis-specific immunosurveillance in lung cancer.

    Chockley, Peter J / Chen, Jun / Chen, Guoan / Beer, David G / Standiford, Theodore J / Keshamouni, Venkateshwar G

    The Journal of clinical investigation

    2018  Volume 128, Issue 4, Page(s) 1384–1396

    Abstract: During epithelial-mesenchymal transition (EMT) epithelial cancer cells transdifferentiate into highly motile, invasive, mesenchymal-like cells, giving rise to disseminating tumor cells. Few of these disseminated cells successfully metastasize. Immune ... ...

    Abstract During epithelial-mesenchymal transition (EMT) epithelial cancer cells transdifferentiate into highly motile, invasive, mesenchymal-like cells, giving rise to disseminating tumor cells. Few of these disseminated cells successfully metastasize. Immune cells and inflammation in the tumor microenvironment were shown to drive EMT, but few studies investigated the consequences of EMT for tumor immunosurveillance. In addition to initiating metastasis, we demonstrate that EMT confers increased susceptibility to natural killer (NK) cells and contributes, in part, to the inefficiency of the metastatic process. Depletion of NK cells allowed spontaneous metastasis without affecting primary tumor growth. EMT-induced modulation of E-cadherin and cell adhesion molecule 1 (CADM1) mediated increased susceptibility to NK cytotoxicity. Higher CADM1 expression correlates with improved patient survival in 2 lung and 1 breast adenocarcinoma patient cohorts and decreased metastasis. Our observations reveal a novel NK-mediated, metastasis-specific immunosurveillance in lung cancer and present a window of opportunity for preventing metastasis by boosting NK cell activity.
    MeSH term(s) A549 Cells ; Animals ; Carcinoma, Lewis Lung/genetics ; Carcinoma, Lewis Lung/immunology ; Carcinoma, Lewis Lung/pathology ; Cell Adhesion Molecule-1/genetics ; Cell Adhesion Molecule-1/immunology ; Epithelial-Mesenchymal Transition/genetics ; Epithelial-Mesenchymal Transition/immunology ; Female ; Humans ; Immunity, Cellular ; Immunologic Surveillance ; Killer Cells, Natural/immunology ; Killer Cells, Natural/pathology ; Lung Neoplasms/genetics ; Lung Neoplasms/immunology ; Lung Neoplasms/pathology ; Male ; Mice ; Mice, Knockout ; Neoplasm Proteins/genetics ; Neoplasm Proteins/immunology ; Tumor Microenvironment/immunology
    Chemical Substances CADM1 protein, human ; Cadm1 protein, mouse ; Cell Adhesion Molecule-1 ; Neoplasm Proteins
    Language English
    Publishing date 2018-02-26
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI97611
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  8. Article ; Online: Building Career Paths for Ph.D., Basic and Translational Scientists in Clinical Departments in the United States: An Official American Thoracic Society Workshop Report.

    Moore, Bethany B / Ballinger, Megan N / Bauer, Natalie N / Blackwell, Timothy S / Borok, Zea / Budinger, G R Scott / Camoretti-Mercado, Blanca / Erzurum, Serpil C / Himes, Blanca E / Keshamouni, Venkateshwar G / Kulkarni, Hrishikesh S / Mallampalli, Rama K / Mariani, Thomas J / Martinez, Fernando J / McCombs, Janet E / Newcomb, Dawn C / Johnston, Richard A / O'Reilly, Michael A / Prakash, Y S /
    Ridge, Karen M / Sime, Patricia J / Sperling, Anne I / Violette, Shelia / Wilkes, David S / Königshoff, Melanie

    Annals of the American Thoracic Society

    2023  Volume 20, Issue 8, Page(s) 1077–1087

    Abstract: Rationale: ...

    Abstract Rationale:
    MeSH term(s) Adult ; United States ; Humans ; Child ; Academic Medical Centers ; Personnel Selection ; Leadership ; Physicians ; Faculty, Medical
    Language English
    Publishing date 2023-08-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2717461-X
    ISSN 2325-6621 ; 1943-5665 ; 2325-6621
    ISSN (online) 2325-6621 ; 1943-5665
    ISSN 2325-6621
    DOI 10.1513/AnnalsATS.202304-305ST
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  9. Article ; Online: Development of potent dimeric inhibitors of GAS41 YEATS domain.

    Listunov, Dymytrii / Linhares, Brian M / Kim, EunGi / Winkler, Alyssa / Simes, Miranda L / Weaver, Sidney / Cho, Hyo Je / Rizo, Alexandrea / Zolov, Sergey / Keshamouni, Venkateshwar G / Grembecka, Jolanta / Cierpicki, Tomasz

    Cell chemical biology

    2021  Volume 28, Issue 12, Page(s) 1716–1727.e6

    Abstract: GAS41 is an emerging oncogene overexpressed and implicated in multiple cancers, including non-small cell lung cancer (NSCLC). GAS41 is a dimeric protein that contains the YEATS domain, which is involved in the recognition of lysine-acylated histones. ... ...

    Abstract GAS41 is an emerging oncogene overexpressed and implicated in multiple cancers, including non-small cell lung cancer (NSCLC). GAS41 is a dimeric protein that contains the YEATS domain, which is involved in the recognition of lysine-acylated histones. Here, we report the development of GAS41 YEATS inhibitors by employing a fragment-based screening approach. These inhibitors bind to GAS41 YEATS domain in a channel constituting a recognition site for acylated lysine on histone proteins. To enhance inhibitory activity, we developed a dimeric analog with nanomolar activity that blocks interactions of GAS41 with acetylated histone H3. Our lead compound engages GAS41 in cells, blocks proliferation of NSCLC cells, and modulates expression of GAS41-dependent genes, validating on-target mechanism of action. This study demonstrates that disruption of GAS41 protein-protein interactions may represent an attractive approach to target lung cancer cells. This work exemplifies the use of bivalent inhibitors as a general strategy to block challenging protein-protein interactions.
    MeSH term(s) Amides/chemistry ; Amides/pharmacology ; Antineoplastic Agents/chemistry ; Antineoplastic Agents/pharmacology ; Carcinoma, Non-Small-Cell Lung/drug therapy ; Carcinoma, Non-Small-Cell Lung/metabolism ; Carcinoma, Non-Small-Cell Lung/pathology ; Cell Proliferation/drug effects ; Cells, Cultured ; Drug Screening Assays, Antitumor ; Female ; Humans ; Lung Neoplasms/drug therapy ; Lung Neoplasms/metabolism ; Lung Neoplasms/pathology ; Male ; Molecular Structure ; Protein Interaction Domains and Motifs/drug effects ; Thiophenes/chemistry ; Thiophenes/pharmacology ; Transcription Factors/antagonists & inhibitors ; Transcription Factors/metabolism
    Chemical Substances Amides ; Antineoplastic Agents ; Thiophenes ; Transcription Factors ; YEATS4 protein, human
    Language English
    Publishing date 2021-07-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ISSN 2451-9448
    ISSN (online) 2451-9448
    DOI 10.1016/j.chembiol.2021.06.010
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Epithelial-mesenchymal transition in tumor metastasis: a method to the madness.

    Keshamouni, Venkateshwar G / Schiemann, William P

    Future oncology (London, England)

    2009  Volume 5, Issue 8, Page(s) 1109–1111

    MeSH term(s) Animals ; Cell Differentiation/physiology ; Epithelium/pathology ; Humans ; Mesoderm/pathology ; Metaplasia ; Neoplasm Metastasis/pathology
    Language English
    Publishing date 2009-10-22
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2274956-1
    ISSN 1744-8301 ; 1479-6694
    ISSN (online) 1744-8301
    ISSN 1479-6694
    DOI 10.2217/fon.09.87
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