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  1. Article ; Online: The cross talk between cancer cells and their microenvironments.

    Witz, Isaac P

    Biochemical and biophysical research communications

    2022  Volume 633, Page(s) 59–60

    MeSH term(s) Tumor Microenvironment ; Neoplasms
    Language English
    Publishing date 2022-09-12
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't
    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.2022.09.066
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 116: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Book ; Conference proceedings: Proceedings of the 4th International Conference on Tumor Microenvironment

    Witz, Isaac P.

    progression, therapy and prevention ; Florence, Italy, March 6 - 10, 2007

    2007  

    Event/congress International Conference on Tumor Microenvironment (4, 2007, Florenz)
    Author's details ed. Isaac P. Witz
    Language English
    Size IX, 174 S. : Ill., graph. Darst.
    Publisher Medimond
    Publishing place Bologna
    Publishing country Italy
    Document type Book ; Conference proceedings
    HBZ-ID HT015390367
    ISBN 978-88-7587-346-2 ; 88-7587-346-1
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2008 A 622 order for loan Magazin

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  3. Book ; Conference proceedings: Proceedings of the 3rd International Conference on Tumor Microenvironment

    Witz, Isaac P.

    progression, therapy and prevention ; Prague, Czech Republic, October 12 - 16, 2004

    2005  

    Event/congress International Conference on Tumor Microenvironment (3, 2004, Prag)
    Author's details ed. Isaac P. Witz
    Language English
    Size IX, 148 S. : graph. Darst.
    Publisher Medimond
    Publishing place Bologna
    Publishing country Italy
    Document type Book ; Conference proceedings
    HBZ-ID HT014559383
    ISBN 88-7587-135-3 ; 978-88-7587-135-2
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2005 A 5197 order for loan Magazin

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  4. Book ; Conference proceedings: Proceedings of the 2nd International Conference on Tumor Microenvironment

    Witz, Isaac P.

    progression, therapy & prevention ; Baden, Austria, June 25 - 29, 2002

    2002  

    Event/congress International Conference on Tumor Microenvironment (2, 2002, BadenNiederösterreich)
    Author's details ed. Isaac P. Witz
    Language English
    Size X, 247 S. : Ill., graph. Darst.
    Publisher Monduzzi
    Publishing place Bologna
    Publishing country Italy
    Document type Book ; Conference proceedings
    HBZ-ID HT013819242
    ISBN 88-323-2625-6 ; 978-88-323-2625-3
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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    2003 A 4600 order for loan Magazin

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  5. Article ; Online: Site-specific metastasis: A cooperation between cancer cells and the metastatic microenvironment.

    Izraely, Sivan / Witz, Isaac P

    International journal of cancer

    2020  Volume 148, Issue 6, Page(s) 1308–1322

    Abstract: The conclusion derived from the information provided in this review is that disseminating tumor cells (DTC) collaborate with the microenvironment of a future metastatic organ site in the establishment of organ-specific metastasis. We review the basic ... ...

    Abstract The conclusion derived from the information provided in this review is that disseminating tumor cells (DTC) collaborate with the microenvironment of a future metastatic organ site in the establishment of organ-specific metastasis. We review the basic principles of site-specific metastasis and the contribution of the cross talk between DTC and the microenvironment of metastatic sites (metastatic microenvironment [MME]) to the establishment of the organ-specific premetastatic niche; the targeted migration of DTC to the endothelium of the future organ-specific metastasis; the transmigration of DTC to this site and the seeding and colonization of DTC in their future MME. We also discuss the role played by DTC-MME interactions on tumor dormancy and on the differential response of tumor cells residing in different MMEs to antitumor therapy. Finally, we summarize some studies dealing with the effects of the MME on a unique site-specific metastasis-brain metastasis.
    MeSH term(s) Animals ; Humans ; Neoplasm Metastasis/pathology ; Neoplastic Cells, Circulating/pathology ; Tumor Microenvironment/physiology
    Language English
    Publishing date 2020-08-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 218257-9
    ISSN 1097-0215 ; 0020-7136
    ISSN (online) 1097-0215
    ISSN 0020-7136
    DOI 10.1002/ijc.33247
    Database MEDical Literature Analysis and Retrieval System OnLINE

    Full text online

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 478: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 576: Show issues

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  6. Article ; Online: A history of exploring cancer in context.

    Maman, Shelly / Witz, Isaac P

    Nature reviews. Cancer

    2018  Volume 18, Issue 6, Page(s) 359–376

    Abstract: The concept that progression of cancer is regulated by interactions of cancer cells with their microenvironment was postulated by Stephen Paget over a century ago. Contemporary tumour microenvironment (TME) research focuses on the identification of ... ...

    Abstract The concept that progression of cancer is regulated by interactions of cancer cells with their microenvironment was postulated by Stephen Paget over a century ago. Contemporary tumour microenvironment (TME) research focuses on the identification of tumour-interacting microenvironmental constituents, such as resident or infiltrating non-tumour cells, soluble factors and extracellular matrix components, and the large variety of mechanisms by which these constituents regulate and shape the malignant phenotype of tumour cells. In this Timeline article, we review the developmental phases of the TME paradigm since its initial description. While illuminating controversies, we discuss the importance of interactions between various microenvironmental components and tumour cells and provide an overview and assessment of therapeutic opportunities and modalities by which the TME can be targeted.
    MeSH term(s) Biomedical Research/history ; Cancer-Associated Fibroblasts ; Cell Movement ; Disease Progression ; Extracellular Matrix/metabolism ; Gene Expression Regulation, Neoplastic/genetics ; History, 20th Century ; History, 21st Century ; Humans ; Immunoglobulins/immunology ; Inflammation/immunology ; Lymphocytes/immunology ; Lymphocytes, Tumor-Infiltrating/immunology ; Metabolomics ; Microbiota ; Myeloid Cells/immunology ; Neoplasm Metastasis ; Neoplasms/blood supply ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/pathology ; Neoplastic Stem Cells ; Neovascularization, Pathologic ; Tumor Microenvironment
    Chemical Substances Immunoglobulins
    Language English
    Publishing date 2018-05-30
    Publishing country England
    Document type Historical Article ; Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2062767-1
    ISSN 1474-1768 ; 1474-175X
    ISSN (online) 1474-1768
    ISSN 1474-175X
    DOI 10.1038/s41568-018-0006-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5563: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MG 24: Show issues

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  7. Article: Heterogeneity in the Metastatic Microenvironment: JunB-Expressing Microglia Cells as Potential Drivers of Melanoma Brain Metastasis Progression.

    Adir, Orit / Sagi-Assif, Orit / Meshel, Tsipi / Ben-Menachem, Shlomit / Pasmanik-Chor, Metsada / Hoon, Dave S B / Witz, Isaac P / Izraely, Sivan

    Cancers

    2023  Volume 15, Issue 20

    Abstract: Reciprocal signaling between melanoma brain metastatic (MBM) cells and microglia reprograms the phenotype of both interaction partners, including upregulation of the transcription factor JunB in microglia. Here, we aimed to elucidate the impact of ... ...

    Abstract Reciprocal signaling between melanoma brain metastatic (MBM) cells and microglia reprograms the phenotype of both interaction partners, including upregulation of the transcription factor JunB in microglia. Here, we aimed to elucidate the impact of microglial JunB upregulation on MBM progression. For molecular profiling, we employed RNA-seq and reverse-phase protein array (RPPA). To test microglial JunB functions, we generated microglia variants stably overexpressing JunB (JunB
    Language English
    Publishing date 2023-10-13
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers15204979
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Book: In situ expression of tumor immunity

    Witz, Isaac P.

    (Contemporary topics in immunobiology ; 10)

    1980  

    Author's details ed. by Isaac P. Witz
    Series title Contemporary topics in immunobiology ; 10
    Collection
    Keywords Immunbiologie
    Subject Immunobiologie
    Language English
    Size XVIII, 348 S.
    Publisher Plenum Pr
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT004797074
    ISBN 0-306-40387-0 ; 978-0-306-40387-3
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    Se 168 -10- verfügbar in Königswinter Königswinter

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  9. Article ; Online: A heterodimer of α and β hemoglobin chains functions as an innate anticancer agent.

    Chelladurai, Maharrish / Xu, Dan / Izraely, Sivan / Ben-Menachem, Shlomit / Bengaiev, Roman / Sagi-Assif, Orit / Yuan, Weirong / Pasmanik Chor, Metsada / Hoon, Dave S / Lu, Wuyuan / Witz, Isaac P

    International journal of cancer

    2023  Volume 154, Issue 3, Page(s) 561–572

    Abstract: Metastatic (as well as tumor) microenvironments contain both cancer-promoting and cancer-restraining factors. The balance between these opposing forces determines the fate of cancer cells that disseminate to secondary organ sites. In search for ... ...

    Abstract Metastatic (as well as tumor) microenvironments contain both cancer-promoting and cancer-restraining factors. The balance between these opposing forces determines the fate of cancer cells that disseminate to secondary organ sites. In search for microenvironmental drivers or inhibitors of metastasis, we identified, in a previous study, the beta subunit of hemoglobin (HBB) as a lung-derived antimetastatic factor. In the present study, exploring mechanisms regulating melanoma brain metastasis, we discovered that brain-derived factors restrain proliferation and induce apoptosis and necrosis of brain-metastasizing melanoma cells. Employing various purification procedures, we identified a heterodimer composed of hemoglobin alpha and beta chains that perform these antimetastatic functions. Neither the alpha nor the beta subunit alone was inhibitory. An alpha/beta chain dimer chemically purified from human hemoglobin inhibited the cell viability of primary melanomas, melanoma brain metastasis (MBM), and breast cancer cell lines. The dimer-induced DNA damage, cell cycle arrest at the SubG1 phase, apoptosis, and significant necrosis in four MBM cell lines. Proteomic analysis of dimer-treated MBM cells revealed that the dimer downregulates the expression of BRD4, GAB2, and IRS2 proteins, playing crucial roles in cancer cell sustainability and progression. Thus, we hypothesize that the hemoglobin dimer functions as a resistance factor against brain-metastasizing cancer cells.
    MeSH term(s) Humans ; Melanoma/genetics ; Nuclear Proteins ; Proteomics ; Transcription Factors ; Brain Neoplasms/genetics ; Hemoglobins ; Antineoplastic Agents/pharmacology ; Necrosis ; Cell Line, Tumor ; Tumor Microenvironment ; Bromodomain Containing Proteins ; Cell Cycle Proteins
    Chemical Substances Nuclear Proteins ; Transcription Factors ; Hemoglobins ; Antineoplastic Agents ; BRD4 protein, human ; Bromodomain Containing Proteins ; Cell Cycle Proteins
    Language English
    Publishing date 2023-09-07
    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.34702
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 478: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)
    Zs.MO 576: Show issues

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  10. Article ; Online: The Vicious Cycle of Melanoma-Microglia Crosstalk: Inter-Melanoma Variations in the Brain-Metastasis-Promoting IL-6/JAK/STAT3 Signaling Pathway.

    Izraely, Sivan / Ben-Menachem, Shlomit / Malka, Sapir / Sagi-Assif, Orit / Bustos, Matias A / Adir, Orit / Meshel, Tsipi / Chelladurai, Maharrish / Ryu, Suyeon / Ramos, Romela I / Pasmanik-Chor, Metsada / Hoon, Dave S B / Witz, Isaac P

    Cells

    2023  Volume 12, Issue 11

    Abstract: Previous studies from our lab demonstrated that the crosstalk between brain-metastasizing melanoma cells and microglia, the macrophage-like cells of the central nervous system, fuels progression to metastasis. In the present study, an in-depth ... ...

    Abstract Previous studies from our lab demonstrated that the crosstalk between brain-metastasizing melanoma cells and microglia, the macrophage-like cells of the central nervous system, fuels progression to metastasis. In the present study, an in-depth investigation of melanoma-microglia interactions elucidated a pro-metastatic molecular mechanism that drives a vicious melanoma-brain-metastasis cycle. We employed RNA-Sequencing, HTG miRNA whole transcriptome assay, and reverse phase protein arrays (RPPA) to analyze the impact of melanoma-microglia interactions on sustainability and progression of four different human brain-metastasizing melanoma cell lines. Microglia cells exposed to melanoma-derived IL-6 exhibited upregulated levels of STAT3 phosphorylation and SOCS3 expression, which, in turn, promoted melanoma cell viability and metastatic potential. IL-6/STAT3 pathway inhibitors diminished the pro-metastatic functions of microglia and reduced melanoma progression. SOCS3 overexpression in microglia cells evoked microglial support in melanoma brain metastasis by increasing melanoma cell migration and proliferation. Different melanomas exhibited heterogeneity in their microglia-activating capacity as well as in their response to microglia-derived signals. In spite of this reality and based on the results of the present study, we concluded that the activation of the IL-6/STAT3/SOCS3 pathway in microglia is a major mechanism by which reciprocal melanoma-microglia signaling engineers the interacting microglia to reinforce the progression of melanoma brain metastasis. This mechanism may operate differently in different melanomas.
    MeSH term(s) Humans ; Microglia/metabolism ; Interleukin-6/metabolism ; Signal Transduction ; Suppressor of Cytokine Signaling Proteins/genetics ; Suppressor of Cytokine Signaling Proteins/metabolism ; Melanoma/pathology ; Brain Neoplasms/metabolism ; Brain/metabolism ; STAT3 Transcription Factor/metabolism
    Chemical Substances Interleukin-6 ; Suppressor of Cytokine Signaling Proteins ; STAT3 protein, human ; STAT3 Transcription Factor
    Language English
    Publishing date 2023-05-30
    Publishing country Switzerland
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells12111513
    Database MEDical Literature Analysis and Retrieval System OnLINE

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