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  1. Article: Emergence of

    Kufe, Donald W

    Cancers

    2022  Volume 14, Issue 19

    Abstract: ... ...

    Abstract The
    Language English
    Publishing date 2022-09-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers14194805
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article: Chronic activation of MUC1-C in wound repair promotes progression to cancer stem cells.

    Kufe, Donald W

    Journal of cancer metastasis and treatment

    2022  Volume 8

    Abstract: ... ...

    Abstract The
    Language English
    Publishing date 2022-03-31
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2819994-7
    ISSN 2394-4722
    ISSN 2394-4722
    DOI 10.20517/2394-4722.2022.03
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  3. Article ; Online: MUC1-C in chronic inflammation and carcinogenesis; emergence as a target for cancer treatment.

    Kufe, Donald W

    Carcinogenesis

    2020  Volume 41, Issue 9, Page(s) 1173–1183

    Abstract: Chronic inflammation is a highly prevalent consequence of changes in environmental and lifestyle factors that contribute to the development of cancer. The basis for this critical association has largely remained unclear. The MUC1 gene evolved in mammals ... ...

    Abstract Chronic inflammation is a highly prevalent consequence of changes in environmental and lifestyle factors that contribute to the development of cancer. The basis for this critical association has largely remained unclear. The MUC1 gene evolved in mammals to protect epithelia from the external environment. The MUC1-C subunit promotes responses found in wound healing and cancer. MUC1-C induces EMT, epigenetic reprogramming, dedifferentiation and pluripotency factor expression, which when prolonged in chronic inflammation promote cancer progression. As discussed in this review, MUC1-C also drives drug resistance and immune evasion, and is an important target for cancer therapeutics now under development.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Carcinogenesis/drug effects ; Carcinogenesis/metabolism ; Carcinogenesis/pathology ; Gene Expression Regulation, Neoplastic/drug effects ; Humans ; Inflammation/drug therapy ; Inflammation/metabolism ; Inflammation/pathology ; Mucin-1/genetics ; Mucin-1/metabolism ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/pathology
    Chemical Substances Antineoplastic Agents ; Mucin-1
    Language English
    Publishing date 2020-07-24
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 603134-1
    ISSN 1460-2180 ; 0143-3334
    ISSN (online) 1460-2180
    ISSN 0143-3334
    DOI 10.1093/carcin/bgaa082
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1558: Show issues Location:
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  4. Article: MUC1-C is a target of salinomycin in inducing ferroptosis of cancer stem cells.

    Daimon, Tatsuaki / Bhattacharya, Atrayee / Wang, Keyi / Haratake, Naoki / Nakashoji, Ayako / Ozawa, Hiroki / Morimoto, Yoshihiro / Yamashita, Nami / Kosaka, Takeo / Oya, Mototsugu / Kufe, Donald W

    Cell death discovery

    2024  Volume 10, Issue 1, Page(s) 9

    Abstract: The oncogenic MUC1-C transmembrane protein is a critical effector of the cancer stem cell (CSC) state. Addiction to MUC1-C for self-renewal in the progression of human cancers has emphasized the need for development of anti-MUC1-C agents. However, there ... ...

    Abstract The oncogenic MUC1-C transmembrane protein is a critical effector of the cancer stem cell (CSC) state. Addiction to MUC1-C for self-renewal in the progression of human cancers has emphasized the need for development of anti-MUC1-C agents. However, there are presently no approved small molecules for targeting MUC1-C-dependent CSCs. In screening for small molecules, we identified salinomycin (SAL), an inducer of ferroptosis, as a potent inhibitor of MUC1-C signaling. We demonstrate that SAL suppresses MUC1-C expression by disrupting a NF-κB/MUC1-C auto-inductive circuit that is necessary for ferroptosis resistance. Our results show that SAL-induced MUC1-C suppression downregulates a MUC1-C→MYC pathway that activates genes encoding (i) glutathione-disulfide reductase (GSR), and (ii) the LDL receptor related protein 8 (LRP8), which inhibit ferroptosis by generating GSH and regulating selenium levels, respectively. GSR and LRP8 contribute to the function of glutathione peroxidase 4 (GPX4), an essential negative regulator of ferroptotic cell death. We demonstrate that targeting MUC1-C genetically or with the GO-203 peptide inhibitor suppresses GPX4 expression and GPX activity in association with the induction of ferroptosis. Studies of CSCs enriched by serial passage as tumorspheres further demonstrate that the effects of SAL are mediated by downregulation of MUC1-C and thereby overcoming resistance to ferroptosis. As confirmation of these results, rescue of MUC1-C downregulation with the MUC1-C cytoplasmic domain (i) reversed the suppression of GSR, LRP8 and GPX4 expression, and (ii) attenuated the induction of ferroptosis. These findings identify SAL as a unique small molecule inhibitor of MUC1-C signaling and demonstrate that MUC1-C is an important effector of resistance to ferroptosis.
    Language English
    Publishing date 2024-01-05
    Publishing country United States
    Document type Journal Article
    ISSN 2058-7716
    ISSN 2058-7716
    DOI 10.1038/s41420-023-01772-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Book: Cancer medicine

    Holland, James F. / Frei, Emil / Kufe, Donald W.

    2006  

    Title variant Cancer medicine 7 ; Holland - Frei cancer medicine 7
    Institution American Association for Cancer Research
    Author's details Holland ; Frei. Ed. Donald W. Kufe ... AACR American Association for Cancer Research
    Keywords Neoplasms
    Language English
    Size XXIII, 2328 S. : Ill., graph. Darst.
    Edition 7. [ed.]
    Publisher Decker
    Publishing place Hamilton u.a.
    Publishing country Canada
    Document type Book
    Note Zugang zu Online-Edition "Cancer medicine 7" über Website ; 6. Aufl. in 2 Bänden erschienen
    HBZ-ID HT014706750
    ISBN 1-55009-307-X ; 978-1-55009-307-0
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2006 C 69 order for loan Magazin
    2010 C 36 order for loan Magazin

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  6. Article ; Online: Functional targeting of the MUC1 oncogene in human cancers.

    Kufe, Donald W

    Cancer biology & therapy

    2009  Volume 8, Issue 13, Page(s) 1197–1203

    MeSH term(s) Amino Acid Sequence ; Antineoplastic Agents/therapeutic use ; Cell Transformation, Neoplastic/genetics ; Humans ; Molecular Sequence Data ; Mucin-1/genetics ; Mucin-1/metabolism ; Mutation ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Protein Subunits/genetics ; Protein Subunits/metabolism ; Signal Transduction/drug effects
    Chemical Substances Antineoplastic Agents ; MUC1 protein, human ; Mucin-1 ; Protein Subunits
    Language English
    Publishing date 2009-07-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2146305-0
    ISSN 1555-8576 ; 1538-4047
    ISSN (online) 1555-8576
    ISSN 1538-4047
    DOI 10.4161/cbt.8.13.8844
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5887: Show issues Location:
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  7. Book: Cancer medicine / 1

    Holland, James F. / Frei, Emil / Kufe, Donald W.

    2003  

    Institution American Cancer Society
    Author's details Holland ; Frei. Ed. Donald W. Kufe ... An approved publication of the American Cancer Society
    Collection Cancer medicine
    Language English
    Size XXIV, 1191, 40 S. : Ill., graph. Darst.
    Publisher Decker
    Publishing place Hamilton u.a.
    Publishing country Canada
    Document type Book
    HBZ-ID HT013751443
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2005 C 133 order for loan Magazin
    2008 C 95 order for loan Magazin

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  8. Book: Cancer medicine / 2

    Holland, James F. / Frei, Emil / Kufe, Donald W.

    2003  

    Institution American Cancer Society
    Author's details Holland ; Frei. Ed. Donald W. Kufe ... An approved publication of the American Cancer Society
    Collection Cancer medicine
    Language English
    Size XXIV S., S. 1196 - 2699, 40 S. : Ill., graph. Darst.
    Publisher Decker
    Publishing place Hamilton u.a.
    Publishing country Canada
    Document type Book
    HBZ-ID HT013751519
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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  9. Article ; Online: MUC1-C is necessary for SHP2 activation and BRAF inhibitor resistance in BRAF(V600E) mutant colorectal cancer.

    Morimoto, Yoshihiro / Yamashita, Nami / Hirose, Haruka / Fushimi, Atsushi / Haratake, Naoki / Daimon, Tatsuaki / Bhattacharya, Atrayee / Ahmad, Rehan / Suzuki, Yozo / Takahashi, Hidekazu / Kufe, Donald W

    Cancer letters

    2023  Volume 559, Page(s) 216116

    Abstract: Colorectal cancers (CRCs) harboring the BRAF(V600E) mutation are associated with aggressive disease and resistance to BRAF inhibitors by feedback activation of the receptor tyrosine kinase (RTK)→RAS→MAPK pathway. The oncogenic MUC1-C protein promotes ... ...

    Abstract Colorectal cancers (CRCs) harboring the BRAF(V600E) mutation are associated with aggressive disease and resistance to BRAF inhibitors by feedback activation of the receptor tyrosine kinase (RTK)→RAS→MAPK pathway. The oncogenic MUC1-C protein promotes progression of colitis to CRC; whereas there is no known involvement of MUC1-C in BRAF(V600E) CRCs. The present work demonstrates that MUC1 expression is significantly upregulated in BRAF(V600E) vs wild-type CRCs. We show that BRAF(V600E) CRC cells are dependent on MUC1-C for proliferation and BRAF inhibitor (BRAFi) resistance. Mechanistically, MUC1-C integrates induction of MYC in driving cell cycle progression with activation of the SHP2 phosphotyrosine phosphatase, which enhances RTK-mediated RAS→ERK signaling. We demonstrate that targeting MUC1-C genetically and pharmacologically suppresses (i) activation of MYC, (ii) induction of the NOTCH1 stemness factor, and (iii) the capacity for self-renewal. We also show that MUC1-C associates with SHP2 and is required for SHP2 activation in driving BRAFi-induced feedback of ERK signaling. In this way, targeting MUC1-C in BRAFi-resistant BRAF(V600E) CRC tumors inhibits growth and sensitizes to BRAF inhibition. These findings demonstrate that MUC1-C is a target for the treatment of BRAF(V600E) CRCs and for reversing their resistance to BRAF inhibitors by suppressing the feedback MAPK pathway.
    MeSH term(s) Humans ; Cell Line, Tumor ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/metabolism ; Mucin-1/genetics ; Mutation ; Protein Kinase Inhibitors/pharmacology ; Proto-Oncogene Proteins B-raf ; Receptor Protein-Tyrosine Kinases/genetics ; Signal Transduction
    Chemical Substances BRAF protein, human (EC 2.7.11.1) ; MUC1 protein, human ; Mucin-1 ; Protein Kinase Inhibitors ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1) ; PTPN11 protein, human (EC 3.1.3.48)
    Language English
    Publishing date 2023-03-05
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2023.216116
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1177: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  10. Article ; Online: Mucins in cancer: function, prognosis and therapy.

    Kufe, Donald W

    Nature reviews. Cancer

    2009  Volume 9, Issue 12, Page(s) 874–885

    Abstract: Epithelia are protected from adverse conditions by a mucous barrier. The secreted and transmembrane mucins that constitute the mucous barrier are largely unrecognized as effectors of carcinogenesis. However, both types of mucins are intimately involved ... ...

    Abstract Epithelia are protected from adverse conditions by a mucous barrier. The secreted and transmembrane mucins that constitute the mucous barrier are largely unrecognized as effectors of carcinogenesis. However, both types of mucins are intimately involved in inflammation and cancer. Moreover, diverse human malignancies overexpress transmembrane mucins to exploit their role in signalling cell growth and survival. Mucins have thus been identified as markers of adverse prognosis and as attractive therapeutic targets. Notably, the findings that certain transmembrane mucins induce transformation and promote tumour progression have provided the experimental basis for demonstrating that inhibitors of their function are effective as anti-tumour agents in preclinical models.
    MeSH term(s) Antineoplastic Agents ; Biomarkers, Tumor/metabolism ; Cell Transformation, Neoplastic/metabolism ; Drug Design ; Humans ; Mucins/antagonists & inhibitors ; Mucins/metabolism ; Neoplasms/diagnosis ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Receptor Protein-Tyrosine Kinases/metabolism
    Chemical Substances Antineoplastic Agents ; Biomarkers, Tumor ; Mucins ; Receptor Protein-Tyrosine Kinases (EC 2.7.10.1)
    Language English
    Publishing date 2009-12-24
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2062767-1
    ISSN 1474-1768 ; 1474-175X
    ISSN (online) 1474-1768
    ISSN 1474-175X
    DOI 10.1038/nrc2761
    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:
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    Zs.MG 24: Show issues

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