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  1. Article: Special Issue: Cancer Metastasis and Therapeutic Resistance.

    Yeh, Elizabeth S

    Biomedicines

    2023  Volume 11, Issue 5

    Abstract: Metastasis and resistance to cancer therapeutics are critical barriers to curing cancer. This special issue entitled "Cancer Metastasis and Therapeutic Resistance" contains nine original contributions. The articles span a variety of human cancers, ... ...

    Abstract Metastasis and resistance to cancer therapeutics are critical barriers to curing cancer. This special issue entitled "Cancer Metastasis and Therapeutic Resistance" contains nine original contributions. The articles span a variety of human cancers, including breast, lung, brain, prostate, and skin and touch upon significant areas of interest such as cancer stem cell function, cancer immunology, and glycosylation.
    Language English
    Publishing date 2023-05-03
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines11051347
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Mass Spectrometry-Based Glycoproteomic Workflows for Cancer Biomarker Discovery.

    Doud, Emma H / Yeh, Elizabeth S

    Technology in cancer research & treatment

    2023  Volume 22, Page(s) 15330338221148811

    Abstract: Glycosylation has a clear role in cancer initiation and progression, with numerous studies identifying distinct glycan features or specific glycoproteoforms associated with cancer. Common findings include that aggressive cancers tend to have higher ... ...

    Abstract Glycosylation has a clear role in cancer initiation and progression, with numerous studies identifying distinct glycan features or specific glycoproteoforms associated with cancer. Common findings include that aggressive cancers tend to have higher expression levels of enzymes that regulate glycosylation as well as glycoproteins with greater levels of complexity, increased branching, and enhanced chain length
    MeSH term(s) Humans ; Biomarkers, Tumor/metabolism ; Workflow ; Glycosylation ; Mass Spectrometry/methods ; Neoplasms/diagnosis ; Neoplasms/genetics ; Polysaccharides/metabolism
    Chemical Substances Biomarkers, Tumor ; Polysaccharides
    Language English
    Publishing date 2023-01-19
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2146365-7
    ISSN 1533-0338 ; 1533-0346
    ISSN (online) 1533-0338
    ISSN 1533-0346
    DOI 10.1177/15330338221148811
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5871: 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)
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  3. Article: Mapping the Anti-Cancer Activity of α-Connexin Carboxyl-Terminal (aCT1) Peptide in Resistant HER2+ Breast Cancer.

    Baker, Kimberly M / Abt, Melissa / Doud, Emma H / Oblak, Adrian L / Yeh, Elizabeth S

    Cancers

    2024  Volume 16, Issue 2

    Abstract: Connexin 43 (Cx43) is a protein encoded by ... ...

    Abstract Connexin 43 (Cx43) is a protein encoded by the
    Language English
    Publishing date 2024-01-19
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers16020423
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  4. Article: HUNK

    Ramos-Solis, Nicole / Dilday, Tinslee / Kritikos, Alex E / Yeh, Elizabeth S

    Biomedicines

    2022  Volume 10, Issue 12

    Abstract: Hormonally upregulated neu-associated kinase (HUNK) is a serine/threonine (S/T) protein kinase related to the adenosine monophosphate-activated protein kinase (AMPK) family of kinases. HUNK was originally discovered using a screen to identify kinases ... ...

    Abstract Hormonally upregulated neu-associated kinase (HUNK) is a serine/threonine (S/T) protein kinase related to the adenosine monophosphate-activated protein kinase (AMPK) family of kinases. HUNK was originally discovered using a screen to identify kinases expressed in the mouse mammary gland. Therefore, the majority of studies to date have been carried out in models specific to this tissue, and the kinase was named to reflect its mammary gland-specific physiology and pathology. Prior studies show a clear pathogenic role for HUNK in breast cancer. HUNK is upregulated in response to oncogenic HER2/neu and Akt, and there is strong evidence that HUNK is critical for the survival of breast cancer cells. Further evidence shows that inhibiting HUNK using a variety of breast cancer models, including those that are resistant, inhibits tumorigenesis and metastasis. However, HUNK alterations are infrequent. Here, the incidence and consequence of HUNK alterations in breast cancer is reviewed using data mined from the online database cBioPortal and considered in relation to prior research studies.
    Language English
    Publishing date 2022-11-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2720867-9
    ISSN 2227-9059
    ISSN 2227-9059
    DOI 10.3390/biomedicines10123072
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  5. Article ; Online: Identification and characterization of a potent and selective HUNK inhibitor for treatment of HER2+ breast cancer.

    Dilday, Tinslee / Abt, Melissa / Ramos-Solís, Nicole / Dayal, Neetu / Larocque, Elizabeth / Oblak, Adrian L / Sintim, Herman O / Yeh, Elizabeth S

    Cell chemical biology

    2024  

    Abstract: Human epidermal growth factor receptor 2 (HER2)-targeted agents have proven to be effective, however, the development of resistance to these agents has become an obstacle in treating HER2+ breast cancer. Evidence implicates HUNK as an anti-cancer target ... ...

    Abstract Human epidermal growth factor receptor 2 (HER2)-targeted agents have proven to be effective, however, the development of resistance to these agents has become an obstacle in treating HER2+ breast cancer. Evidence implicates HUNK as an anti-cancer target for primary and resistant HER2+ breast cancers. In this study, a selective inhibitor of HUNK is characterized alongside a phosphorylation event in a downstream substrate of HUNK as a marker for HUNK activity in HER2+ breast cancer. Rubicon has been established as a substrate of HUNK that is phosphorylated at serine (S) 92. Findings indicate that HUNK-mediated phosphorylation of Rubicon at S92 promotes both autophagy and tumorigenesis in HER2/neu+ breast cancer. HUNK inhibition prevents Rubicon S92 phosphorylation in HER2/neu+ breast cancer models and inhibits tumorigenesis. This study characterizes a downstream phosphorylation event as a measure of HUNK activity and identifies a selective HUNK inhibitor that has meaningful efficacy toward HER2+ breast cancer.
    Language English
    Publishing date 2024-01-25
    Publishing country United States
    Document type Journal Article
    ISSN 2451-9448
    ISSN (online) 2451-9448
    DOI 10.1016/j.chembiol.2024.01.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: The Potential for Connexin Hemichannels to Drive Breast Cancer Progression through Regulation of the Inflammatory Response.

    Rhett, J Matthew / Yeh, Elizabeth S

    International journal of molecular sciences

    2018  Volume 19, Issue 4

    Abstract: Over the past few decades, connexin hemichannels have become recognized as major players in modulating the inflammatory response. Chronic inflammation is documented to promote tumorigenesis and is a critical component of tumor progression. Furthermore, ... ...

    Abstract Over the past few decades, connexin hemichannels have become recognized as major players in modulating the inflammatory response. Chronic inflammation is documented to promote tumorigenesis and is a critical component of tumor progression. Furthermore, inflammation is strongly linked to angiogenesis, immunotolerance, invasiveness, metastasis, and resistance in breast cancers. In this review, the literature on the role of connexin hemichannels in inflammation is summarized, and the potential role for hemichannel-mediated inflammation in driving breast cancer progression is discussed. Lastly, the potential for connexin-based therapeutics to modulate the inflammatory component of the tumor microenvironment as an avenue for the treatment of breast cancer is also discussed.
    MeSH term(s) Breast Neoplasms/immunology ; Breast Neoplasms/metabolism ; Connexins/immunology ; Connexins/metabolism ; Disease Progression ; Female ; Humans ; Inflammation/immunology ; Inflammation/metabolism
    Chemical Substances Connexins
    Language English
    Publishing date 2018-03-30
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms19041043
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  7. Article: Autophagy and Apoptotic Crosstalk: Mechanism of Therapeutic Resistance in HER2-Positive Breast Cancer.

    Zambrano, Joelle / Yeh, Elizabeth S

    Breast cancer : basic and clinical research

    2016  Volume 10, Page(s) 13–23

    Abstract: While breast cancer patients benefit from the use of HER2 inhibitors, many fail therapy and become resistant to treatment, indicating a critical need to prevent treatment failure. A number of studies have emerged that highlight the catabolic process of ... ...

    Abstract While breast cancer patients benefit from the use of HER2 inhibitors, many fail therapy and become resistant to treatment, indicating a critical need to prevent treatment failure. A number of studies have emerged that highlight the catabolic process of autophagy in breast cancer as a mechanism of resistance to chemotherapy and targeted inhibitors. Furthermore, recent research has begun to dissect how autophagy signaling crosstalks with apoptotic signaling. Thus, a possible strategy in fighting resistance is to couple targeting of apoptotic and autophagy signaling pathways. In this review, we discuss how cellular response by autophagy circumvents cell death to promote resistance of breast cancers to HER2 inhibitors, as well as the potential avenues of therapeutic intervention.
    Language English
    Publishing date 2016-03-13
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2423804-1
    ISSN 1178-2234
    ISSN 1178-2234
    DOI 10.4137/BCBCR.S32791
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Uncoupling of p97 ATPase activity has a dominant negative effect on protein extraction.

    Rycenga, Halley B / Wolfe, Kelly B / Yeh, Elizabeth S / Long, David T

    Scientific reports

    2019  Volume 9, Issue 1, Page(s) 10329

    Abstract: p97 is a highly abundant, homohexameric AAA+ ATPase that performs a variety of essential cellular functions. Characterized as a ubiquitin-selective chaperone, p97 recognizes proteins conjugated to K48-linked polyubiquitin chains and promotes their ... ...

    Abstract p97 is a highly abundant, homohexameric AAA+ ATPase that performs a variety of essential cellular functions. Characterized as a ubiquitin-selective chaperone, p97 recognizes proteins conjugated to K48-linked polyubiquitin chains and promotes their removal from chromatin and other molecular complexes. Changes in p97 expression or activity are associated with the development of cancer and several related neurodegenerative disorders. Although pathogenic p97 mutations cluster in and around p97's ATPase domains, mutant proteins display normal or elevated ATPase activity. Here, we show that one of the most common p97 mutations (R155C) retains ATPase activity, but is functionally defective. p97-R155C can be recruited to ubiquitinated substrates on chromatin, but is unable to promote substrate removal. As a result, p97-R155C acts as a dominant negative, blocking protein extraction by a similar mechanism to that observed when p97's ATPase activity is inhibited or inactivated. However, unlike ATPase-deficient proteins, p97-R155C consumes excess ATP, which can hinder high-energy processes. Together, our results shed new insight into how pathogenic mutations in p97 alter its cellular function, with implications for understanding the etiology and treatment of p97-associated diseases.
    MeSH term(s) Adenosine Triphosphatases/chemistry ; Adenosine Triphosphatases/genetics ; Adenosine Triphosphatases/metabolism ; Amino Acid Substitution ; Animals ; Cell Line, Tumor ; Chromatin/metabolism ; DNA/metabolism ; Female ; Humans ; In Vitro Techniques ; Mutant Proteins/chemistry ; Mutant Proteins/genetics ; Mutant Proteins/metabolism ; Mutation, Missense ; Neoplasms/enzymology ; Neoplasms/genetics ; Nuclear Proteins/chemistry ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Oocytes/metabolism ; Protein Subunits ; Recombinant Proteins/chemistry ; Recombinant Proteins/genetics ; Recombinant Proteins/metabolism ; Substrate Specificity ; Ubiquitin/metabolism ; Xenopus laevis
    Chemical Substances Chromatin ; Mutant Proteins ; Nuclear Proteins ; Protein Subunits ; Recombinant Proteins ; Ubiquitin ; DNA (9007-49-2) ; Adenosine Triphosphatases (EC 3.6.1.-) ; p97 ATPase (EC 3.6.1.-)
    Language English
    Publishing date 2019-07-17
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-019-46949-4
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Hormonally up-regulated neu-associated kinase: A novel target for breast cancer progression.

    Zambrano, Joelle N / Neely, Benjamin A / Yeh, Elizabeth S

    Pharmacological research

    2017  Volume 119, Page(s) 188–194

    Abstract: Hormonally up-regulated neu-associated Kinase (Hunk) is a protein kinase that was originally identified in the murine mammary gland and has been shown to be highly expressed in Human Epidermal Growth Factor Receptor 2 positive ( ... ...

    Abstract Hormonally up-regulated neu-associated Kinase (Hunk) is a protein kinase that was originally identified in the murine mammary gland and has been shown to be highly expressed in Human Epidermal Growth Factor Receptor 2 positive (HER2
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; Breast/drug effects ; Breast/metabolism ; Breast/pathology ; Breast Neoplasms/drug therapy ; Breast Neoplasms/metabolism ; Breast Neoplasms/pathology ; Drug Resistance, Neoplasm ; Female ; Humans ; Molecular Targeted Therapy/methods ; Neoplasm Metastasis/pathology ; Neoplasm Metastasis/prevention & control ; Protein Serine-Threonine Kinases/analysis ; Protein Serine-Threonine Kinases/metabolism ; Receptor, ErbB-2/analysis ; Receptor, ErbB-2/metabolism
    Chemical Substances Antineoplastic Agents ; ERBB2 protein, human (EC 2.7.10.1) ; Receptor, ErbB-2 (EC 2.7.10.1) ; HUNK protein, human (EC 2.7.11.1) ; Protein Serine-Threonine Kinases (EC 2.7.11.1)
    Language English
    Publishing date 2017-02-09
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1003347-6
    ISSN 1096-1186 ; 0031-6989 ; 1043-6618
    ISSN (online) 1096-1186
    ISSN 0031-6989 ; 1043-6618
    DOI 10.1016/j.phrs.2017.02.007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 721: 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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  10. Article: Tumor-associated macrophages: unwitting accomplices in breast cancer malignancy.

    Williams, Carly Bess / Yeh, Elizabeth S / Soloff, Adam C

    NPJ breast cancer

    2016  Volume 2

    Abstract: Deleterious inflammation is a primary feature of breast cancer. Accumulating evidence demonstrates that macrophages, the most abundant leukocyte population in mammary tumors, have a critical role at each stage of cancer progression. Such tumor-associated ...

    Abstract Deleterious inflammation is a primary feature of breast cancer. Accumulating evidence demonstrates that macrophages, the most abundant leukocyte population in mammary tumors, have a critical role at each stage of cancer progression. Such tumor-associated macrophages facilitate neoplastic transformation, tumor immune evasion and the subsequent metastatic cascade. Herein, we discuss the dynamic process whereby molecular and cellular features of the tumor microenvironment act to license tissue-repair mechanisms of macrophages, fostering angiogenesis, metastasis and the support of cancer stem cells. We illustrate how tumors induce, then exploit trophic macrophages to subvert innate and adaptive immune responses capable of destroying malignant cells. Finally, we discuss compelling evidence from murine models of cancer and early clinical trials in support of macrophage-targeted intervention strategies with the potential to dramatically reduce breast cancer morbidity and mortality.
    Language English
    Publishing date 2016-01-20
    Publishing country United States
    Document type Journal Article
    ISSN 2374-4677
    ISSN 2374-4677
    DOI 10.1038/npjbcancer.2015.25
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