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  1. Article ; Online: Omaveloxolone attenuates squamous cell carcinoma growth and disease severity in an Epidermolysis Bullosa mouse model.

    Cohen-Nowak, Adam J / Cohen, Alexa J / Correia, Emily D / Portocarrero, Carla P / South, Andrew P / Nikbakht, Neda

    Experimental dermatology

    2022  Volume 31, Issue 7, Page(s) 1083–1088

    Abstract: Patients with epidermolysis bullosa (EB) are susceptible to development of squamous cell carcinomas (SCC) at sites of chronic inflammation and fibrosis. While triterpenoids such as RTA 408 (Omaveloxolone) have been shown to reduce inflammation and ... ...

    Abstract Patients with epidermolysis bullosa (EB) are susceptible to development of squamous cell carcinomas (SCC) at sites of chronic inflammation and fibrosis. While triterpenoids such as RTA 408 (Omaveloxolone) have been shown to reduce inflammation and inhibit tumour growth in various cancer models, the utility of this class of drugs in the treatment of SCC has not been investigated. Given the dual anti-inflammatory and anti-neoplastic properties of triterpenoids, we hypothesized RTA 408 would be an effective treatment for SCCs that arise in the chronic inflammatory setting in EB. We tested the effects of topical RTA 408 on a mouse model of non-Herlitz, junctional EB. RTA 408 significantly reduced phenotypic severity in the affected ears of Lamc2jeb mice. In cultures, RTA 408 reduced cell viability in EB-associated SCC cell lines and normal human epidermal keratinocytes. When administered in vivo, RTA 408 inhibited SCC tumour growth in mice without cutaneous or systemic toxicity. These results suggest that RTA 408 can be a promising new therapy to reduce inflammation and inhibit SCC growth in patients with EB.
    MeSH term(s) Animals ; Carcinoma, Squamous Cell/metabolism ; Epidermolysis Bullosa/pathology ; Epidermolysis Bullosa Dystrophica ; Humans ; Inflammation ; Mice ; Severity of Illness Index ; Skin Neoplasms/metabolism ; Triterpenes/pharmacology ; Triterpenes/therapeutic use
    Chemical Substances Triterpenes ; omaveloxolone (G69Z98951Q)
    Language English
    Publishing date 2022-03-31
    Publishing country Denmark
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1130936-2
    ISSN 1600-0625 ; 0906-6705
    ISSN (online) 1600-0625
    ISSN 0906-6705
    DOI 10.1111/exd.14564
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3508: 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)

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  2. Article ; Online: Akt is required for Stat5 activation and mammary differentiation.

    Chen, Chien-Chung / Boxer, Robert B / Stairs, Douglas B / Portocarrero, Carla P / Horton, Rachel H / Alvarez, James V / Birnbaum, Morris J / Chodosh, Lewis A

    Breast cancer research : BCR

    2010  Volume 12, Issue 5, Page(s) R72

    Abstract: Introduction: The Akt pathway plays a central role in regulating cell survival, proliferation and metabolism, and is one of the most commonly activated pathways in human cancer. A role for Akt in epithelial differentiation, however, has not been ... ...

    Abstract Introduction: The Akt pathway plays a central role in regulating cell survival, proliferation and metabolism, and is one of the most commonly activated pathways in human cancer. A role for Akt in epithelial differentiation, however, has not been established. We previously reported that mice lacking Akt1, but not Akt2, exhibit a pronounced metabolic defect during late pregnancy and lactation that results from a failure to upregulate Glut1 as well as several lipid synthetic enzymes. Despite this metabolic defect, however, both Akt1-deficient and Akt2-deficient mice exhibit normal mammary epithelial differentiation and Stat5 activation.
    Methods: In light of the overlapping functions of Akt family members, we considered the possibility that Akt may play an essential role in regulating mammary epithelial development that is not evident in Akt1-deficient mice due to compensation by other Akt isoforms. To address this possibility, we interbred mice bearing targeted deletions in Akt1 and Akt2 and determined the effect on mammary differentiation during pregnancy and lactation.
    Results: Deletion of one allele of Akt2 in Akt1-deficient mice resulted in a severe defect in Stat5 activation during late pregnancy that was accompanied by a global failure of terminal mammary epithelial cell differentiation, as manifested by the near-complete loss in production of the three principal components of milk: lactose, lipid, and milk proteins. This defect was due, in part, to a failure of pregnant Akt1(-/-);Akt2(+/-) mice to upregulate the positive regulator of Prlr-Jak-Stat5 signaling, Id2, or to downregulate the negative regulators of Prlr-Jak-Stat5 signaling, caveolin-1 and Socs2.
    Conclusions: Our findings demonstrate an unexpected requirement for Akt in Prlr-Jak-Stat5 signaling and establish Akt as an essential central regulator of mammary epithelial differentiation and lactation.
    MeSH term(s) Animals ; Cell Differentiation ; Cell Proliferation ; Cell Survival ; Female ; Janus Kinases/metabolism ; Lactation ; Mammary Glands, Animal/cytology ; Mammary Glands, Animal/metabolism ; Mice ; Mice, Knockout ; Milk Proteins/biosynthesis ; Organ Culture Techniques ; Proto-Oncogene Proteins c-akt/genetics ; Proto-Oncogene Proteins c-akt/metabolism ; STAT5 Transcription Factor/metabolism ; Signal Transduction
    Chemical Substances Milk Proteins ; STAT5 Transcription Factor ; Janus Kinases (EC 2.7.10.2) ; Akt1 protein, mouse (EC 2.7.11.1) ; Akt2 protein, mouse (EC 2.7.11.1) ; Akt3 protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1)
    Language English
    Publishing date 2010-09-17
    Publishing country England
    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.
    ZDB-ID 2015059-3
    ISSN 1465-542X ; 1465-5411
    ISSN (online) 1465-542X
    ISSN 1465-5411
    DOI 10.1186/bcr2640
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5494: 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)

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  3. Article: Isoform-specific requirement for Akt1 in the developmental regulation of cellular metabolism during lactation.

    Boxer, Robert B / Stairs, Douglas B / Dugan, Katherine D / Notarfrancesco, Kathleen L / Portocarrero, Carla P / Keister, Blaine A / Belka, George K / Cho, Han / Rathmell, Jeffrey C / Thompson, Craig B / Birnbaum, Morris J / Chodosh, Lewis A

    Cell metabolism

    2006  Volume 4, Issue 6, Page(s) 475–490

    Abstract: The metabolic demands and synthetic capacity of the lactating mammary gland exceed that of any other tissue, thereby providing a useful paradigm for understanding the developmental regulation of cellular metabolism. By evaluating mice bearing targeted ... ...

    Abstract The metabolic demands and synthetic capacity of the lactating mammary gland exceed that of any other tissue, thereby providing a useful paradigm for understanding the developmental regulation of cellular metabolism. By evaluating mice bearing targeted deletions in Akt1 or Akt2, we demonstrate that Akt1 is specifically required for lactating mice to synthesize sufficient quantities of milk to support their offspring. Whereas cellular proliferation, differentiation, and apoptosis are unaffected, loss of Akt1 disrupts the coordinate regulation of metabolic pathways that normally occurs at the onset of lactation. This results in a failure to upregulate glucose uptake, Glut1 surface localization, lipid synthesis, and multiple lipogenic enzymes, as well as a failure to downregulate lipid catabolic enzymes. These findings demonstrate that Akt1 is required in an isoform-specific manner for orchestrating many of the developmental changes in cellular metabolism that occur at the onset of lactation and establish a role for Akt1 in glucose metabolism.
    MeSH term(s) Animals ; Female ; Glucose/metabolism ; Glucose Transporter Type 1/metabolism ; Isoenzymes/deficiency ; Isoenzymes/metabolism ; Lactation/genetics ; Lactation/metabolism ; Lipids/biosynthesis ; Mice ; Mice, Knockout ; Milk/metabolism ; Protein Transport/genetics ; Proto-Oncogene Proteins c-akt/deficiency ; Proto-Oncogene Proteins c-akt/metabolism
    Chemical Substances Glucose Transporter Type 1 ; Isoenzymes ; Lipids ; Slc2a1 protein, mouse ; Akt1 protein, mouse (EC 2.7.11.1) ; Akt2 protein, mouse (EC 2.7.11.1) ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2006-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2176834-1
    ISSN 1932-7420 ; 1550-4131
    ISSN (online) 1932-7420
    ISSN 1550-4131
    DOI 10.1016/j.cmet.2006.10.011
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6169: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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  4. Article: The transcriptional repressor Snail promotes mammary tumor recurrence.

    Moody, Susan E / Perez, Denise / Pan, Tien-chi / Sarkisian, Christopher J / Portocarrero, Carla P / Sterner, Christopher J / Notorfrancesco, Kathleen L / Cardiff, Robert D / Chodosh, Lewis A

    Cancer cell

    2005  Volume 8, Issue 3, Page(s) 197–209

    Abstract: Breast cancer recurrence is a fundamental clinical manifestation of tumor progression and represents the principal cause of death from this disease. Using a conditional transgenic mouse model for the recurrence of HER2/neu-induced mammary tumors, we ... ...

    Abstract Breast cancer recurrence is a fundamental clinical manifestation of tumor progression and represents the principal cause of death from this disease. Using a conditional transgenic mouse model for the recurrence of HER2/neu-induced mammary tumors, we demonstrate that the transcriptional repressor Snail is spontaneously upregulated in recurrent tumors in vivo and that recurrence is accompanied by epithelial-to-mesenchymal transition (EMT). Consistent with a causal role for Snail in these processes, we show that Snail is sufficient to induce EMT in primary tumor cells, that Snail is sufficient to promote mammary tumor recurrence in vivo, and that high levels of Snail predict decreased relapse-free survival in women with breast cancer. In aggregate, our observations strongly implicate Snail in the process of breast cancer recurrence.
    MeSH term(s) Animals ; Breast Neoplasms/genetics ; Epithelial Cells/pathology ; Female ; Gene Expression Regulation, Neoplastic ; Humans ; Mammary Neoplasms, Experimental/genetics ; Mammary Neoplasms, Experimental/pathology ; Mesoderm/pathology ; Mice ; Mice, Transgenic ; Neoplasm Recurrence, Local/genetics ; Neoplasm Recurrence, Local/pathology ; Receptor, ErbB-2/genetics ; Snail Family Transcription Factors ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Snail Family Transcription Factors ; Transcription Factors ; Receptor, ErbB-2 (EC 2.7.10.1)
    Language English
    Publishing date 2005-09
    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, P.H.S.
    ZDB-ID 2078448-X
    ISSN 1878-3686 ; 1535-6108
    ISSN (online) 1878-3686
    ISSN 1535-6108
    DOI 10.1016/j.ccr.2005.07.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5650: 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 104: Show issues

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