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  1. Article ; Online: Pandemic and the PCMR.

    Setaluri, Vijayasaradhi

    Pigment cell & melanoma research

    2020  Volume 33, Issue 4, Page(s) 526

    MeSH term(s) COVID-19/epidemiology ; Humans ; Pandemics ; Periodicals as Topic ; SARS-CoV-2/physiology
    Keywords covid19
    Language English
    Publishing date 2020-06-02
    Publishing country England
    Document type Editorial
    ZDB-ID 2409570-9
    ISSN 1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
    ISSN (online) 1755-148X ; 1600-0749
    ISSN 0893-5785 ; 1755-1471
    DOI 10.1111/pcmr.12901
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2444: 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: Life as Editor.

    Setaluri, Vijayasaradhi

    Pigment cell & melanoma research

    2019  Volume 32, Issue 3, Page(s) 344

    MeSH term(s) Biomedical Research ; Humans ; Melanoma ; Periodicals as Topic/standards ; Pigmentation ; Publishing/standards
    Language English
    Publishing date 2019-04-21
    Publishing country England
    Document type Editorial
    ZDB-ID 2409570-9
    ISSN 1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
    ISSN (online) 1755-148X ; 1600-0749
    ISSN 0893-5785 ; 1755-1471
    DOI 10.1111/pcmr.12786
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    Zs.A 2444: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: Where are all the women scientists in pigment cell and melanoma research?

    Setaluri, Vijayasaradhi

    Pigment cell & melanoma research

    2018  Volume 31, Issue 4, Page(s) 456

    MeSH term(s) Biomedical Research ; Female ; Humans ; Melanoma ; Women, Working
    Language English
    Publishing date 2018-08-01
    Publishing country England
    Document type Editorial
    ZDB-ID 2409570-9
    ISSN 1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
    ISSN (online) 1755-148X ; 1600-0749
    ISSN 0893-5785 ; 1755-1471
    DOI 10.1111/pcmr.12713
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2444: 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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  5. Article ; Online: Epilogue.

    Setaluri, Vijayasaradhi / Helfaer, Evan P And Marion

    Pigment cell & melanoma research

    2023  Volume 36, Issue 6, Page(s) 454

    Language English
    Publishing date 2023-10-30
    Publishing country England
    Document type Editorial
    ZDB-ID 2409570-9
    ISSN 1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
    ISSN (online) 1755-148X ; 1600-0749
    ISSN 0893-5785 ; 1755-1471
    DOI 10.1111/pcmr.13143
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2444: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    ab Jg. 2022: Lesesaal (EG)

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  6. Article ; Online: 2018, Forward, Going Online and all that...

    Setaluri, Vijayasaradhi

    Pigment cell & melanoma research

    2017  Volume 31, Issue 1, Page(s) 6

    MeSH term(s) Biomedical Research ; Humans ; Internet ; Periodicals as Topic ; Publishing
    Language English
    Publishing date 2017-12-22
    Publishing country England
    Document type Editorial
    ZDB-ID 2409570-9
    ISSN 1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
    ISSN (online) 1755-148X ; 1600-0749
    ISSN 0893-5785 ; 1755-1471
    DOI 10.1111/pcmr.12679
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2444: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Autophagy as a melanocytic self-defense mechanism.

    Setaluri, Vijayasaradhi

    The Journal of investigative dermatology

    2015  Volume 135, Issue 5, Page(s) 1215–1217

    Abstract: Defects in autophagy have implications for melanocyte survival and manifestations of skin pigmentary disorders. Zhang et al. (2015) show that mouse melanocytes lacking the autophagy protein Atg7 undergo premature senescence in vitro and accumulate ... ...

    Abstract Defects in autophagy have implications for melanocyte survival and manifestations of skin pigmentary disorders. Zhang et al. (2015) show that mouse melanocytes lacking the autophagy protein Atg7 undergo premature senescence in vitro and accumulate products of oxidative damage, despite activation of the redox response. Interestingly, contrary to previous findings, the melanocyte-specific deficiency in autophagy did not cause major defects in melanosome biogenesis, nor did it produce visually striking changes in mouse coat color.
    MeSH term(s) Aging, Premature/physiopathology ; Animals ; Antioxidants/metabolism ; Autophagy/physiology ; Cellular Senescence/physiology ; Humans ; Melanocytes/metabolism ; Melanocytes/pathology
    Chemical Substances Antioxidants
    Language English
    Publishing date 2015-04-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80136-7
    ISSN 1523-1747 ; 0022-202X
    ISSN (online) 1523-1747
    ISSN 0022-202X
    DOI 10.1038/jid.2015.19
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  8. Article ; Online: Connecting the dots: Melanoma cell of origin, tumor cell plasticity, trans-differentiation, and drug resistance.

    Castro-Pérez, Edgardo / Singh, Mithalesh / Sadangi, Shreyans / Mela-Sánchez, Carmen / Setaluri, Vijayasaradhi

    Pigment cell & melanoma research

    2023  Volume 36, Issue 5, Page(s) 330–347

    Abstract: Melanoma, a lethal malignancy that arises from melanocytes, exhibits a multiplicity of clinico-pathologically distinct subtypes in sun-exposed and non-sun-exposed areas. Melanocytes are derived from multipotent neural crest cells and are present in ... ...

    Abstract Melanoma, a lethal malignancy that arises from melanocytes, exhibits a multiplicity of clinico-pathologically distinct subtypes in sun-exposed and non-sun-exposed areas. Melanocytes are derived from multipotent neural crest cells and are present in diverse anatomical locations, including skin, eyes, and various mucosal membranes. Tissue-resident melanocyte stem cells and melanocyte precursors contribute to melanocyte renewal. Elegant studies using mouse genetic models have shown that melanoma can arise from either melanocyte stem cells or differentiated pigment-producing melanocytes depending on a combination of tissue and anatomical site of origin and activation of oncogenic mutations (or overexpression) and/or the repression in expression or inactivating mutations in tumor suppressors. This variation raises the possibility that different subtypes of human melanomas (even subsets within each subtype) may also be a manifestation of malignancies of distinct cells of origin. Melanoma is known to exhibit phenotypic plasticity and trans-differentiation (defined as a tendency to differentiate into cell lineages other than the original lineage from which the tumor arose) along vascular and neural lineages. Additionally, stem cell-like properties such as pseudo-epithelial-to-mesenchymal (EMT-like) transition and expression of stem cell-related genes have also been associated with the development of melanoma drug resistance. Recent studies that employed reprogramming melanoma cells to induced pluripotent stem cells have uncovered potential relationships between melanoma plasticity, trans-differentiation, and drug resistance and implications for cell or origin of human cutaneous melanoma. This review provides a comprehensive summary of the current state of knowledge on melanoma cell of origin and the relationship between tumor cell plasticity and drug resistance.
    MeSH term(s) Animals ; Mice ; Humans ; Melanoma/pathology ; Skin Neoplasms/pathology ; Cell Plasticity ; Melanocytes/metabolism ; Cell Differentiation ; Drug Resistance ; Induced Pluripotent Stem Cells/metabolism ; Neural Crest/metabolism
    Language English
    Publishing date 2023-05-03
    Publishing country England
    Document type Journal Article ; Review ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2409570-9
    ISSN 1755-148X ; 1600-0749 ; 0893-5785 ; 1755-1471
    ISSN (online) 1755-148X ; 1600-0749
    ISSN 0893-5785 ; 1755-1471
    DOI 10.1111/pcmr.13092
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2444: 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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  9. Article: EPAC mediates the dual role of cAMP signaling in melanoma.

    Rodriguez, Carlos I / Setaluri, Vijayasaradhi

    Oncoscience

    2018  Volume 6, Issue 1-2, Page(s) 283–284

    Language English
    Publishing date 2018-08-22
    Publishing country United States
    Document type Journal Article
    ISSN 2331-4737
    ISSN 2331-4737
    DOI 10.18632/oncoscience.463
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Role of dual specificity phosphatases (DUSPs) in melanoma cellular plasticity and drug resistance.

    Singh, Mithalesh K / Altameemi, Sarah / Lares, Marcos / Newton, Michael A / Setaluri, Vijayasaradhi

    Scientific reports

    2022  Volume 12, Issue 1, Page(s) 14395

    Abstract: Melanoma cells exhibit phenotypic plasticity that allows transition from a proliferative and differentiated phenotype to a more invasive and undifferentiated or transdifferentiated phenotype often associated with drug resistance. The mechanisms that ... ...

    Abstract Melanoma cells exhibit phenotypic plasticity that allows transition from a proliferative and differentiated phenotype to a more invasive and undifferentiated or transdifferentiated phenotype often associated with drug resistance. The mechanisms that control melanoma phenotype plasticity and its role in drug resistance are not fully understood. We previously demonstrated that emergence of MAPK inhibitor (MAPKi)-resistance phenotype is associated with decreased expression of stem cell proliferation genes and increased expression of MAPK inactivation genes, including dual specificity phosphatases (DUSPs). Several members of the DUSP family genes, specifically DUSP1, -3, -8 and -9, are expressed in primary and metastatic melanoma cell lines and pre-and post BRAFi treated melanoma cells. Here, we show that knockdown of DUSP1 or DUSP8 or treatment with BCI, a pharmacological inhibitor of DUSP1/6 decrease the survival of MAPKi-resistant cells and sensitizes them to BRAFi and MEKi. Pharmacological inhibition of DUSP1/6 upregulated nestin, a neural crest stem cell marker, in both MAPKi-sensitive cells and cells with acquired MAPKi-resistance. In contrast, treatment with BCI resulted in upregulation of MAP2, a neuronal differentiation marker, only in MAPKi-sensitive cells but caused downregulation of both MAP2 and GFAP, a glial marker, in all MAPKi-resistant cell lines. These data suggest that DUSP proteins are involved in the regulation of cellular plasticity cells and melanoma drug resistance and are potential targets for treatment of MAPKi-resistant melanoma.
    MeSH term(s) Cell Line, Tumor ; Cell Plasticity/genetics ; Drug Resistance, Neoplasm/genetics ; Dual-Specificity Phosphatases/genetics ; Humans ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/pathology ; Protein Kinase Inhibitors/pharmacology
    Chemical Substances Protein Kinase Inhibitors ; Dual-Specificity Phosphatases (EC 3.1.3.48)
    Language English
    Publishing date 2022-08-23
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-022-18578-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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