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  1. AU="Wilson H. Miller, Jr."
  2. AU="Beena Thomas"
  3. AU=Mercury Oblaise A
  4. AU="Jeongjun Kim"
  5. AU="Marks, Evan A. N."
  6. AU="Thomson, Tina"
  7. AU="Lazaros Iliadis"
  8. AU="Guglielmo, Letterio"
  9. AU="Wilson, Brandon"
  10. AU=Hammerman Marc R.
  11. AU=Bromfield Mahiri
  12. AU=Hunt John T
  13. AU="Nock, Annike Morgane"
  14. AU="Benitah, Salvador Aznar"
  15. AU="Axelgaard, Esben"
  16. AU="Kachingwe, Martin"
  17. AU="Yokoyama, Ryuto"
  18. AU="Luck, Jennifer N"
  19. AU="Min Soo Kim"
  20. AU="Piotr Dylewicz"
  21. AU="Mankel, A"
  22. AU="Lia, Andrea"
  23. AU=Wang Yong
  24. AU="Mckay, Victoria"
  25. AU="Yanqun Liu"
  26. AU="Doyon, Yannick"
  27. AU=Ho-Yen Colan M
  28. AU="Tarnawski, Miroslaw"
  29. AU="Mark Pickering"
  30. AU=Felson Marcus
  31. AU="Antje Garten"
  32. AU="Pijpers, Judith"
  33. AU=Ciacchini Benedetta AU=Ciacchini Benedetta

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  1. Artikel ; Online: Peroxisome disruption alters lipid metabolism and potentiates antitumor response with MAPK-targeted therapy in melanoma

    Fan Huang / Feiyang Cai / Michael S. Dahabieh / Kshemaka Gunawardena / Ali Talebi / Jonas Dehairs / Farah El-Turk / Jae Yeon Park / Mengqi Li / Christophe Goncalves / Natascha Gagnon / Jie Su / Judith H. LaPierre / Perrine Gaub / Jean-Sébastien Joyal / John J. Mitchell / Johannes V. Swinnen / Wilson H. Miller Jr. / Sonia V. del Rincón

    The Journal of Clinical Investigation, Vol 133, Iss

    2023  Band 20

    Abstract: Melanomas reprogram their metabolism to rapidly adapt to therapy-induced stress conditions, allowing them to persist and ultimately develop resistance. We report that a subpopulation of melanoma cells tolerate MAPK pathway inhibitors (MAPKis) through a ... ...

    Abstract Melanomas reprogram their metabolism to rapidly adapt to therapy-induced stress conditions, allowing them to persist and ultimately develop resistance. We report that a subpopulation of melanoma cells tolerate MAPK pathway inhibitors (MAPKis) through a concerted metabolic reprogramming mediated by peroxisomes and UDP-glucose ceramide glycosyltransferase (UGCG). Compromising peroxisome biogenesis, by repressing PEX3 expression, potentiated the proapoptotic effects of MAPKis via an induction of ceramides, an effect limited by UGCG-mediated ceramide metabolism. Cotargeting PEX3 and UGCG selectively eliminated a subset of metabolically active, drug-tolerant CD36+ melanoma persister cells, thereby sensitizing melanoma to MAPKis and delaying resistance. Increased levels of peroxisomal genes and UGCG were found in patient-derived MAPKi-relapsed melanomas, and simultaneously inhibiting PEX3 and UGCG restored MAPKi sensitivity in multiple models of therapy resistance. Finally, combination therapy consisting of a newly identified inhibitor of the PEX3-PEX19 interaction, a UGCG inhibitor, and MAPKis demonstrated potent antitumor activity in preclinical melanoma models, thus representing a promising approach for melanoma treatment.
    Schlagwörter Oncology ; Medicine ; R
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2023-10-01T00:00:00Z
    Verlag American Society for Clinical Investigation
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: NPM and BRG1 Mediate Transcriptional Resistance to Retinoic Acid in Acute Promyelocytic Leukemia

    Jessica N. Nichol / Matthew D. Galbraith / Claudia L. Kleinman / Joaquín M. Espinosa / Wilson H. Miller Jr.

    Cell Reports, Vol 14, Iss 12, Pp 2938-

    2016  Band 2949

    Abstract: Perturbation in the transcriptional control of genes driving differentiation is an established paradigm whereby oncogenic fusion proteins promote leukemia. From a retinoic acid (RA)-sensitive acute promyelocytic leukemia (APL) cell line, we derived an RA- ...

    Abstract Perturbation in the transcriptional control of genes driving differentiation is an established paradigm whereby oncogenic fusion proteins promote leukemia. From a retinoic acid (RA)-sensitive acute promyelocytic leukemia (APL) cell line, we derived an RA-resistant clone characterized by a block in transcription initiation, despite maintaining wild-type PML/RARA expression. We uncovered an aberrant interaction among PML/RARA, nucleophosmin (NPM), and topoisomerase II beta (TOP2B). Surprisingly, RA stimulation in these cells results in enhanced chromatin association of the nucleosome remodeler BRG1. Inhibition of NPM or TOP2B abrogated BRG1 recruitment. Furthermore, NPM inhibition and targeting BRG1 restored differentiation when combined with RA. Here, we demonstrate a role for NPM and BRG1 in obstructing RA differentiation and implicate chromatin remodeling in mediating therapeutic resistance in malignancies. NPM mutations are the most common genetic change in patients with acute leukemia (AML); therefore, our model may be applicable to other more common leukemias driven by NPM.
    Schlagwörter Biology (General) ; QH301-705.5
    Sprache Englisch
    Erscheinungsdatum 2016-03-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Optimized protocol for immunophenotyping of melanoma and tumor-bearing skin from mouse

    Sai Sakktee Krisna / Christophe Goncalves / Natascha Gagnon / Fan Huang / Dany Plourde / Wilson H. Miller, Jr. / Jörg H. Fritz / Sonia V. del Rincon

    STAR Protocols, Vol 2, Iss 3, Pp 100627- (2021)

    2021  

    Abstract: Summary: While isolating immune cells from spleens and lungs is routinely achieved using flow cytometry, it is challenging to isolate viable immune cells from skin. Here, we describe a step-by-step protocol for skin digestion using a murine melanoma ... ...

    Abstract Summary: While isolating immune cells from spleens and lungs is routinely achieved using flow cytometry, it is challenging to isolate viable immune cells from skin. Here, we describe a step-by-step protocol for skin digestion using a murine melanoma model, which is amenable for detection of low abundant immune cell populations including group 2 innate lymphoid cells.
    Schlagwörter Cancer ; Cell isolation ; Flow Cytometry/Mass Cytometry ; Immunology ; Model Organisms ; Science (General) ; Q1-390
    Sprache Englisch
    Erscheinungsdatum 2021-09-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

    Volltext online

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