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  1. AU="Perlee, Sarah"
  2. AU="Atamanalp, Refik Selim"
  3. AU="Costa, Bruno Buranello"
  4. AU="Kohler, Beatriz"
  5. AU="Tabata, Toshinori"
  6. AU="Sun, Shijing"
  7. AU="Kufeji D."
  8. AU="Kohani, Sayeh"
  9. AU="Wong, John Cm"
  10. AU="Hua LI"
  11. AU="Özkan, Yasemin"
  12. AU=Quirmbach Diana
  13. AU="Corpstein, Clairissa D"
  14. AU="Motel-Klingebiel, Andreas"
  15. AU="Brown, Randy A"
  16. AU="Feng, Yaying"
  17. AU="Lussi, A"
  18. AU="Yeon Susan B"
  19. AU="Abaci, Irem"
  20. AU="Lin, Xiaode"
  21. AU="Mendez, Luis"
  22. AU=Alzahrani Faisal A AU=Alzahrani Faisal A
  23. AU="Heidi G Standke"
  24. AU="Banville, Isabelle"
  25. AU=Morrow Lee E
  26. AU="Cuss, Chad W."
  27. AU="Carter, Paul (Interviewpartner)"
  28. AU=Lubozynski M F
  29. AU="Yves, Ville"
  30. AU="Bayer, Emily A"
  31. AU=Roesch Saskia
  32. AU="Tam, Benjamin"
  33. AU="Mori, Kousuke"
  34. AU="Steuer, Melanie"
  35. AU="Sood Hemant"
  36. AU="Jennifer Schaff"
  37. AU="Maji, Manideepa"
  38. AU=Evans Heather L
  39. AU="Cheng, Shuai"
  40. AU="Zalis, Joshua"

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  1. Artikel: A zebrafish system for identifying genetic dependencies in melanocytes and melanoma.

    Perlee, Sarah / Ma, Yilun / Hunter, Miranda V / Swanson, Jacob B / Ming, Zhitao / Xia, Julia / Lionnet, Timothee / McGrail, Maura / White, Richard

    bioRxiv : the preprint server for biology

    2024  

    Abstract: The advent of large-scale sequencing in both development and disease has identified large numbers of candidate genes that may be linked to important phenotypes. Validating the function of these candidates in vivo is challenging, due to low efficiency and ...

    Abstract The advent of large-scale sequencing in both development and disease has identified large numbers of candidate genes that may be linked to important phenotypes. Validating the function of these candidates in vivo is challenging, due to low efficiency and low throughput of most model systems. This is especially the case in skin cells such as melanocytes, where the background mutation rate is high. We have developed a rapid and scalable system for assessing the role of candidate genes in a melanocyte specific manner using zebrafish. We generated transgenic zebrafish in which Cas9 was knocked-in to the endogenous mitfa locus, a master transcription factor of the melanocyte lineage. By introducing single guide RNA expression cassettes into mitfaCas9 embryos, we were able to achieve highly efficient melanocyte-specific mutation of genes important for melanocyte patterning and survival. These animals can be used to screen for dominant or recessive pigment defects in both the F0 generation (3 days) and F1 generation (3 months). We also utilized the mitfaCas9 line to study the role of melanoma genetic dependencies such as SOX10, demonstrating that loss of SOX10 reduces melanoma initiation yet promotes tumor progression by a switch to a SOX9hi state. This SOX10 to SOX9 switch has previously been observed in human patients, indicating that our system can be used to rapidly uncover biological states with relevance to human disease. Our high efficiency genetic approach can be readily applied to other cell lineages, with relevance to both development and disease.
    Sprache Englisch
    Erscheinungsdatum 2024-03-28
    Erscheinungsland United States
    Dokumenttyp Preprint
    DOI 10.1101/2024.03.22.586101
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: SETD1A regulates transcriptional pause release of heme biosynthesis genes in leukemia.

    Hoshii, Takayuki / Perlee, Sarah / Kikuchi, Sota / Rahmutulla, Bahityar / Fukuyo, Masaki / Masuda, Takeshi / Ohtsuki, Sumio / Soga, Tomoyoshi / Nabet, Behnam / Kaneda, Atsushi

    Cell reports

    2022  Band 41, Heft 9, Seite(n) 111727

    Abstract: Histone methyltransferase SETD1A is critical for acute myeloid leukemia (AML) cell survival, but the molecular mechanism driving SETD1A gene regulation remains elusive. To delineate the role of SETD1A, we utilize a protein degrader technology to induce ... ...

    Abstract Histone methyltransferase SETD1A is critical for acute myeloid leukemia (AML) cell survival, but the molecular mechanism driving SETD1A gene regulation remains elusive. To delineate the role of SETD1A, we utilize a protein degrader technology to induce rapid SETD1A degradation in AML cell lines. SETD1A degradation results in immediate downregulation of transcripts associated with DNA repair and heme biosynthesis pathways. CRISPR-based functional analyses and metabolomics reveal an essential role of SETD1A to maintain mitochondrial respiration in AML cells. These SETD1A targets are enriched in head-to-head (H2H) genes. SETD1A degradation disrupts a non-enzymatic SETD1A domain-dependent cyclin K function, increases the Ser5P RNA polymerase II (RNAPII) at the transcriptional start site (TSS), and induces the promoter-proximal pausing of RNAPII in a strand-specific manner. This study reveals a non-enzymatic role for SETD1A in transcriptional pause release and provides insight into the mechanism of RNAPII pausing and its function in cancer.
    Mesh-Begriff(e) Humans ; Leukemia ; Metabolomics ; Down-Regulation ; DNA Repair ; RNA Polymerase II ; Heme ; Histone-Lysine N-Methyltransferase/genetics
    Chemische Substanzen RNA Polymerase II (EC 2.7.7.-) ; Heme (42VZT0U6YR) ; Setd1A protein, human (EC 2.1.1.43) ; Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
    Sprache Englisch
    Erscheinungsdatum 2022-11-17
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2022.111727
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  3. Artikel ; Online: SETD1A function in leukemia is mediated through interaction with mitotic regulators BuGZ/BUB3.

    Perlee, Sarah / Kikuchi, Sota / Nakadai, Tomoyoshi / Masuda, Takeshi / Ohtsuki, Sumio / Matsumoto, Makoto / Rahmutulla, Bahityar / Fukuyo, Masaki / Cifani, Paolo / Kentsis, Alex / Roeder, Robert G / Kaneda, Atsushi / Hoshii, Takayuki

    EMBO reports

    2023  Band 24, Heft 10, Seite(n) e57108

    Abstract: The H3K4 methyltransferase SETD1A plays a crucial role in leukemia cell survival through its noncatalytic FLOS domain-mediated recruitment of cyclin K and regulation of DNA damage response genes. In this study, we identify a functional nuclear ... ...

    Abstract The H3K4 methyltransferase SETD1A plays a crucial role in leukemia cell survival through its noncatalytic FLOS domain-mediated recruitment of cyclin K and regulation of DNA damage response genes. In this study, we identify a functional nuclear localization signal in and interaction partners of the FLOS domain. Our screen for FLOS domain-binding partners reveals that the SETD1A FLOS domain binds mitosis-associated proteins BuGZ/BUB3. Inhibition of both cyclin K and BuGZ/BUB3-binding motifs in SETD1A shows synergistic antileukemic effects. BuGZ/BUB3 localize to SETD1A-bound promoter-TSS regions and SETD1A-negative H3K4me1-positive enhancer regions adjacent to SETD1A target genes. The GLEBS motif and intrinsically disordered region of BuGZ are required for both SETD1A-binding and leukemia cell proliferation. Cell-cycle-specific SETD1A restoration assays indicate that SETD1A expression at the G1/S phase of the cell cycle promotes both the expression of DNA damage response genes and cell cycle progression in leukemia cells.
    Mesh-Begriff(e) Humans ; Mitosis/genetics ; Cyclins/genetics ; Cyclins/metabolism ; Cell Cycle/genetics ; Cell Cycle Proteins/metabolism ; Leukemia/genetics ; Poly-ADP-Ribose Binding Proteins/genetics
    Chemische Substanzen Cyclins ; Cell Cycle Proteins ; BUB3 protein, human ; Poly-ADP-Ribose Binding Proteins
    Sprache Englisch
    Erscheinungsdatum 2023-08-03
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2020896-0
    ISSN 1469-3178 ; 1469-221X
    ISSN (online) 1469-3178
    ISSN 1469-221X
    DOI 10.15252/embr.202357108
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel ; Online: EWI-2 Inhibits Cell-Cell Fusion at the HIV-1 Virological Presynapse.

    Whitaker, Emily E / Matheson, Nicholas J / Perlee, Sarah / Munson, Phillip B / Symeonides, Menelaos / Thali, Markus

    Viruses

    2019  Band 11, Heft 12

    Abstract: Cell-to-cell transfer of virus particles at the Env-dependent virological synapse (VS) is a highly efficient mode of HIV-1 transmission. While cell-cell fusion could be triggered at the VS, leading to the formation of syncytia and preventing exponential ... ...

    Abstract Cell-to-cell transfer of virus particles at the Env-dependent virological synapse (VS) is a highly efficient mode of HIV-1 transmission. While cell-cell fusion could be triggered at the VS, leading to the formation of syncytia and preventing exponential growth of the infected cell population, this is strongly inhibited by both viral (Gag) and host (ezrin and tetraspanins) proteins. Here, we identify EWI-2, a protein that was previously shown to associate with ezrin and tetraspanins, as a host factor that contributes to the inhibition of Env-mediated cell-cell fusion. Using quantitative fluorescence microscopy, shRNA knockdowns, and cell-cell fusion assays, we show that EWI-2 accumulates at the presynaptic terminal (i.e., the producer cell side of the VS), where it contributes to the fusion-preventing activities of the other viral and cellular components. We also find that EWI-2, like tetraspanins, is downregulated upon HIV-1 infection, most likely by Vpu. Despite the strong inhibition of fusion at the VS, T cell-based syncytia do form
    Mesh-Begriff(e) Antigens, CD/genetics ; Antigens, CD/metabolism ; Cell Fusion ; Cell Line ; Down-Regulation ; Giant Cells/physiology ; Giant Cells/virology ; HIV Infections/virology ; HIV-1/genetics ; HIV-1/physiology ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Presynaptic Terminals/physiology ; Presynaptic Terminals/virology ; RNA, Small Interfering/genetics ; T-Lymphocytes/virology ; Virion/physiology
    Chemische Substanzen Antigens, CD ; IGSF8 protein, human ; Membrane Proteins ; RNA, Small Interfering
    Sprache Englisch
    Erscheinungsdatum 2019-11-20
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2516098-9
    ISSN 1999-4915 ; 1999-4915
    ISSN (online) 1999-4915
    ISSN 1999-4915
    DOI 10.3390/v11121082
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: GABA Regulates Electrical Activity and Tumor Initiation in Melanoma.

    Tagore, Mohita / Hergenreder, Emiliano / Perlee, Sarah C / Cruz, Nelly M / Menocal, Laura / Suresh, Shruthy / Chan, Eric / Baron, Maayan / Melendez, Stephanie / Dave, Asim / Chatila, Walid K / Nsengimana, Jeremie / Koche, Richard P / Hollmann, Travis J / Ideker, Trey / Studer, Lorenz / Schietinger, Andrea / White, Richard M

    Cancer discovery

    2023  Band 13, Heft 10, Seite(n) 2270–2291

    Abstract: Oncogenes can initiate tumors only in certain cellular contexts, which is referred to as oncogenic competence. In melanoma, whether cells in the microenvironment can endow such competence remains unclear. Using a combination of zebrafish transgenesis ... ...

    Abstract Oncogenes can initiate tumors only in certain cellular contexts, which is referred to as oncogenic competence. In melanoma, whether cells in the microenvironment can endow such competence remains unclear. Using a combination of zebrafish transgenesis coupled with human tissues, we demonstrate that GABAergic signaling between keratinocytes and melanocytes promotes melanoma initiation by BRAFV600E. GABA is synthesized in melanoma cells, which then acts on GABA-A receptors in keratinocytes. Electron microscopy demonstrates specialized cell-cell junctions between keratinocytes and melanoma cells, and multielectrode array analysis shows that GABA acts to inhibit electrical activity in melanoma/keratinocyte cocultures. Genetic and pharmacologic perturbation of GABA synthesis abrogates melanoma initiation in vivo. These data suggest that GABAergic signaling across the skin microenvironment regulates the ability of oncogenes to initiate melanoma.
    Significance: This study shows evidence of GABA-mediated regulation of electrical activity between melanoma cells and keratinocytes, providing a new mechanism by which the microenvironment promotes tumor initiation. This provides insights into the role of the skin microenvironment in early melanomas while identifying GABA as a potential therapeutic target in melanoma. See related commentary by Ceol, p. 2128. This article is featured in Selected Articles from This Issue, p. 2109.
    Mesh-Begriff(e) Animals ; Humans ; Melanoma/drug therapy ; Melanoma/genetics ; Melanoma/pathology ; Zebrafish ; Melanocytes/pathology ; Skin ; Keratinocytes ; Cell Transformation, Neoplastic/genetics ; gamma-Aminobutyric Acid ; Tumor Microenvironment
    Chemische Substanzen gamma-Aminobutyric Acid (56-12-2)
    Sprache Englisch
    Erscheinungsdatum 2023-08-08
    Erscheinungsland United States
    Dokumenttyp Journal Article
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-23-0389
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Developmental chromatin programs determine oncogenic competence in melanoma.

    Baggiolini, Arianna / Callahan, Scott J / Montal, Emily / Weiss, Joshua M / Trieu, Tuan / Tagore, Mohita M / Tischfield, Sam E / Walsh, Ryan M / Suresh, Shruthy / Fan, Yujie / Campbell, Nathaniel R / Perlee, Sarah C / Saurat, Nathalie / Hunter, Miranda V / Simon-Vermot, Theresa / Huang, Ting-Hsiang / Ma, Yilun / Hollmann, Travis / Tickoo, Satish K /
    Taylor, Barry S / Khurana, Ekta / Koche, Richard P / Studer, Lorenz / White, Richard M

    Science (New York, N.Y.)

    2021  Band 373, Heft 6559, Seite(n) eabc1048

    Abstract: Oncogenes only transform cells under certain cellular contexts, a phenomenon called oncogenic competence. Using a combination of a human pluripotent stem cell–derived cancer model along with zebrafish transgenesis, we demonstrate that the transforming ... ...

    Abstract Oncogenes only transform cells under certain cellular contexts, a phenomenon called oncogenic competence. Using a combination of a human pluripotent stem cell–derived cancer model along with zebrafish transgenesis, we demonstrate that the transforming ability of BRAF
    Mesh-Begriff(e) ATPases Associated with Diverse Cellular Activities/genetics ; ATPases Associated with Diverse Cellular Activities/metabolism ; Animals ; Animals, Genetically Modified ; Carcinogenesis/genetics ; Carcinogenesis/pathology ; Chromatin/genetics ; Chromatin/metabolism ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Humans ; Melanocytes/metabolism ; Melanocytes/pathology ; Melanoma/genetics ; Melanoma/pathology ; Mice ; Neoplasms, Experimental ; Neoplastic Stem Cells/pathology ; Neural Crest/metabolism ; Neural Crest/pathology ; Pluripotent Stem Cells/pathology ; Proto-Oncogene Proteins B-raf/genetics ; Proto-Oncogene Proteins B-raf/metabolism ; SOXE Transcription Factors/genetics ; SOXE Transcription Factors/metabolism ; Transcription, Genetic ; Zebrafish
    Chemische Substanzen Chromatin ; DNA-Binding Proteins ; SOX10 protein, human ; SOXE Transcription Factors ; BRAF protein, human (EC 2.7.11.1) ; Proto-Oncogene Proteins B-raf (EC 2.7.11.1) ; ATAD2 protein, human (EC 3.6.1.3) ; ATPases Associated with Diverse Cellular Activities (EC 3.6.4.-)
    Sprache Englisch
    Erscheinungsdatum 2021-09-03
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 128410-1
    ISSN 1095-9203 ; 0036-8075
    ISSN (online) 1095-9203
    ISSN 0036-8075
    DOI 10.1126/science.abc1048
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  7. Artikel ; Online: IKAROS and MENIN coordinate therapeutically actionable leukemogenic gene expression in MLL-r acute myeloid leukemia.

    Aubrey, Brandon J / Cutler, Jevon A / Bourgeois, Wallace / Donovan, Katherine A / Gu, Shengqing / Hatton, Charlie / Perlee, Sarah / Perner, Florian / Rahnamoun, Homa / Theall, Alexandra C P / Henrich, Jill A / Zhu, Qian / Nowak, Radosław P / Kim, Young Joon / Parvin, Salma / Cremer, Anjali / Olsen, Sarah Naomi / Eleuteri, Nicholas A / Pikman, Yana /
    McGeehan, Gerard M / Stegmaier, Kimberly / Letai, Anthony / Fischer, Eric S / Liu, X Shirley / Armstrong, Scott A

    Nature cancer

    2022  Band 3, Heft 5, Seite(n) 595–613

    Abstract: Acute myeloid leukemia (AML) remains difficult to treat and requires new therapeutic approaches. Potent inhibitors of the chromatin-associated protein MENIN have recently entered human clinical trials, opening new therapeutic opportunities for some ... ...

    Abstract Acute myeloid leukemia (AML) remains difficult to treat and requires new therapeutic approaches. Potent inhibitors of the chromatin-associated protein MENIN have recently entered human clinical trials, opening new therapeutic opportunities for some genetic subtypes of this disease. Using genome-scale functional genetic screens, we identified IKAROS (encoded by IKZF1) as an essential transcription factor in KMT2A (MLL1)-rearranged (MLL-r) AML that maintains leukemogenic gene expression while also repressing pathways for tumor suppression, immune regulation and cellular differentiation. Furthermore, IKAROS displays an unexpected functional cooperativity and extensive chromatin co-occupancy with mixed lineage leukemia (MLL)1-MENIN and the regulator MEIS1 and an extensive hematopoietic transcriptional complex involving homeobox (HOX)A10, MEIS1 and IKAROS. This dependency could be therapeutically exploited by inducing IKAROS protein degradation with immunomodulatory imide drugs (IMiDs). Finally, we demonstrate that combined IKAROS degradation and MENIN inhibition effectively disrupts leukemogenic transcriptional networks, resulting in synergistic killing of leukemia cells and providing a paradigm for improved drug targeting of transcription and an opportunity for rapid clinical translation.
    Mesh-Begriff(e) Chromatin ; Gene Expression ; Humans ; Ikaros Transcription Factor/metabolism ; Leukemia, Myeloid, Acute/drug therapy ; Myeloid Ecotropic Viral Integration Site 1 Protein/genetics ; Transcription Factors/genetics
    Chemische Substanzen Chromatin ; Myeloid Ecotropic Viral Integration Site 1 Protein ; Transcription Factors ; Ikaros Transcription Factor (148971-36-2)
    Sprache Englisch
    Erscheinungsdatum 2022-05-09
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ISSN 2662-1347
    ISSN (online) 2662-1347
    DOI 10.1038/s43018-022-00366-1
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  8. Artikel ; Online: Cooperation between melanoma cell states promotes metastasis through heterotypic cluster formation.

    Campbell, Nathaniel R / Rao, Anjali / Hunter, Miranda V / Sznurkowska, Magdalena K / Briker, Luzia / Zhang, Maomao / Baron, Maayan / Heilmann, Silja / Deforet, Maxime / Kenny, Colin / Ferretti, Lorenza P / Huang, Ting-Hsiang / Perlee, Sarah / Garg, Manik / Nsengimana, Jérémie / Saini, Massimo / Montal, Emily / Tagore, Mohita / Newton-Bishop, Julia /
    Middleton, Mark R / Corrie, Pippa / Adams, David J / Rabbie, Roy / Aceto, Nicola / Levesque, Mitchell P / Cornell, Robert A / Yanai, Itai / Xavier, Joao B / White, Richard M

    Developmental cell

    2021  Band 56, Heft 20, Seite(n) 2808–2825.e10

    Abstract: Melanomas can have multiple coexisting cell states, including proliferative (PRO) versus invasive (INV) subpopulations that represent a "go or grow" trade-off; however, how these populations interact is poorly understood. Using a combination of zebrafish ...

    Abstract Melanomas can have multiple coexisting cell states, including proliferative (PRO) versus invasive (INV) subpopulations that represent a "go or grow" trade-off; however, how these populations interact is poorly understood. Using a combination of zebrafish modeling and analysis of patient samples, we show that INV and PRO cells form spatially structured heterotypic clusters and cooperate in the seeding of metastasis, maintaining cell state heterogeneity. INV cells adhere tightly to each other and form clusters with a rim of PRO cells. Intravital imaging demonstrated cooperation in which INV cells facilitate dissemination of less metastatic PRO cells. We identified the TFAP2 neural crest transcription factor as a master regulator of clustering and PRO/INV states. Isolation of clusters from patients with metastatic melanoma revealed a subset with heterotypic PRO-INV clusters. Our data suggest a framework for the co-existence of these two divergent cell populations, in which heterotypic clusters promote metastasis via cell-cell cooperation.
    Mesh-Begriff(e) Animals ; Cluster Analysis ; Gene Expression Regulation, Neoplastic/physiology ; Melanoma/metabolism ; Melanoma/pathology ; Neoplasm Metastasis/pathology ; Neoplastic Cells, Circulating/pathology ; Neural Crest/pathology ; Zebrafish
    Sprache Englisch
    Erscheinungsdatum 2021-09-15
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2021.08.018
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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