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  1. Article: Outpatient anesthesia for oral surgery in a juvenile with Leigh disease.

    Ellis, Zachary / Bloomer, Charles

    Anesthesia progress

    2005  Volume 52, Issue 2, Page(s) 70–73

    Abstract: ... in a juvenile with Leigh disease, a progressive neurodegenerative disorder related to respiratory chain deficiency. This syndrome ...

    Abstract We report a case of anesthesia for elective outpatient third molar extraction in a juvenile with Leigh disease, a progressive neurodegenerative disorder related to respiratory chain deficiency. This syndrome usually presents in infancy and is characterized by nervous system dysfunction and respiratory abnormalities. Anesthesia has been reported to aggravate respiratory symptoms and frequently precipitate respiratory failure. Preoperative swallowing difficulty or respiratory symptoms should be carefully diagnosed, because they can be a warning sign of postoperative complications or mortality. Adverse effects of anesthesia may quickly lead into metabolic acidosis. Anesthetics should be carefully chosen that do not interfere with mitochondrial respiration, which can lead to lactic acidosis.
    MeSH term(s) Adolescent ; Ambulatory Surgical Procedures ; Anesthesia, Dental ; Anesthetics, Intravenous/administration & dosage ; Anesthetics, Local/administration & dosage ; Dental Care for Chronically Ill ; Elective Surgical Procedures ; Female ; Humans ; Leigh Disease/physiopathology ; Lidocaine/administration & dosage ; Mandibular Nerve/drug effects ; Molar, Third/surgery ; Nerve Block ; Propofol/administration & dosage ; Tooth Extraction
    Chemical Substances Anesthetics, Intravenous ; Anesthetics, Local ; Lidocaine (98PI200987) ; Propofol (YI7VU623SF)
    Language English
    Publishing date 2005
    Publishing country United States
    Document type Case Reports ; Journal Article
    ZDB-ID 603800-1
    ISSN 1878-7177 ; 0003-3006
    ISSN (online) 1878-7177
    ISSN 0003-3006
    DOI 10.2344/0003-3006(2005)52[70:OAFOSI]2.0.CO;2
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  2. Article ; Online: Polycomb Directed Cell Fate Decisions in Development and Cancer.

    German, Beatriz / Ellis, Leigh

    Epigenomes

    2022  Volume 6, Issue 3

    Abstract: The polycomb group (PcG) proteins are a subset of transcription regulators highly conserved throughout evolution. Their principal role is to epigenetically modify chromatin landscapes and control the expression of master transcriptional programs to ... ...

    Abstract The polycomb group (PcG) proteins are a subset of transcription regulators highly conserved throughout evolution. Their principal role is to epigenetically modify chromatin landscapes and control the expression of master transcriptional programs to determine cellular identity. The two mayor PcG protein complexes that have been identified in mammals to date are Polycomb Repressive Complex 1 (PRC1) and 2 (PRC2). These protein complexes selectively repress gene expression via the induction of covalent post-translational histone modifications, promoting chromatin structure stabilization. PRC2 catalyzes the histone H3 methylation at lysine 27 (H3K27me1/2/3), inducing heterochromatin structures. This activity is controlled by the formation of a multi-subunit complex, which includes enhancer of zeste (EZH2), embryonic ectoderm development protein (EED), and suppressor of zeste 12 (SUZ12). This review will summarize the latest insights into how PRC2 in mammalian cells regulates transcription to orchestrate the temporal and tissue-specific expression of genes to determine cell identity and cell-fate decisions. We will specifically describe how PRC2 dysregulation in different cell types can promote phenotypic plasticity and/or non-mutational epigenetic reprogramming, inducing the development of highly aggressive epithelial neuroendocrine carcinomas, including prostate, small cell lung, and Merkel cell cancer. With this, EZH2 has emerged as an important actionable therapeutic target in such cancers.
    Language English
    Publishing date 2022-09-06
    Publishing country Switzerland
    Document type Journal Article ; Review
    ISSN 2075-4655
    ISSN (online) 2075-4655
    DOI 10.3390/epigenomes6030028
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  3. Article ; Online: Understanding cancer lineage plasticity: reversing therapeutic resistance in metastatic prostate cancer.

    Ellis, Leigh

    Pharmacogenomics

    2017  Volume 18, Issue 7, Page(s) 597–600

    MeSH term(s) Animals ; Cell Lineage/physiology ; Cell Plasticity/physiology ; Drug Resistance, Neoplasm/physiology ; Humans ; Male ; Prostatic Neoplasms, Castration-Resistant/pathology
    Language English
    Publishing date 2017
    Publishing country England
    Document type Journal Article
    ZDB-ID 2019513-8
    ISSN 1744-8042 ; 1462-2416
    ISSN (online) 1744-8042
    ISSN 1462-2416
    DOI 10.2217/pgs-2017-0039
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  4. Article: Polycomb Directed Cell Fate Decisions in Development and Cancer

    German, Beatriz / Ellis, Leigh

    Epigenomes. 2022 Sept. 06, v. 6, no. 3

    2022  

    Abstract: The polycomb group (PcG) proteins are a subset of transcription regulators highly conserved throughout evolution. Their principal role is to epigenetically modify chromatin landscapes and control the expression of master transcriptional programs to ... ...

    Abstract The polycomb group (PcG) proteins are a subset of transcription regulators highly conserved throughout evolution. Their principal role is to epigenetically modify chromatin landscapes and control the expression of master transcriptional programs to determine cellular identity. The two mayor PcG protein complexes that have been identified in mammals to date are Polycomb Repressive Complex 1 (PRC1) and 2 (PRC2). These protein complexes selectively repress gene expression via the induction of covalent post-translational histone modifications, promoting chromatin structure stabilization. PRC2 catalyzes the histone H3 methylation at lysine 27 (H3K27me1/2/3), inducing heterochromatin structures. This activity is controlled by the formation of a multi-subunit complex, which includes enhancer of zeste (EZH2), embryonic ectoderm development protein (EED), and suppressor of zeste 12 (SUZ12). This review will summarize the latest insights into how PRC2 in mammalian cells regulates transcription to orchestrate the temporal and tissue-specific expression of genes to determine cell identity and cell-fate decisions. We will specifically describe how PRC2 dysregulation in different cell types can promote phenotypic plasticity and/or non-mutational epigenetic reprogramming, inducing the development of highly aggressive epithelial neuroendocrine carcinomas, including prostate, small cell lung, and Merkel cell cancer. With this, EZH2 has emerged as an important actionable therapeutic target in such cancers.
    Keywords ectoderm ; epigenetics ; epithelium ; evolution ; gene expression ; heterochromatin ; histones ; lungs ; lysine ; mammals ; methylation ; phenotypic plasticity ; therapeutics ; transcription (genetics)
    Language English
    Dates of publication 2022-0906
    Publishing place Multidisciplinary Digital Publishing Institute
    Document type Article
    ISSN 2075-4655
    DOI 10.3390/epigenomes6030028
    Database NAL-Catalogue (AGRICOLA)

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  5. Article ; Online: Determination of synthetic lethal interactions to provide therapeutic direction to end aggressive prostate cancer.

    Ellis, Leigh

    Future oncology (London, England)

    2015  Volume 11, Issue 10, Page(s) 1451–1454

    MeSH term(s) Animals ; Disease Progression ; Drug Synergism ; Epistasis, Genetic ; Humans ; Male ; Molecular Targeted Therapy ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology
    Language English
    Publishing date 2015
    Publishing country England
    Document type Editorial
    ZDB-ID 2184533-5
    ISSN 1744-8301 ; 1479-6694
    ISSN (online) 1744-8301
    ISSN 1479-6694
    DOI 10.2217/fon.15.61
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  6. Article ; Online: Targeting Glutamine Metabolism in Prostate Cancer.

    Bhowmick, Neil / Posadas, Edwin / Ellis, Leigh / Freedland, Stephen J / Vizio, Dolores Di / Freeman, Michael R / Theodorescu, Dan / Figlin, Robert / Gong, Jun

    Frontiers in bioscience (Elite edition)

    2023  Volume 15, Issue 1, Page(s) 2

    Abstract: Glutamine is a conditionally essential amino acid important for cancer cell proliferation through intermediary metabolism leading ... ...

    Abstract Glutamine is a conditionally essential amino acid important for cancer cell proliferation through intermediary metabolism leading to
    MeSH term(s) Male ; Humans ; Glutamine/metabolism ; Prostatic Neoplasms/drug therapy ; Signal Transduction ; Homeostasis ; Oxidation-Reduction ; Tumor Microenvironment
    Chemical Substances Glutamine (0RH81L854J)
    Language English
    Publishing date 2023-04-13
    Publishing country Singapore
    Document type Journal Article ; Review ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 2565080-4
    ISSN 1945-0508 ; 1945-0494
    ISSN (online) 1945-0508
    ISSN 1945-0494
    DOI 10.31083/j.fbe1501002
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    Zs.A 6871: Show issues Location:
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  7. Article: Phenotypic Plasticity - Alternate Transcriptional Programs Driving Treatment Resistant Prostate Cancer.

    Nanda, Jagpreet Singh / Koganti, Praveen / Perri, Graziela / Ellis, Leigh

    Critical reviews in oncogenesis

    2022  Volume 27, Issue 1, Page(s) 45–60

    Abstract: Androgen deprivation therapy (ADT) that antagonizes androgen receptor (AR) signaling has made significant increases to overall survival of prostate cancer patients. However, ADT is not curative, and patients eventually progress to castration resistant ... ...

    Abstract Androgen deprivation therapy (ADT) that antagonizes androgen receptor (AR) signaling has made significant increases to overall survival of prostate cancer patients. However, ADT is not curative, and patients eventually progress to castration resistant disease (CRPC). It has become evident that a subset of prostate cancers acquire ADT resistance through mechanisms independent of AR alteration or reprogramming of AR signaling. This approximately involves a quarter of prostate cancers progressing on ADT. Collectively, these tumors evolve via phenotypic plasticity and display the activation of developmental and stemness gene signatures as well as transitional programs including an epithelial-mesenchymal phenotype. Currently, no successful treatments exist for prostate cancer patients to inhibit or reverse prostate tumor progression that utilizes mechanisms of epi-plasticity. This overview will discuss epigenetic mechanisms that mediate phenotypic plasticity and the potential for targeting the epigenome to create a novel direction for combination strategies involving epigenetic therapy to provide durable response.
    MeSH term(s) Adaptation, Physiological ; Androgen Antagonists/therapeutic use ; Humans ; Male ; Prostatic Neoplasms, Castration-Resistant/drug therapy ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/pathology ; Receptors, Androgen/genetics ; Signal Transduction/genetics
    Chemical Substances Androgen Antagonists ; Receptors, Androgen
    Language English
    Publishing date 2022-09-26
    Publishing country United States
    Document type Journal Article ; Review ; 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 1036388-9
    ISSN 0893-9675
    ISSN 0893-9675
    DOI 10.1615/CritRevOncog.2022043096
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    Zs.A 2587: Show issues Location:
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  8. Article ; Online: LSD1: A single target to combat lineage plasticity in lethal prostate cancer.

    Ellis, Leigh / Loda, Massimo

    Proceedings of the National Academy of Sciences of the United States of America

    2018  Volume 115, Issue 18, Page(s) 4530–4531

    MeSH term(s) Cell Line, Tumor ; Histone Demethylases ; Humans ; Male ; Prostatic Neoplasms
    Chemical Substances Histone Demethylases (EC 1.14.11.-)
    Language English
    Publishing date 2018-04-16
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.1804205115
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    Zs.A 1148: Show issues Location:
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  9. Article: MYBL2 drives prostate cancer plasticity and identifies CDK2 as a therapeutic vulnerability in RB1-loss and neuroendocrine prostate cancer.

    German, Beatriz / Singh, Jagpreet N / Fonseca, Marcos AdS / Burkhart, Deborah L / Sheahan, Anjali / Bergom, Hannah / Morel, Katherine L / Beltran, Himisha / Hwang, Justin H / Lawrenson, Kate / Ellis, Leigh

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Phenotypic plasticity is a recognized mechanism driving therapeutic resistance in prostate cancer (PCa) patients. While underlying molecular causations driving phenotypic plasticity have been identified, therapeutic success is yet to be achieved. To ... ...

    Abstract Phenotypic plasticity is a recognized mechanism driving therapeutic resistance in prostate cancer (PCa) patients. While underlying molecular causations driving phenotypic plasticity have been identified, therapeutic success is yet to be achieved. To identify putative master regulator transcription factors (MR-TF) driving phenotypic plasticity in PCa, this work utilized a multiomic approach using genetically engineered mouse models of prostate cancer combined with patient data to identify MYBL2 as a significantly enriched transcription factor in PCa exhibiting phenotypic plasticity. Genetic inhibition of
    Significance: PCa that escapes therapy targeting the androgen receptor signaling pathways via phenotypic plasticity are currently untreatable. Our study identifies MYBL2 as a MR-TF in phenotypic plastic PCa and implicates CDK2 inhibition as novel therapeutic target for this most lethal subtype of PCa.
    Language English
    Publishing date 2024-02-02
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.31.578216
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  10. Article ; Online: Epigenetic reprogramming: A key mechanism driving therapeutic resistance.

    Sheahan, Anjali V / Ellis, Leigh

    Urologic oncology

    2018  Volume 36, Issue 8, Page(s) 375–379

    Abstract: Prostate cancer initiation, development and progression is driven by androgen receptor (AR) signaling. Androgen deprivation therapy is the primary treatment for patients that present with locally advanced or metastatic disease. However, androgen ... ...

    Abstract Prostate cancer initiation, development and progression is driven by androgen receptor (AR) signaling. Androgen deprivation therapy is the primary treatment for patients that present with locally advanced or metastatic disease. However, androgen deprivation therapy is not curative, and patients will progress to castrate-resistant disease (CRPC). Although most patient's progress to CRPC via restoration of AR signaling (CRPC-Ad), approximately a quarter of patients will progress via mechanisms independent of AR signaling. This highly lethal phenotype is termed aggressive variant prostate cancer (AVPC). Data from clinical and preclinical studies demonstrate that AVPC involves combinatorial loss-of-function mutations in key tumor suppressor genes, low to absent AR levels, and re-expression of reprogramming, stem, and neuroendocrine related gene signatures. Further, AVPC is shown to evolve from a CRPC-Ad phenotype. Overall, lineage plasticity underlying progression to AVPC is thought to be provoked by genome-wide chromatin remodeling. Here, we will discuss an emerging focus on key drivers of chromatin remodeling in AVPC, and how their identification could provide noninvasive biomarkers to predict or detect AVPC emergence, and therapeutic targets to prevent or reverse progression to AVPC.
    MeSH term(s) Disease Progression ; Drug Resistance, Neoplasm/genetics ; Epigenomics/methods ; Humans ; Male ; Prostatic Neoplasms, Castration-Resistant/genetics ; Prostatic Neoplasms, Castration-Resistant/pathology
    Language English
    Publishing date 2018-02-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1336505-8
    ISSN 1873-2496 ; 1078-1439
    ISSN (online) 1873-2496
    ISSN 1078-1439
    DOI 10.1016/j.urolonc.2017.12.021
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