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  1. Article ; Online: Oncogenesis by E2A-PBX1 in ALL: RUNX and more.

    Licht, Jonathan D

    Blood

    2020  Volume 136, Issue 1, Page(s) 3–4

    MeSH term(s) Carcinogenesis/genetics ; Cell Transformation, Neoplastic ; Core Binding Factor Alpha 2 Subunit/genetics ; Humans ; Precursor Cell Lymphoblastic Leukemia-Lymphoma
    Chemical Substances Core Binding Factor Alpha 2 Subunit ; RUNX1 protein, human
    Language English
    Publishing date 2020-07-02
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood.2020005879
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    In stock of ZB MED Cologne/Königswinter

    Uh III Zs.140: Show issues Location:
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    Zs.MO 364: Show issues

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  2. Article ; Online: Histone H3 G34 Tail Mutations in Cancer: Actions in

    Licht, Jonathan D

    Cancer discovery

    2020  Volume 10, Issue 12, Page(s) 1794–1796

    Abstract: Sequencing of cancer genomes has demonstrated that driver mutations occur in every component of the transcriptional machinery including histones that comprise the nucleosome. Histone mutations may affect the "tail" residues subject to post-translational ... ...

    Abstract Sequencing of cancer genomes has demonstrated that driver mutations occur in every component of the transcriptional machinery including histones that comprise the nucleosome. Histone mutations may affect the "tail" residues subject to post-translational modification and can compromise the structural integrity of the histone octamer.
    MeSH term(s) Cell Differentiation ; Chromatin/genetics ; Gene Expression ; Giant Cell Tumor of Bone ; Histones/genetics ; Humans ; Mutation ; Nucleosomes/genetics ; Osteoblasts
    Chemical Substances Chromatin ; Histones ; Nucleosomes
    Language English
    Publishing date 2020-12-01
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-20-1396
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    Zs.A 6916: Show issues Location:
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  3. Article ; Online: Leveraging epigenetics to enhance the efficacy of immunotherapy.

    Licht, Jonathan D / Bennett, Richard L

    Clinical epigenetics

    2021  Volume 13, Issue 1, Page(s) 115

    Abstract: Background: Epigenetic mechanisms regulate chromatin accessibility patterns that govern interaction of transcription machinery with genes and their cis-regulatory elements. Mutations that affect epigenetic mechanisms are common in cancer. Because ... ...

    Abstract Background: Epigenetic mechanisms regulate chromatin accessibility patterns that govern interaction of transcription machinery with genes and their cis-regulatory elements. Mutations that affect epigenetic mechanisms are common in cancer. Because epigenetic modifications are reversible many anticancer strategies targeting these mechanisms are currently under development and in clinical trials.
    Main body: Here we review evidence suggesting that epigenetic therapeutics can deactivate immunosuppressive gene expression or reprogram tumor cells to activate antigen presentation mechanisms. In addition, the dysregulation of epigenetic mechanisms commonly observed in cancer may alter the immunogenicity of tumor cells and effectiveness of immunotherapies.
    Conclusions: Therapeutics targeting epigenetic mechanisms may be helpful to counter immune evasion and improve the effectiveness of immunotherapies.
    MeSH term(s) Epigenesis, Genetic/immunology ; Epigenomics/methods ; Humans ; Immunotherapy/methods ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/therapy
    Language English
    Publishing date 2021-05-17
    Publishing country Germany
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 2553921-8
    ISSN 1868-7083 ; 1868-7075
    ISSN (online) 1868-7083
    ISSN 1868-7075
    DOI 10.1186/s13148-021-01100-x
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  4. Article: DISORDERED HISTONE METHYLATION IN HEMATOLOGICAL MALIGNANCIES THE CASE OF UTX/KDM6A.

    Licht, Jonathan D

    Transactions of the American Clinical and Climatological Association

    2018  Volume 129, Page(s) 24–36

    Abstract: Alterations of epigenetic proteins that modulate the gene repressive lysine 27 on histone H3 (H3K27me) are recurrent features in cancers, including multiple myeloma (MM). The histone demethylase UTX/KDM6A, mutated in up to 10% of cases of MM activates ... ...

    Abstract Alterations of epigenetic proteins that modulate the gene repressive lysine 27 on histone H3 (H3K27me) are recurrent features in cancers, including multiple myeloma (MM). The histone demethylase UTX/KDM6A, mutated in up to 10% of cases of MM activates genes by removing the H3K27me3 repressive histone mark, counteracting EZH2. RNA-sequencing studies showed that UTX upregulated genes in association with loss of H3K27me. Treatment of MM cell lines with an EZH2 inhibitor preferentially slowed growth of
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Cell Death ; Cell Line, Tumor ; Enhancer of Zeste Homolog 2 Protein/antagonists & inhibitors ; Enhancer of Zeste Homolog 2 Protein/genetics ; Enhancer of Zeste Homolog 2 Protein/metabolism ; Epigenesis, Genetic ; Female ; Gene Expression Regulation, Neoplastic ; Histone Demethylases/genetics ; Histone Demethylases/metabolism ; Histones/metabolism ; Humans ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/metabolism ; Methylation ; Mice, Inbred C57BL ; Mice, Nude ; Multiple Myeloma/drug therapy ; Multiple Myeloma/genetics ; Multiple Myeloma/metabolism ; Multiple Myeloma/pathology ; Mutation ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Proto-Oncogene Proteins c-bcl-6/genetics ; Proto-Oncogene Proteins c-bcl-6/metabolism ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Xenograft Model Antitumor Assays
    Chemical Substances Antineoplastic Agents ; BCL6 protein, human ; Histones ; Interferon Regulatory Factors ; MYC protein, human ; Nuclear Proteins ; Proto-Oncogene Proteins c-bcl-6 ; Proto-Oncogene Proteins c-myc ; interferon regulatory factor-4 ; Histone Demethylases (EC 1.14.11.-) ; UTX protein, human (EC 1.14.11.-) ; EZH2 protein, human (EC 2.1.1.43) ; Enhancer of Zeste Homolog 2 Protein (EC 2.1.1.43)
    Language English
    Publishing date 2018-08-30
    Publishing country United States
    Document type Journal Article
    ZDB-ID 603823-2
    ISSN 0065-7778
    ISSN 0065-7778
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.B 4: Show issues Location:
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  5. Article ; Online: SETD2: a complex role in blood malignancy.

    Licht, Jonathan D

    Blood

    2017  Volume 130, Issue 24, Page(s) 2576–2578

    MeSH term(s) Histone-Lysine N-Methyltransferase ; Humans ; Neoplasms
    Chemical Substances Histone-Lysine N-Methyltransferase (EC 2.1.1.43)
    Language English
    Publishing date 2017-12-14
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2017-10-811927
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  6. Article ; Online: Histone mutations in cancer.

    Espinoza Pereira, Kimberly N / Shan, Jixiu / Licht, Jonathan D / Bennett, Richard L

    Biochemical Society transactions

    2023  Volume 51, Issue 5, Page(s) 1749–1763

    Abstract: Genes encoding histone proteins are recurrently mutated in tumor samples, and these mutations may impact nucleosome stability, histone post-translational modification, or chromatin dynamics. The prevalence of histone mutations across diverse cancer types ...

    Abstract Genes encoding histone proteins are recurrently mutated in tumor samples, and these mutations may impact nucleosome stability, histone post-translational modification, or chromatin dynamics. The prevalence of histone mutations across diverse cancer types suggest that normal chromatin structure is a barrier to tumorigenesis. Oncohistone mutations disrupt chromatin structure and gene regulatory mechanisms, resulting in aberrant gene expression and the development of cancer phenotypes. Examples of oncohistones include the histone H3 K27M mutation found in pediatric brain cancers that blocks post-translational modification of the H3 N-terminal tail and the histone H2B E76K mutation found in some solid tumors that disrupts nucleosome stability. Oncohistones may comprise a limited fraction of the total histone pool yet cause global effects on chromatin structure and drive cancer phenotypes. Here, we survey histone mutations in cancer and review their function and role in tumorigenesis.
    MeSH term(s) Humans ; Child ; Histones/metabolism ; Nucleosomes/genetics ; Mutation ; Neoplasms/genetics ; Neoplasms/pathology ; Chromatin ; Carcinogenesis/genetics ; Cell Transformation, Neoplastic/genetics
    Chemical Substances Histones ; Nucleosomes ; Chromatin
    Language English
    Publishing date 2023-09-18
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 184237-7
    ISSN 1470-8752 ; 0300-5127
    ISSN (online) 1470-8752
    ISSN 0300-5127
    DOI 10.1042/BST20210567
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    Zs.A 944: Show issues Location:
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  7. Article ; Online: DNA Methylation Inhibitors in Cancer Therapy: The Immunity Dimension.

    Licht, Jonathan D

    Cell

    2015  Volume 162, Issue 5, Page(s) 938–939

    Abstract: DNA demethylating agents are approved for some blood malignancies and are under active investigation in solid tumors, but how these drugs work has remained unclear. In this issue of Cell, two groups show that these agents activate a toxic cellular ... ...

    Abstract DNA demethylating agents are approved for some blood malignancies and are under active investigation in solid tumors, but how these drugs work has remained unclear. In this issue of Cell, two groups show that these agents activate a toxic cellular antiviral program through transcriptional activation of endogenous retroviral sequences.
    MeSH term(s) Animals ; Antimetabolites, Antineoplastic/pharmacology ; Azacitidine/analogs & derivatives ; Colorectal Neoplasms/drug therapy ; Colorectal Neoplasms/immunology ; DNA Methylation/drug effects ; Female ; Humans ; Interferon Type I/immunology ; Melanoma/immunology ; Melanoma/therapy
    Chemical Substances Antimetabolites, Antineoplastic ; Interferon Type I ; Azacitidine (M801H13NRU)
    Language English
    Publishing date 2015-08-27
    Publishing country United States
    Document type Comment ; Journal Article
    ZDB-ID 187009-9
    ISSN 1097-4172 ; 0092-8674
    ISSN (online) 1097-4172
    ISSN 0092-8674
    DOI 10.1016/j.cell.2015.08.005
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    Zs.A 1167: Show issues Location:
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    Zs.MG 58: Show issues

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  8. Article ; Online: FQI1: a transcription-methylation switch for cancer.

    Guryanova, Olga A / Licht, Jonathan D

    Oncotarget

    2017  Volume 8, Issue 8, Page(s) 12536–12537

    MeSH term(s) Carcinoma, Hepatocellular/genetics ; DNA Methylation ; Humans ; Liver Neoplasms/genetics ; Transcription Factors
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2017-02-02
    Publishing country United States
    Document type News ; Comment
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.15087
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  9. Article ; Online: Cancer incidence after asthma diagnosis: Evidence from a large clinical research network in the United States.

    Guo, Yi / Bian, Jiang / Chen, Zhaoyi / Fishe, Jennifer N / Zhang, Dongyu / Braithwaite, Dejana / George, Thomas J / Shenkman, Elizabeth A / Licht, Jonathan D

    Cancer medicine

    2023  Volume 12, Issue 10, Page(s) 11871–11877

    Abstract: Background: Prior studies on the association between asthma and cancer show inconsistent results. This study aimed to generate additional evidence on the association between asthma and cancer, both overall, and by cancer type, in the United States.: ... ...

    Abstract Background: Prior studies on the association between asthma and cancer show inconsistent results. This study aimed to generate additional evidence on the association between asthma and cancer, both overall, and by cancer type, in the United States.
    Method: We conducted a retrospective cohort study using 2012-2020 electronic health records and claims data in the OneFlorida+ clinical research network. Our study population included a cohort of adult patients with asthma (n = 90,021) and a matching cohort of adult patients without asthma (n = 270,063). We built Cox proportional hazards models to examine the association between asthma diagnosis and subsequent cancer risk.
    Results: Our results showed that asthma patients were more likely to develop cancer compared to patients without asthma in multivariable analysis (hazard ratio [HR] = 1.36, 99% confidence interval [CI] = 1.29-1.44). Elevated cancer risk was observed in asthma patients without (HR = 1.60; 99% CI: 1.50-1.71) or with (HR = 1.11; 99% CI: 1.03-1.21) inhaled steroid use. However, in analyses of specific cancer types, cancer risk was elevated for nine of 13 cancers in asthma patients without inhaled steroid use but only for two of 13 cancers in asthma patients with inhaled steroid use, suggesting a protective effect of inhaled steroid use on cancer.
    Conclusion: This is the first study to report a positive association between asthma and overall cancer risk in the US population. More in-depth studies using real-word data are needed to further explore the causal mechanisms of asthma on cancer risk.
    MeSH term(s) Adult ; Humans ; United States/epidemiology ; Retrospective Studies ; Incidence ; Administration, Inhalation ; Asthma/diagnosis ; Asthma/epidemiology ; Asthma/drug therapy ; Steroids ; Neoplasms/diagnosis ; Neoplasms/epidemiology
    Chemical Substances Steroids
    Language English
    Publishing date 2023-03-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2659751-2
    ISSN 2045-7634 ; 2045-7634
    ISSN (online) 2045-7634
    ISSN 2045-7634
    DOI 10.1002/cam4.5875
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  10. Article: HIRA-mediated loading of histone variant H3.3 controls androgen-induced transcription by regulation of AR/BRD4 complex assembly at enhancers.

    Morozov, Viacheslav M / Riva, Alberto / Sarwar, Sadia / Kim, WanJu / Li, Jianping / Zhou, Lei / Licht, Jonathan D / Daaka, Yehia / Ishov, Alexander M

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Incorporation of histone variant H3.3 comprises active territories of chromatin. Exploring the function of H3.3 in prostate cancer (PC), we found that knockout (KO) of H3.3 chaperone HIRA suppresses PC growth : Key points: *H3.3 at enhancers promotes ... ...

    Abstract Incorporation of histone variant H3.3 comprises active territories of chromatin. Exploring the function of H3.3 in prostate cancer (PC), we found that knockout (KO) of H3.3 chaperone HIRA suppresses PC growth
    Key points: *H3.3 at enhancers promotes acetylation of H3K27Ac and retention of AR/BRD4 complex for transcription regulation*Knockout of H3.3 chaperone HIRA suppresses PC cells growth and deregulates androgen-induced transcription*H3.3/HIRA pathway regulates both AR and GR, suggesting a common HIRA/H3.3 mechanism of nuclear receptors function.
    Language English
    Publishing date 2023-05-08
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.05.08.536256
    Database MEDical Literature Analysis and Retrieval System OnLINE

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