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  1. Article ; Online: Corrigendum: Identifying a missing lineage driver in a subset of lung neuroendocrine tumors.

    Pozo, Karine / Minna, John D / Johnson, Jane E

    Genes & development

    2018  Volume 32, Issue 17-18, Page(s) 1266

    Language English
    Publishing date 2018-09-01
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.319129.118
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 2292: Show issues Location:
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  2. Article: The Emerging Role of Cdk5 in Cancer.

    Pozo, Karine / Bibb, James A

    Trends in cancer

    2016  Volume 2, Issue 10, Page(s) 606–618

    Abstract: Cdk5 is an atypical cyclin-dependent kinase that is well characterized for its role in the central nervous system rather than in the cell cycle. However Cdk5 has been recently implicated in the development and progression of a variety of cancers ... ...

    Abstract Cdk5 is an atypical cyclin-dependent kinase that is well characterized for its role in the central nervous system rather than in the cell cycle. However Cdk5 has been recently implicated in the development and progression of a variety of cancers including breast, lung, colon, pancreatic, melanoma, thyroid and brain tumors. This broad pro-tumorigenic role makes Cdk5 a promising drug target for the development of new cancer therapies. Here we review the contribution of Cdk5 to molecular mechanisms that confer upon tumors the ability to grow, proliferate and disseminate to secondary organs, as well as resistance to chemotherapies. We subsequently discuss existing and new strategies for targeting Cdk5 and its downstream mechanisms as anti-cancer treatments.
    Language English
    Publishing date 2016-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2852626-0
    ISSN 2405-8033 ; 2405-8025 ; 2405-8033
    ISSN (online) 2405-8033 ; 2405-8025
    ISSN 2405-8033
    DOI 10.1016/j.trecan.2016.09.001
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Identifying a missing lineage driver in a subset of lung neuroendocrine tumors.

    Pozo, Karine / Minna, John D / Johnson, Jane E

    Genes & development

    2018  Volume 32, Issue 13-14, Page(s) 865–867

    Abstract: Tumor heterogeneity of a primary histologic cancer type has major implications for cancer research and therapeutics. An important and understudied aspect of this heterogeneity is the role of transcription factors that serve as "lineage oncogenes" in a ... ...

    Abstract Tumor heterogeneity of a primary histologic cancer type has major implications for cancer research and therapeutics. An important and understudied aspect of this heterogeneity is the role of transcription factors that serve as "lineage oncogenes" in a tumor type. A demonstration that different subgroups have distinct dependencies on lineage-specific transcription factors is highlighted in a relatively homogenous cancer type: the pulmonary neuroendocrine cancer small cell lung carcinoma (SCLC). Identification of these factors is providing new insights into the origin of the heterogeneity and subtype-specific vulnerabilities in SCLC and provides a template for studying heterogeneity in other cancer types.
    MeSH term(s) Carcinoma, Neuroendocrine/physiopathology ; Cell Lineage ; Genetic Heterogeneity ; Humans ; Lung Neoplasms/physiopathology ; Mutation ; Small Cell Lung Carcinoma/physiopathology ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Transcription Factors
    Language English
    Publishing date 2018-06-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 806684-x
    ISSN 1549-5477 ; 0890-9369
    ISSN (online) 1549-5477
    ISSN 0890-9369
    DOI 10.1101/gad.316943.118
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Different Originating Cells Underlie Intertumoral Heterogeneity in Lung Neuroendocrine Tumors.

    Pozo, Karine / Kelenis, Demetra P / Minna, John D / Johnson, Jane E

    Cancer discovery

    2018  Volume 8, Issue 10, Page(s) 1216–1218

    MeSH term(s) Animals ; Lung Neoplasms ; Mice ; Mutation ; Neuroendocrine Tumors ; Small Cell Lung Carcinoma
    Language English
    Publishing date 2018-03-15
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-18-0979
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  5. Article ; Online: ASCL1, NKX2-1, and PROX1 co-regulate subtype-specific genes in small-cell lung cancer.

    Pozo, Karine / Kollipara, Rahul K / Kelenis, Demetra P / Rodarte, Kathia E / Ullrich, Morgan S / Zhang, Xiaoyang / Minna, John D / Johnson, Jane E

    iScience

    2021  Volume 24, Issue 9, Page(s) 102953

    Abstract: Lineage-defining transcription factors (LTFs) play key roles in small-cell lung cancer (SCLC) pathophysiology. Delineating the LTF-regulated genes operative in SCLC could provide a road map to identify SCLC dependencies. We integrated chromatin landscape ...

    Abstract Lineage-defining transcription factors (LTFs) play key roles in small-cell lung cancer (SCLC) pathophysiology. Delineating the LTF-regulated genes operative in SCLC could provide a road map to identify SCLC dependencies. We integrated chromatin landscape and transcriptome analyses of patient-derived SCLC preclinical models to identify super-enhancers (SEs) and their associated genes in the ASCL1-, NEUROD1-, and POU2F3-high SCLC subtypes. We find SE signatures predict LTF-based classification of SCLC, and the SE-associated genes are enriched with those defined as common essential genes in DepMap. In addition, in ASCL1-high SCLC, we show ASCL1 complexes with NKX2-1 and PROX1 to co-regulate genes functioning in NOTCH signaling, catecholamine biosynthesis, and cell-cycle processes. Depletion of ASCL1 demonstrates it is a key dependency factor in preclinical SCLC models and directly regulates multiple DepMap-defined essential genes. We provide LTF/SE-based subtype-specific gene sets for SCLC for further therapeutic investigation.
    Language English
    Publishing date 2021-08-05
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2021.102953
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Intrinsic DNA binding properties demonstrated for lineage-specifying basic helix-loop-helix transcription factors.

    Casey, Bradford H / Kollipara, Rahul K / Pozo, Karine / Johnson, Jane E

    Genome research

    2018  Volume 28, Issue 4, Page(s) 484–496

    Abstract: During development, transcription factors select distinct gene programs, providing the necessary regulatory complexity for temporal and tissue-specific gene expression. How related factors retain specificity, especially when they recognize the same DNA ... ...

    Abstract During development, transcription factors select distinct gene programs, providing the necessary regulatory complexity for temporal and tissue-specific gene expression. How related factors retain specificity, especially when they recognize the same DNA motifs, is not understood. We address this paradox using basic helix-loop-helix (bHLH) transcription factors ASCL1, ASCL2, and MYOD1, crucial mediators of lineage specification. In vivo, these factors recognize the same DNA motifs, yet bind largely different genomic sites and regulate distinct transcriptional programs. This suggests that their ability to identify regulatory targets is defined either by the cellular environment of the partially defined lineages in which they are endogenously expressed, or by intrinsic properties of the factors themselves. To distinguish between these mechanisms, we directly compared the chromatin binding properties of this subset of bHLH factors when ectopically expressed in embryonic stem cells, presenting them with a common chromatin landscape and cellular components. We find that these factors retain distinct binding sites; thus, specificity of binding is an intrinsic property not requiring a restricted landscape or lineage-specific cofactors. Although the ASCL factors and MYOD1 have some distinct DNA motif preference, it is not sufficient to explain the extent of the differential binding. All three factors can bind inaccessible chromatin and induce changes in chromatin accessibility and H3K27ac. A reiterated pattern of DNA binding motifs is uniquely enriched in inaccessible chromatin at sites bound by these bHLH factors. These combined properties define a subclass of lineage-specific bHLH factors and provide context for their central roles in development and disease.
    MeSH term(s) Amino Acid Sequence/genetics ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Binding Sites ; Chromatin/genetics ; DNA-Binding Proteins/genetics ; Gene Expression Regulation ; Genome ; Humans ; MyoD Protein/genetics ; Nucleotide Motifs/genetics ; Protein Binding/genetics
    Chemical Substances ASCL1 protein, human ; ASCL2 protein, human ; Basic Helix-Loop-Helix Transcription Factors ; Chromatin ; DNA-Binding Proteins ; MyoD Protein ; MyoD1 myogenic differentiation protein
    Language English
    Publishing date 2018-03-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1284872-4
    ISSN 1549-5469 ; 1088-9051 ; 1054-9803
    ISSN (online) 1549-5469
    ISSN 1088-9051 ; 1054-9803
    DOI 10.1101/gr.224360.117
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    Zs.A 3729: Show issues Location:
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  7. Article ; Online: Correction to: Exposure to mild blast forces induces neuropathological effects, neurophysiological deficits and biochemical changes.

    Hernandez, Adan / Tan, Chunfeng / Plattner, Florian / Logsdon, Aric F / Pozo, Karine / Yousuf, Mohammad A / Singh, Tanvir / Turner, Ryan C / Lucke-Wold, Brandon P / Huber, Jason D / Rosen, Charles L / Bibb, James A

    Molecular brain

    2021  Volume 14, Issue 1, Page(s) 164

    Language English
    Publishing date 2021-11-10
    Publishing country England
    Document type Published Erratum
    ZDB-ID 2436057-0
    ISSN 1756-6606 ; 1756-6606
    ISSN (online) 1756-6606
    ISSN 1756-6606
    DOI 10.1186/s13041-021-00872-w
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  8. Article ; Online: Inhibition of Karyopherin β1-Mediated Nuclear Import Disrupts Oncogenic Lineage-Defining Transcription Factor Activity in Small Cell Lung Cancer.

    Kelenis, Demetra P / Rodarte, Kathia E / Kollipara, Rahul K / Pozo, Karine / Choudhuri, Shreoshi Pal / Spainhower, Kyle B / Wait, Sarah J / Stastny, Victor / Oliver, Trudy G / Johnson, Jane E

    Cancer research

    2022  Volume 82, Issue 17, Page(s) 3058–3073

    Abstract: Genomic studies support the classification of small cell lung cancer (SCLC) into subtypes based on the expression of lineage-defining transcription factors ASCL1 and NEUROD1, which together are expressed in ∼86% of SCLC. ASCL1 and NEUROD1 activate SCLC ... ...

    Abstract Genomic studies support the classification of small cell lung cancer (SCLC) into subtypes based on the expression of lineage-defining transcription factors ASCL1 and NEUROD1, which together are expressed in ∼86% of SCLC. ASCL1 and NEUROD1 activate SCLC oncogene expression, drive distinct transcriptional programs, and maintain the in vitro growth and oncogenic properties of ASCL1 or NEUROD1-expressing SCLC. ASCL1 is also required for tumor formation in SCLC mouse models. A strategy to inhibit the activity of these oncogenic drivers may therefore provide both a targeted therapy for the predominant SCLC subtypes and a tool to investigate the underlying lineage plasticity of established SCLC tumors. However, there are no known agents that inhibit ASCL1 or NEUROD1 function. In this study, we identify a novel strategy to pharmacologically target ASCL1 and NEUROD1 activity in SCLC by exploiting the nuclear localization required for the function of these transcription factors. Karyopherin β1 (KPNB1) was identified as a nuclear import receptor for both ASCL1 and NEUROD1 in SCLC, and inhibition of KPNB1 led to impaired ASCL1 and NEUROD1 nuclear accumulation and transcriptional activity. Pharmacologic targeting of KPNB1 preferentially disrupted the growth of ASCL1+ and NEUROD1+ SCLC cells in vitro and suppressed ASCL1+ tumor growth in vivo, an effect mediated by a combination of impaired ASCL1 downstream target expression, cell-cycle activity, and proteostasis. These findings broaden the support for targeting nuclear transport as an anticancer therapeutic strategy and have implications for targeting lineage-transcription factors in tumors beyond SCLC.
    Significance: The identification of KPNB1 as a nuclear import receptor for lineage-defining transcription factors in SCLC reveals a viable therapeutic strategy for cancer treatment.
    MeSH term(s) Active Transport, Cell Nucleus ; Animals ; Basic Helix-Loop-Helix Transcription Factors/genetics ; Basic Helix-Loop-Helix Transcription Factors/metabolism ; Carcinogenesis/genetics ; Cell Line, Tumor ; Gene Expression Regulation, Neoplastic ; Karyopherins/metabolism ; Lung Neoplasms/drug therapy ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Mice ; Oncogenes ; Small Cell Lung Carcinoma/drug therapy ; Small Cell Lung Carcinoma/genetics ; Small Cell Lung Carcinoma/metabolism ; Transcription Factors/genetics ; Transcription Factors/metabolism
    Chemical Substances Basic Helix-Loop-Helix Transcription Factors ; Karyopherins ; Transcription Factors
    Language English
    Publishing date 2022-12-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-21-3713
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Breaking Bad: how does a neuronal protein cause neuroendocrine cancer?

    Pozo, Karine / Nwariaku, Fiemu E / Bibb, James A

    Oncotarget

    2013  Volume 5, Issue 1, Page(s) 5–6

    MeSH term(s) Animals ; Carrier Proteins ; Cell Cycle Proteins ; DNA-Binding Proteins ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Retinoblastoma Protein/physiology ; Transcription Factors/physiology
    Chemical Substances Carrier Proteins ; Cell Cycle Proteins ; DNA-Binding Proteins ; Retinoblastoma Protein ; Transcription Factors
    Language English
    Publishing date 2013-12-25
    Publishing country United States
    Document type Editorial ; Comment
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.1710
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  10. Article ; Online: Unraveling mechanisms of homeostatic synaptic plasticity.

    Pozo, Karine / Goda, Yukiko

    Neuron

    2010  Volume 66, Issue 3, Page(s) 337–351

    Abstract: Homeostatic synaptic plasticity is a negative feedback mechanism that neurons use to offset excessive excitation or inhibition by adjusting their synaptic strengths. Recent findings reveal a complex web of signaling processes involved in this ... ...

    Abstract Homeostatic synaptic plasticity is a negative feedback mechanism that neurons use to offset excessive excitation or inhibition by adjusting their synaptic strengths. Recent findings reveal a complex web of signaling processes involved in this compensatory form of synaptic strength regulation, and in contrast to the popular view of homeostatic plasticity as a slow, global phenomenon, neurons may also rapidly tune the efficacy of individual synapses on demand. Here we review our current understanding of cellular and molecular mechanisms of homeostatic synaptic plasticity.
    MeSH term(s) Animals ; Homeostasis/physiology ; Models, Neurological ; Nerve Net/physiology ; Neuronal Plasticity/physiology ; Neurons/physiology ; Synapses/physiology ; Synaptic Transmission/physiology
    Language English
    Publishing date 2010-05-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 808167-0
    ISSN 1097-4199 ; 0896-6273
    ISSN (online) 1097-4199
    ISSN 0896-6273
    DOI 10.1016/j.neuron.2010.04.028
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