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  1. Article ; Online: Triple-negative breast tumors are dependent on mutant p53 for growth and survival.

    Dibra, Denada / Moyer, Sydney M / El-Naggar, Adel K / Qi, Yuan / Su, Xiaoping / Lozano, Guillermina

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

    2023  Volume 120, Issue 34, Page(s) e2308807120

    Abstract: ... ...

    Abstract The
    MeSH term(s) Animals ; Humans ; Mice ; Genes, p53 ; Mutation ; Mutation, Missense ; Triple Negative Breast Neoplasms/metabolism ; Tumor Microenvironment ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Tumor Suppressor Protein p53 ; Trp53 protein, mouse
    Language English
    Publishing date 2023-08-14
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2308807120
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  2. Article ; Online: Mutant p53 protects triple-negative breast adenocarcinomas from ferroptosis in vivo.

    Dibra, Denada / Xiong, Shunbin / Moyer, Sydney M / El-Naggar, Adel K / Qi, Yuan / Su, Xiaoping / Kong, Elisabeth K / Korkut, Anil / Lozano, Guillermina

    Science advances

    2024  Volume 10, Issue 7, Page(s) eadk1835

    Abstract: ... ...

    Abstract The
    MeSH term(s) Animals ; Humans ; Mice ; Adenocarcinoma ; Cell Line, Tumor ; Ferroptosis/genetics ; Triple Negative Breast Neoplasms/pathology ; Tumor Microenvironment ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Tumor Suppressor Protein p53 ; Trp53 protein, mouse
    Language English
    Publishing date 2024-02-14
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adk1835
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  3. Article ; Online: Aberrant cell state plasticity mediated by developmental reprogramming precedes colorectal cancer initiation.

    Bala, Pratyusha / Rennhack, Jonathan P / Aitymbayev, Daulet / Morris, Clare / Moyer, Sydney M / Duronio, Gina N / Doan, Paul / Li, Zhixin / Liang, Xiaoyan / Hornick, Jason L / Yurgelun, Matthew B / Hahn, William C / Sethi, Nilay S

    Science advances

    2023  Volume 9, Issue 13, Page(s) eadf0927

    Abstract: Cell state plasticity is carefully regulated in adult epithelia to prevent cancer. The aberrant expansion of the normally restricted capability for cell state plasticity in neoplasia is poorly defined. Using genetically engineered and carcinogen-induced ... ...

    Abstract Cell state plasticity is carefully regulated in adult epithelia to prevent cancer. The aberrant expansion of the normally restricted capability for cell state plasticity in neoplasia is poorly defined. Using genetically engineered and carcinogen-induced mouse models of intestinal neoplasia, we observed that impaired differentiation is a conserved event preceding cancer development. Single-cell RNA sequencing (scRNA-seq) of premalignant lesions from mouse models and a patient with hereditary polyposis revealed that cancer initiates by adopting an aberrant transcriptional state characterized by regenerative activity, marked by
    MeSH term(s) Mice ; Animals ; Intestines ; Colorectal Neoplasms/genetics ; Colorectal Neoplasms/pathology ; Cell Differentiation ; Adenoma/genetics ; Adenoma/pathology
    Language English
    Publishing date 2023-03-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adf0927
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  4. Article ; Online: p53 drives a transcriptional program that elicits a non-cell-autonomous response and alters cell state in vivo.

    Moyer, Sydney M / Wasylishen, Amanda R / Qi, Yuan / Fowlkes, Natalie / Su, Xiaoping / Lozano, Guillermina

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

    2020  Volume 117, Issue 38, Page(s) 23663–23673

    Abstract: Cell stress and DNA damage activate the tumor suppressor p53, triggering transcriptional activation of a myriad of target genes. The molecular, morphological, and physiological consequences of this activation remain poorly understood in vivo. We ... ...

    Abstract Cell stress and DNA damage activate the tumor suppressor p53, triggering transcriptional activation of a myriad of target genes. The molecular, morphological, and physiological consequences of this activation remain poorly understood in vivo. We activated a p53 transcriptional program in mice by deletion of
    MeSH term(s) Animals ; Chromatin Immunoprecipitation ; Female ; Intestine, Small/cytology ; Intestine, Small/metabolism ; Male ; Mice ; Mice, Transgenic ; Organ Specificity/genetics ; Pancreas/cytology ; Pancreas/metabolism ; Proto-Oncogene Proteins c-mdm2/genetics ; Single-Cell Analysis ; Transcriptome/genetics ; Tumor Suppressor Protein p53/analysis ; Tumor Suppressor Protein p53/genetics ; Tumor Suppressor Protein p53/metabolism
    Chemical Substances Trp53 protein, mouse ; Tumor Suppressor Protein p53 ; Mdm2 protein, mouse (EC 2.3.2.27) ; Proto-Oncogene Proteins c-mdm2 (EC 2.3.2.27)
    Language English
    Publishing date 2020-09-08
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2008474117
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1148: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Mdm proteins: critical regulators of embry ogenesis and homeostasis.

    Moyer, Sydney M / Larsson, Connie A / Lozano, Guillermina

    Journal of molecular cell biology

    2017  

    Abstract: Mdm2 and Mdm4 are negative regulators of the tumor suppressor p53; hence, this relationship is the focus of many cancer related studies. A multitude of experiments across various developmental stages have been conducted to explore the tissue-specific ... ...

    Abstract Mdm2 and Mdm4 are negative regulators of the tumor suppressor p53; hence, this relationship is the focus of many cancer related studies. A multitude of experiments across various developmental stages have been conducted to explore the tissue-specific roles of these proteins in the mouse. When Mdm2 or Mdm4 are deleted in the germline or specific tissues, they display different phenotypic defects, some of which lead to embryonic lethality. Mdm2 loss is often more deleterious than loss of its homolog Mdm4 All tissues experience activation of p53 target genes upon loss of Mdm2 or Mdm4; however, the degree to which the p53 pathway is perturbed is highly tissue-specific and does not correlate to the severity of the morphological phenotypes. Therefore, a need for further understanding of how these proteins regulate p53 activity is warranted, as therapeutic targeting of the p53 pathway is rapidly evolving and gaining attention in the field of cancer research. In this review, we discuss the tissue-specificity of Mdm proteins in regulating p53 and expose the need for investigation at the cell-specific level.
    Language English
    Publishing date 2017-01-15
    Publishing country United States
    Document type Review ; Journal Article
    ZDB-ID 2500949-7
    ISSN 1759-4685 ; 1759-4685
    ISSN (online) 1759-4685
    ISSN 1759-4685
    DOI 10.1093/jmcb/mjx004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: A Ubiquitination Cascade Regulating the Integrated Stress Response and Survival in Carcinomas.

    Cervia, Lisa D / Shibue, Tsukasa / Borah, Ashir A / Gaeta, Benjamin / He, Linh / Leung, Lisa / Li, Naomi / Moyer, Sydney M / Shim, Brian H / Dumont, Nancy / Gonzalez, Alfredo / Bick, Nolan R / Kazachkova, Mariya / Dempster, Joshua M / Krill-Burger, John Michael / Piccioni, Federica / Udeshi, Namrata D / Olive, Meagan E / Carr, Steven A /
    Root, David E / McFarland, James M / Vazquez, Francisca / Hahn, William C

    Cancer discovery

    2022  Volume 13, Issue 3, Page(s) 766–795

    Abstract: Systematic identification of signaling pathways required for the fitness of cancer cells will facilitate the development of new cancer therapies. We used gene essentiality measurements in 1,086 cancer cell lines to identify selective coessentiality ... ...

    Abstract Systematic identification of signaling pathways required for the fitness of cancer cells will facilitate the development of new cancer therapies. We used gene essentiality measurements in 1,086 cancer cell lines to identify selective coessentiality modules and found that a ubiquitin ligase complex composed of UBA6, BIRC6, KCMF1, and UBR4 is required for the survival of a subset of epithelial tumors that exhibit a high degree of aneuploidy. Suppressing BIRC6 in cell lines that are dependent on this complex led to a substantial reduction in cell fitness in vitro and potent tumor regression in vivo. Mechanistically, BIRC6 suppression resulted in selective activation of the integrated stress response (ISR) by stabilization of the heme-regulated inhibitor, a direct ubiquitination target of the UBA6/BIRC6/KCMF1/UBR4 complex. These observations uncover a novel ubiquitination cascade that regulates ISR and highlight the potential of ISR activation as a new therapeutic strategy.
    Significance: We describe the identification of a heretofore unrecognized ubiquitin ligase complex that prevents the aberrant activation of the ISR in a subset of cancer cells. This provides a novel insight on the regulation of ISR and exposes a therapeutic opportunity to selectively eliminate these cancer cells. See related commentary Leli and Koumenis, p. 535. This article is highlighted in the In This Issue feature, p. 517.
    MeSH term(s) Humans ; Ubiquitination ; Cell Line ; Carcinoma ; Signal Transduction ; Ubiquitins
    Chemical Substances Ubiquitins
    Language English
    Publishing date 2022-12-29
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-22-1230
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 6916: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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  7. Article ; Online: Integrated clinical and genomic analysis identifies driver events and molecular evolution of colitis-associated cancers.

    Chatila, Walid K / Walch, Henry / Hechtman, Jaclyn F / Moyer, Sydney M / Sgambati, Valeria / Faleck, David M / Srivastava, Amitabh / Tang, Laura / Benhamida, Jamal / Ismailgeci, Dorina / Campos, Carl / Wu, Fan / Chang, Qing / Vakiani, Efsevia / de Stanchina, Elisa / Weiser, Martin R / Widmar, Maria / Yantiss, Rhonda K / Shah, Manish A /
    Bass, Adam J / Stadler, Zsofia K / Katz, Lior H / Mellinghoff, Ingo K / Sethi, Nilay S / Schultz, Nikolaus / Ganesh, Karuna / Kelsen, David / Yaeger, Rona

    Nature communications

    2023  Volume 14, Issue 1, Page(s) 110

    Abstract: Inflammation has long been recognized to contribute to cancer development, particularly across the gastrointestinal tract. Patients with inflammatory bowel disease have an increased risk for bowel cancers, and it has been posited that a field of genetic ... ...

    Abstract Inflammation has long been recognized to contribute to cancer development, particularly across the gastrointestinal tract. Patients with inflammatory bowel disease have an increased risk for bowel cancers, and it has been posited that a field of genetic changes may underlie this risk. Here, we define the clinical features, genomic landscape, and germline alterations in 174 patients with colitis-associated cancers and sequenced 29 synchronous or isolated dysplasia. TP53 alterations, an early and highly recurrent event in colitis-associated cancers, occur in half of dysplasia, largely as convergent evolution of independent events. Wnt pathway alterations are infrequent, and our data suggest transcriptional rewiring away from Wnt. Sequencing of multiple dysplasia/cancer lesions from mouse models and patients demonstrates rare shared alterations between lesions. These findings suggest neoplastic bowel lesions developing in a background of inflammation experience lineage plasticity away from Wnt activation early during tumorigenesis and largely occur as genetically independent events.
    MeSH term(s) Animals ; Mice ; Colitis-Associated Neoplasms ; Inflammatory Bowel Diseases/genetics ; Genomics ; Hyperplasia ; Inflammation/complications ; Inflammation/genetics ; Evolution, Molecular
    Language English
    Publishing date 2023-01-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-35592-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Daxx maintains endogenous retroviral silencing and restricts cellular plasticity in vivo.

    Wasylishen, Amanda R / Sun, Chang / Moyer, Sydney M / Qi, Yuan / Chau, Gilda P / Aryal, Neeraj K / McAllister, Florencia / Kim, Michael P / Barton, Michelle C / Estrella, Jeannelyn S / Su, Xiaoping / Lozano, Guillermina

    Science advances

    2020  Volume 6, Issue 32, Page(s) eaba8415

    Abstract: Tumor sequencing studies have emphasized the role of epigenetics and altered chromatin homeostasis in cancer. Mutations ... ...

    Abstract Tumor sequencing studies have emphasized the role of epigenetics and altered chromatin homeostasis in cancer. Mutations in
    MeSH term(s) Animals ; Cell Plasticity ; Co-Repressor Proteins/genetics ; Endogenous Retroviruses/genetics ; Mice ; Molecular Chaperones/genetics ; Molecular Chaperones/metabolism ; Neuroendocrine Tumors/genetics ; Neuroendocrine Tumors/metabolism ; Neuroendocrine Tumors/pathology ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Pancreatic Neoplasms/pathology ; X-linked Nuclear Protein/metabolism
    Chemical Substances Co-Repressor Proteins ; Daxx protein, mouse ; Molecular Chaperones ; Nuclear Proteins ; X-linked Nuclear Protein (EC 3.6.4.12)
    Language English
    Publishing date 2020-08-05
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.aba8415
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: VRK1 as a synthetic lethal target in VRK2 promoter-methylated cancers of the nervous system.

    So, Jonathan / Mabe, Nathaniel W / Englinger, Bernhard / Chow, Kin-Hoe / Moyer, Sydney M / Yerrum, Smitha / Trissal, Maria C / Marques, Joana G / Kwon, Jason J / Shim, Brian / Pal, Sangita / Panditharatna, Eshini / Quinn, Thomas / Schaefer, Daniel A / Jeong, Daeun / Mayhew, David L / Hwang, Justin / Beroukhim, Rameen / Ligon, Keith L /
    Stegmaier, Kimberly / Filbin, Mariella G / Hahn, William C

    JCI insight

    2022  Volume 7, Issue 19

    Abstract: Collateral lethality occurs when loss of a gene/protein renders cancer cells dependent on its remaining paralog. Combining genome-scale CRISPR/Cas9 loss-of-function screens with RNA sequencing in over 900 cancer cell lines, we found that cancers of ... ...

    Abstract Collateral lethality occurs when loss of a gene/protein renders cancer cells dependent on its remaining paralog. Combining genome-scale CRISPR/Cas9 loss-of-function screens with RNA sequencing in over 900 cancer cell lines, we found that cancers of nervous system lineage, including adult and pediatric gliomas and neuroblastomas, required the nuclear kinase vaccinia-related kinase 1 (VRK1) for their survival in vivo. VRK1 dependency was inversely correlated with expression of its paralog VRK2. VRK2 knockout sensitized cells to VRK1 loss, and conversely, VRK2 overexpression increased cell fitness in the setting of VRK1 loss. DNA methylation of the VRK2 promoter was associated with low VRK2 expression in human neuroblastomas and adult and pediatric gliomas. Mechanistically, depletion of VRK1 reduced barrier-to-autointegration factor phosphorylation during mitosis, resulting in DNA damage and apoptosis. Together, these studies identify VRK1 as a synthetic lethal target in VRK2 promoter-methylated adult and pediatric gliomas and neuroblastomas.
    MeSH term(s) Child ; Glioma/genetics ; Humans ; Intracellular Signaling Peptides and Proteins ; Nervous System ; Neuroblastoma/genetics ; Protein Serine-Threonine Kinases/genetics ; Vaccinia ; Vaccinia virus
    Chemical Substances Intracellular Signaling Peptides and Proteins ; Protein Serine-Threonine Kinases (EC 2.7.11.1) ; VRK1 protein, human (EC 2.7.11.1) ; VRK2 protein, human (EC 2.7.11.1)
    Language English
    Publishing date 2022-10-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ISSN 2379-3708
    ISSN (online) 2379-3708
    DOI 10.1172/jci.insight.158755
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: VRK1 as a synthetic lethal target in VRK2 promoter–methylated cancers of the nervous system

    Jonathan So / Nathaniel W. Mabe / Bernhard Englinger / Kin-Hoe Chow / Sydney M. Moyer / Smitha Yerrum / Maria C. Trissal / Joana G. Marques / Jason J. Kwon / Brian Shim / Sangita Pal / Eshini Panditharatna / Thomas Quinn / Daniel A. Schaefer / Daeun Jeong / David L. Mayhew / Justin Hwang / Rameen Beroukhim / Keith L. Ligon /
    Kimberly Stegmaier / Mariella G. Filbin / William C. Hahn

    JCI Insight, Vol 7, Iss

    2022  Volume 19

    Abstract: Collateral lethality occurs when loss of a gene/protein renders cancer cells dependent on its remaining paralog. Combining genome-scale CRISPR/Cas9 loss-of-function screens with RNA sequencing in over 900 cancer cell lines, we found that cancers of ... ...

    Abstract Collateral lethality occurs when loss of a gene/protein renders cancer cells dependent on its remaining paralog. Combining genome-scale CRISPR/Cas9 loss-of-function screens with RNA sequencing in over 900 cancer cell lines, we found that cancers of nervous system lineage, including adult and pediatric gliomas and neuroblastomas, required the nuclear kinase vaccinia-related kinase 1 (VRK1) for their survival in vivo. VRK1 dependency was inversely correlated with expression of its paralog VRK2. VRK2 knockout sensitized cells to VRK1 loss, and conversely, VRK2 overexpression increased cell fitness in the setting of VRK1 loss. DNA methylation of the VRK2 promoter was associated with low VRK2 expression in human neuroblastomas and adult and pediatric gliomas. Mechanistically, depletion of VRK1 reduced barrier-to-autointegration factor phosphorylation during mitosis, resulting in DNA damage and apoptosis. Together, these studies identify VRK1 as a synthetic lethal target in VRK2 promoter–methylated adult and pediatric gliomas and neuroblastomas.
    Keywords Oncology ; Medicine ; R
    Subject code 570
    Language English
    Publishing date 2022-10-01T00:00:00Z
    Publisher American Society for Clinical investigation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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