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  1. Article ; Online: Unraveling MYC's Role in Orchestrating Tumor Intrinsic and Tumor Microenvironment Interactions Driving Tumorigenesis and Drug Resistance.

    Doha, Zinab O / Sears, Rosalie C

    Pathophysiology : the official journal of the International Society for Pathophysiology

    2023  Volume 30, Issue 3, Page(s) 400–419

    Abstract: The transcription factor MYC plays a pivotal role in regulating various cellular processes and has been implicated in tumorigenesis across multiple cancer types. MYC has emerged as a master regulator governing tumor intrinsic and tumor microenvironment ... ...

    Abstract The transcription factor MYC plays a pivotal role in regulating various cellular processes and has been implicated in tumorigenesis across multiple cancer types. MYC has emerged as a master regulator governing tumor intrinsic and tumor microenvironment interactions, supporting tumor progression and driving drug resistance. This review paper aims to provide an overview and discussion of the intricate mechanisms through which MYC influences tumorigenesis and therapeutic resistance in cancer. We delve into the signaling pathways and molecular networks orchestrated by MYC in the context of tumor intrinsic characteristics, such as proliferation, replication stress and DNA repair. Furthermore, we explore the impact of MYC on the tumor microenvironment, including immune evasion, angiogenesis and cancer-associated fibroblast remodeling. Understanding MYC's multifaceted role in driving drug resistance and tumor progression is crucial for developing targeted therapies and combination treatments that may effectively combat this devastating disease. Through an analysis of the current literature, this review's goal is to shed light on the complexities of MYC-driven oncogenesis and its potential as a promising therapeutic target.
    Language English
    Publishing date 2023-09-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 1212740-1
    ISSN 1873-149X ; 0928-4680
    ISSN (online) 1873-149X
    ISSN 0928-4680
    DOI 10.3390/pathophysiology30030031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 4137: Show issues Location:
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  2. Article ; Online: Deconstructing Pancreatic Adenocarcinoma by Targeting the Conductor, MYC.

    English, Isabel A / Sears, Rosalie C

    Cancer discovery

    2020  Volume 10, Issue 4, Page(s) 495–497

    Abstract: In this issue ... ...

    Abstract In this issue of
    MeSH term(s) Adenocarcinoma/drug therapy ; Adenocarcinoma/genetics ; Animals ; Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/genetics ; Mice ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/genetics ; Phenotype
    Language English
    Publishing date 2020-04-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 2625242-9
    ISSN 2159-8290 ; 2159-8274
    ISSN (online) 2159-8290
    ISSN 2159-8274
    DOI 10.1158/2159-8290.CD-20-0046
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 6916: Show issues Location:
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  3. Article ; Online: Reprogramming Pancreatic Ductal Adenocarcinoma to Pluripotency.

    Alshaikh, Amani / Grygoryev, Dmytro / Keith, Dove / Sheppard, Brett / Sears, Rosalie C / Kim, Jungsun / Soufi, Abdenour

    Journal of visualized experiments : JoVE

    2024  , Issue 204

    Abstract: The generation of induced pluripotent stem cells (iPSCs) using transcription factors has been achieved from almost any differentiated cell type and has proved highly valuable for research and clinical applications. Interestingly, iPSC reprogramming of ... ...

    Abstract The generation of induced pluripotent stem cells (iPSCs) using transcription factors has been achieved from almost any differentiated cell type and has proved highly valuable for research and clinical applications. Interestingly, iPSC reprogramming of cancer cells, such as pancreatic ductal adenocarcinoma (PDAC), has been shown to revert the invasive PDAC phenotype and override the cancer epigenome. The differentiation of PDAC-derived iPSCs can recapitulate PDAC progression from its early pancreatic intraepithelial neoplasia (PanIN) precursor, revealing the molecular and cellular changes that occur early during PDAC progression. Therefore, PDAC-derived iPSCs can be used to model the earliest stages of PDAC for the discovery of early-detection diagnostic markers. This is particularly important for PDAC patients, who are typically diagnosed at the late metastatic stages due to a lack of reliable biomarkers for the earlier PanIN stages. However, reprogramming cancer cell lines, including PDAC, into pluripotency remains challenging, labor-intensive, and highly variable between different lines. Here, we describe a more consistent protocol for generating iPSCs from various human PDAC cell lines using bicistronic lentiviral vectors. The resulting iPSC lines are stable, showing no dependence on the exogenous expression of reprogramming factors or inducible drugs. Overall, this protocol facilitates the generation of a wide range of PDAC-derived iPSCs, which is essential for discovering early biomarkers that are more specific and representative of PDAC cases.
    MeSH term(s) Humans ; Pancreatic Neoplasms/pathology ; Carcinoma, Pancreatic Ductal/genetics ; Carcinoma, Pancreatic Ductal/pathology ; Induced Pluripotent Stem Cells/metabolism ; Biomarkers, Tumor/metabolism ; Cell Line, Tumor
    Chemical Substances Biomarkers, Tumor
    Language English
    Publishing date 2024-02-02
    Publishing country United States
    Document type Journal Article ; Video-Audio Media
    ZDB-ID 2259946-0
    ISSN 1940-087X ; 1940-087X
    ISSN (online) 1940-087X
    ISSN 1940-087X
    DOI 10.3791/65811
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Targeting the MYC Ubiquitination-Proteasome Degradation Pathway for Cancer Therapy.

    Sun, Xiao-Xin / Li, Yanping / Sears, Rosalie C / Dai, Mu-Shui

    Frontiers in oncology

    2021  Volume 11, Page(s) 679445

    Abstract: Deregulated MYC overexpression and activation contributes to tumor growth and progression. Given the short half-life and unstable nature of the MYC protein, it is not surprising that the oncoprotein is highly ... ...

    Abstract Deregulated MYC overexpression and activation contributes to tumor growth and progression. Given the short half-life and unstable nature of the MYC protein, it is not surprising that the oncoprotein is highly regulated
    Language English
    Publishing date 2021-06-11
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2649216-7
    ISSN 2234-943X
    ISSN 2234-943X
    DOI 10.3389/fonc.2021.679445
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: The use of protein phosphatase 2A activators in combination therapies for pancreas cancer.

    Allen-Petersen, Brittany L / Sears, Rosalie C

    Oncotarget

    2019  Volume 10, Issue 21, Page(s) 2008–2009

    Language English
    Publishing date 2019-03-12
    Publishing country United States
    Document type Editorial
    ZDB-ID 2560162-3
    ISSN 1949-2553 ; 1949-2553
    ISSN (online) 1949-2553
    ISSN 1949-2553
    DOI 10.18632/oncotarget.26772
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Select Stabilization of a Tumor-Suppressive PP2A Heterotrimer.

    Shah, Vidhi M / English, Isabel A / Sears, Rosalie C

    Trends in pharmacological sciences

    2020  Volume 41, Issue 9, Page(s) 595–597

    Abstract: In cancer, suppression of protein phosphatases, such as protein phosphatase 2A (PP2A), that normally counteract kinases, contributes to aberrant signaling. Leonard et al. recently demonstrated that a novel small-molecule activator of PP2A, DT-061, ... ...

    Abstract In cancer, suppression of protein phosphatases, such as protein phosphatase 2A (PP2A), that normally counteract kinases, contributes to aberrant signaling. Leonard et al. recently demonstrated that a novel small-molecule activator of PP2A, DT-061, selectively stabilizes a specific PP2A holoenzyme responsible for dephosphorylating critical oncogenic targets, including MYC. The 3.6-Å cryo-electron microscopy map of the heterotrimer assembly provides insight into the druggable structure of PP2A, guiding future phosphatase therapeutics.
    MeSH term(s) Cryoelectron Microscopy ; Humans ; Neoplasms/drug therapy ; Protein Phosphatase 2/metabolism ; Signal Transduction
    Chemical Substances Protein Phosphatase 2 (EC 3.1.3.16)
    Language English
    Publishing date 2020-07-02
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 282846-7
    ISSN 1873-3735 ; 0165-6147
    ISSN (online) 1873-3735
    ISSN 0165-6147
    DOI 10.1016/j.tips.2020.06.008
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1513: Show issues Location:
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    Zs.MG 6: Show issues

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  7. Article: PIN1 Provides Dynamic Control of MYC in Response to Extrinsic Signals.

    Cohn, Gabriel M / Liefwalker, Daniel F / Langer, Ellen M / Sears, Rosalie C

    Frontiers in cell and developmental biology

    2020  Volume 8, Page(s) 224

    Abstract: PIN1 is a phosphorylation-directed member of the peptidyl- ... ...

    Abstract PIN1 is a phosphorylation-directed member of the peptidyl-prolyl
    Language English
    Publishing date 2020-04-02
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2737824-X
    ISSN 2296-634X
    ISSN 2296-634X
    DOI 10.3389/fcell.2020.00224
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  8. Article: Sendai virus is robust and consistent in delivering genes into human pancreatic cancer cells.

    Grygoryev, Dmytro / Ekstrom, Taelor / Manalo, Elise / Link, Jason M / Alshaikh, Amani / Keith, Dove / Allen-Petersen, Brittany L / Sheppard, Brett / Morgan, Terry / Soufi, Abdenour / Sears, Rosalie C / Kim, Jungsun

    Heliyon

    2024  Volume 10, Issue 5, Page(s) e27221

    Abstract: Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly intratumorally heterogeneous disease that includes several subtypes and is highly plastic. Effective gene delivery to all PDAC cells is essential for modulating gene expression and ... ...

    Abstract Background: Pancreatic ductal adenocarcinoma (PDAC) is a highly intratumorally heterogeneous disease that includes several subtypes and is highly plastic. Effective gene delivery to all PDAC cells is essential for modulating gene expression and identifying potential gene-based therapeutic targets in PDAC. Most current gene delivery systems for pancreatic cells are optimized for islet or acinar cells. Lentiviral vectors are the current main gene delivery vectors for PDAC, but their transduction efficiencies vary depending on pancreatic cell type, and are especially poor for the classical subtype of PDAC cells from both primary tumors and cell lines.
    Methods: We systemically compare transduction efficiencies of glycoprotein G of vesicular stomatitis virus (VSV-G)-pseudotyped lentiviral and Sendai viral vectors in human normal pancreatic ductal and PDAC cells.
    Results: We find that the Sendai viral vector gives the most robust gene delivery efficiency regardless of PDAC cell type. Therefore, we propose using Sendai viral vectors to transduce ectopic genes into PDAC cells.
    Language English
    Publishing date 2024-02-28
    Publishing country England
    Document type Journal Article
    ZDB-ID 2835763-2
    ISSN 2405-8440
    ISSN 2405-8440
    DOI 10.1016/j.heliyon.2024.e27221
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Hypoxia: Friend or Foe for drug delivery in Pancreatic Cancer.

    Shah, Vidhi M / Sheppard, Brett C / Sears, Rosalie C / Alani, Adam Wg

    Cancer letters

    2020  Volume 492, Page(s) 63–70

    Abstract: Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal solid tumors with an overall five-year survival rate of that has only just reached 10%. The tumor microenvironment of PDAC is characterized by desmoplasia, which consist of dense ... ...

    Abstract Pancreatic ductal adenocarcinoma (PDAC) remains one of the most lethal solid tumors with an overall five-year survival rate of that has only just reached 10%. The tumor microenvironment of PDAC is characterized by desmoplasia, which consist of dense stroma of fibroblasts and inflammatory cells, resulting in a hypoxic environment due to limited oxygen diffusion through the tumor. Hypoxia contributes to the aggressive tumor biology by promoting tumor progression, malignancy, and promoting resistance to conventional and targeted therapeutic agents. In depth research in the area has identified that hypoxia modulates the tumor biology through hypoxia inducible factors (HIFs), which not only are the key determinant of pancreatic malignancy but also an important target for therapy. In this review, we summarize the recent advances in understanding hypoxia driven phenotypes, which are responsible for the highly aggressive and metastatic characteristics of pancreatic cancer, and how hypoxia can be exploited as a target for drug delivery.
    MeSH term(s) Carcinoma, Pancreatic Ductal/drug therapy ; Carcinoma, Pancreatic Ductal/immunology ; Carcinoma, Pancreatic Ductal/metabolism ; Cell Hypoxia/physiology ; Drug Resistance, Neoplasm ; Extracellular Matrix/metabolism ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit/antagonists & inhibitors ; Hypoxia-Inducible Factor 1, alpha Subunit/physiology ; Pancreatic Neoplasms/drug therapy ; Pancreatic Neoplasms/immunology ; Pancreatic Neoplasms/metabolism ; Tumor Microenvironment
    Chemical Substances Hypoxia-Inducible Factor 1, alpha Subunit
    Language English
    Publishing date 2020-08-18
    Publishing country Ireland
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 195674-7
    ISSN 1872-7980 ; 0304-3835
    ISSN (online) 1872-7980
    ISSN 0304-3835
    DOI 10.1016/j.canlet.2020.07.041
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 1177: Show issues Location:
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  10. Article ; Online: Mission Possible: Advances in MYC Therapeutic Targeting in Cancer.

    Allen-Petersen, Brittany L / Sears, Rosalie C

    BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy

    2019  Volume 33, Issue 5, Page(s) 539–553

    Abstract: MYC is a master transcriptional regulator that controls almost all cellular processes. Over the last several decades, researchers have strived to define the context-dependent transcriptional gene programs that are controlled by MYC, as well as the ... ...

    Abstract MYC is a master transcriptional regulator that controls almost all cellular processes. Over the last several decades, researchers have strived to define the context-dependent transcriptional gene programs that are controlled by MYC, as well as the mechanisms that regulate MYC function, in an effort to better understand the contribution of this oncoprotein to cancer progression. There are a wealth of data indicating that deregulation of MYC activity occurs in a large number of cancers and significantly contributes to disease progression, metastatic potential, and therapeutic resistance. Although the therapeutic targeting of MYC in cancer is highly desirable, there remain substantial structural and functional challenges that have impeded direct MYC-targeted drug development and efficacy. While efforts to drug the 'undruggable' may seem futile given these challenges and considering the broad reach of MYC, significant strides have been made to identify points of regulation that can be exploited for therapeutic purposes. These include targeting the deregulation of MYC transcription in cancer through small-molecule inhibitors that induce epigenetic silencing or that regulate the G-quadruplex structures within the MYC promoter. Alternatively, compounds that disrupt the DNA-binding activities of MYC have been the long-standing focus of many research groups, since this method would prevent downstream MYC oncogenic activities regardless of upstream alterations. Finally, proteins involved in the post-translational regulation of MYC have been identified as important surrogate targets to reduce MYC activity downstream of aberrant cell stimulatory signals. Given the complex regulation of the MYC signaling pathway, a combination of these approaches may provide the most durable response, but this has yet to be shown. Here, we provide a comprehensive overview of the different therapeutic strategies being employed to target oncogenic MYC function, with a focus on post-translational mechanisms.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Gene Expression Regulation, Neoplastic ; Genes, myc ; Humans ; Molecular Targeted Therapy/methods ; Morpholines/pharmacology ; Neoplasms/drug therapy ; Neoplasms/genetics ; Phosphorylation ; Protein Multimerization/drug effects ; Protein Phosphatase 2/metabolism ; Protein Processing, Post-Translational ; Proto-Oncogene Proteins c-myc/antagonists & inhibitors ; Proto-Oncogene Proteins c-myc/genetics ; Proto-Oncogene Proteins c-myc/metabolism ; Pyrans/pharmacology ; Serine/metabolism
    Chemical Substances Antineoplastic Agents ; Morpholines ; Proto-Oncogene Proteins c-myc ; Pyrans ; SF2523 ; Serine (452VLY9402) ; Protein Phosphatase 2 (EC 3.1.3.16)
    Language English
    Publishing date 2019-08-16
    Publishing country New Zealand
    Document type Journal Article ; Review
    ZDB-ID 1364202-9
    ISSN 1179-190X ; 1173-8804
    ISSN (online) 1179-190X
    ISSN 1173-8804
    DOI 10.1007/s40259-019-00370-5
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    Zs.A 4112: Show issues Location:
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