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  1. Article: The AR-DNA repair axis: insights into prostate cancer aggressiveness.

    Knudsen, Karen E

    The Canadian journal of urology

    2019  Volume 26, Issue 5 Suppl 2, Page(s) 22–23

    Abstract: Despite significant advances in understanding the biology of advanced prostate cancer and approval of novel therapeutic agents, there is no durable cure for metastatic disease. Recent findings unmasked the importance of androgen receptor (AR) signaling ... ...

    Abstract Despite significant advances in understanding the biology of advanced prostate cancer and approval of novel therapeutic agents, there is no durable cure for metastatic disease. Recent findings unmasked the importance of androgen receptor (AR) signaling in regulation of DNA repair, and alterations of the AR-DNA repair factor axis were shown to promote aggressive phenotypes including metastasis. These and related findings underscore the importance of determining impact AR-DNA repair factor alterations on prostate cancer progression.
    MeSH term(s) DNA Repair/physiology ; Humans ; Male ; Prostatic Neoplasms/genetics ; Prostatic Neoplasms/pathology ; Receptors, Androgen/physiology ; Signal Transduction
    Chemical Substances Receptors, Androgen
    Language English
    Publishing date 2019-10-15
    Publishing country Canada
    Document type Journal Article
    ZDB-ID 2064475-9
    ISSN 1195-9479
    ISSN 1195-9479
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5607: Show issues Location:
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  2. Article ; Online: Basic Science and Molecular Genetics of Prostate Cancer Aggressiveness.

    Schiewer, Matthew J / Knudsen, Karen E

    The Urologic clinics of North America

    2021  Volume 48, Issue 3, Page(s) 339–347

    Abstract: Androgen receptor function, tumor cell plasticity, loss of tumor suppressors, and defects in DNA repair genes affect aggressive features of prostate cancer. Prostate cancer development, progression, and aggressive behavior are often attributable to ... ...

    Abstract Androgen receptor function, tumor cell plasticity, loss of tumor suppressors, and defects in DNA repair genes affect aggressive features of prostate cancer. Prostate cancer development, progression, and aggressive behavior are often attributable to function of the androgen receptor. Tumor cell plasticity, neuroendocrine features, and loss of tumor suppressors lend aggressive behavior to prostate cancer cells. DNA repair defects have ramifications for prostate cancer cell behavior.
    Language English
    Publishing date 2021-06-16
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 192293-2
    ISSN 1558-318X ; 0094-0143
    ISSN (online) 1558-318X
    ISSN 0094-0143
    DOI 10.1016/j.ucl.2021.04.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: DNA-PKcs: A Targetable Protumorigenic Protein Kinase.

    Dylgjeri, Emanuela / Knudsen, Karen E

    Cancer research

    2021  Volume 82, Issue 4, Page(s) 523–533

    Abstract: DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is a pleiotropic protein kinase that plays critical roles in cellular processes fundamental to cancer. DNA-PKcs expression and activity are frequently deregulated in multiple hematologic and solid ...

    Abstract DNA-dependent protein kinase catalytic subunit (DNA-PKcs) is a pleiotropic protein kinase that plays critical roles in cellular processes fundamental to cancer. DNA-PKcs expression and activity are frequently deregulated in multiple hematologic and solid tumors and have been tightly linked to poor outcome. Given the potentially influential role of DNA-PKcs in cancer development and progression, therapeutic targeting of this kinase is being tested in preclinical and clinical settings. This review summarizes the latest advances in the field, providing a comprehensive discussion of DNA-PKcs functions in cancer and an update on the clinical assessment of DNA-PK inhibitors in cancer therapy.
    MeSH term(s) Animals ; Clinical Trials as Topic ; DNA-Activated Protein Kinase/antagonists & inhibitors ; DNA-Activated Protein Kinase/genetics ; DNA-Activated Protein Kinase/metabolism ; Energy Metabolism/genetics ; Gene Expression Regulation, Neoplastic ; Humans ; Immunity/genetics ; Neoplasms/drug therapy ; Neoplasms/enzymology ; Neoplasms/genetics ; Protein Biosynthesis/genetics ; Protein Kinase Inhibitors/therapeutic use ; Substrate Specificity ; Tumor Microenvironment/drug effects ; Tumor Microenvironment/genetics
    Chemical Substances Protein Kinase Inhibitors ; DNA-Activated Protein Kinase (EC 2.7.11.1) ; PRKDC protein, human (EC 2.7.11.1)
    Language English
    Publishing date 2021-12-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-21-1756
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Double Trouble: Concomitant

    Mandigo, Amy C / Knudsen, Karen E

    Clinical cancer research : an official journal of the American Association for Cancer Research

    2020  Volume 26, Issue 8, Page(s) 1784–1786

    Abstract: Coordinate single- or two copy loss of ... ...

    Abstract Coordinate single- or two copy loss of the
    MeSH term(s) BRCA2 Protein ; Disease Progression ; Genes, BRCA2 ; Humans ; Male ; Phenotype ; Prostatic Neoplasms/genetics
    Chemical Substances BRCA2 Protein ; BRCA2 protein, human
    Language English
    Publishing date 2020-02-04
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 1225457-5
    ISSN 1557-3265 ; 1078-0432
    ISSN (online) 1557-3265
    ISSN 1078-0432
    DOI 10.1158/1078-0432.CCR-19-4033
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4223: Show issues Location:
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  5. Article ; Online: There and Back Again: The Middle Earth of DNA Repair.

    Knudsen, Karen E

    Molecular cancer research : MCR

    2016  Volume 14, Issue 10, Page(s) 895–897

    Language English
    Publishing date 2016
    Publishing country United States
    Document type Editorial
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-16-0298
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  6. Article ; Online: Expanding Role of Germline DNA Repair Alterations in Prostate Cancer Risk and Early Onset.

    Knudsen, Karen E / Feng, Felix Y

    European urology

    2019  Volume 76, Issue 3, Page(s) 338–339

    MeSH term(s) DNA Repair ; Germ Cells ; Germ-Line Mutation ; Humans ; Male ; Prostatic Neoplasms ; United Kingdom
    Language English
    Publishing date 2019-03-15
    Publishing country Switzerland
    Document type Editorial ; Comment
    ZDB-ID 193790-x
    ISSN 1873-7560 ; 1421-993X ; 0302-2838
    ISSN (online) 1873-7560 ; 1421-993X
    ISSN 0302-2838
    DOI 10.1016/j.eururo.2019.03.005
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    Zs.MO 294: Show issues

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  7. Article: Counterpoint-Prostate Cancer Genomic Analysis: Routine or Research Only?

    Kelly, W Kevin / Knudsen, Karen E

    Oncology (Williston Park, N.Y.)

    2019  Volume 32, Issue 12, Page(s) 607, 630–2

    MeSH term(s) Gene Expression Profiling ; Genomics ; High-Throughput Nucleotide Sequencing ; Humans ; Male ; Prostatic Neoplasms/genetics
    Language English
    Publishing date 2019-01-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1067950-9
    ISSN 0890-9091
    ISSN 0890-9091
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MO 372: Show issues

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  8. Article ; Online: A tripartite approach toward ending cancer as we know it, for everyone: An American Cancer Society perspective.

    Dahut, William L / Kamal, Arif H / Lacasse, Lisa A / Sanders, Kathryn M / Knudsen, Karen E

    Journal of surgical oncology

    2023  Volume 128, Issue 6, Page(s) 931–937

    Abstract: Gaps in the cancer care continuum are vast, both in the United States and globally. The American Cancer Society orchestrates an integrated, tripartite approach toward improving the lives of cancer patients and their families through research, advocacy, ... ...

    Abstract Gaps in the cancer care continuum are vast, both in the United States and globally. The American Cancer Society orchestrates an integrated, tripartite approach toward improving the lives of cancer patients and their families through research, advocacy, and patient support. With a focus on eradicating cancer disparities, the American Cancer Society aims to scale and deploy best practices worldwide through partnerships, to ensure everyone has an opportunity to prevent, detect, treat, and survive cancer.
    MeSH term(s) Humans ; United States ; American Cancer Society ; Neoplasms/prevention & control ; Neoplasms/diagnosis
    Language English
    Publishing date 2023-10-11
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 82063-5
    ISSN 1096-9098 ; 0022-4790
    ISSN (online) 1096-9098
    ISSN 0022-4790
    DOI 10.1002/jso.27463
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    Zs.A 706: Show issues Location:
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  9. Article ; Online: Cancer and the Circadian Clock.

    Shafi, Ayesha A / Knudsen, Karen E

    Cancer research

    2019  Volume 79, Issue 15, Page(s) 3806–3814

    Abstract: The circadian clock is a master regulator of mammalian physiology, regulating daily oscillations of crucial biological processes and behaviors. Notably, circadian disruption has recently been identified as an independent risk factor for cancer and ... ...

    Abstract The circadian clock is a master regulator of mammalian physiology, regulating daily oscillations of crucial biological processes and behaviors. Notably, circadian disruption has recently been identified as an independent risk factor for cancer and classified as a carcinogen. As such, it is imperative to discern the underpinning mechanisms by which circadian disruption alters cancer risk. Emergent data, reviewed herein, demonstrate that circadian regulatory functions play critical roles in several hallmarks of cancer, including control of cell proliferation, cell death, DNA repair, and metabolic alteration. Developing a deeper understanding of circadian-cancer regulation cross-talk holds promise for developing new strategies for cancer interception, prevention, and management.
    MeSH term(s) Animals ; Circadian Clocks/physiology ; Humans ; Neoplasms/genetics ; Neoplasms/metabolism ; Neoplasms/pathology
    Language English
    Publishing date 2019-07-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-19-0566
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: DNA Damage Response in Prostate Cancer.

    Schiewer, Matthew J / Knudsen, Karen E

    Cold Spring Harbor perspectives in medicine

    2019  Volume 9, Issue 1

    Abstract: Prostatic adenocarcinoma (PCa) remains a significant health concern. Although localized PCa can be effectively treated, disseminated disease remains uniformly fatal. PCa is reliant on androgen receptor (AR); as such, first-line therapy for metastatic PCa ...

    Abstract Prostatic adenocarcinoma (PCa) remains a significant health concern. Although localized PCa can be effectively treated, disseminated disease remains uniformly fatal. PCa is reliant on androgen receptor (AR); as such, first-line therapy for metastatic PCa entails suppression of AR signaling. Although initially effective, recurrent tumors reactivate AR function, leading to a lethal stage of disease termed castration-resistant PCa (CRPC). Recent findings implicate AR signaling in control of DNA repair and show that alterations in DNA damage repair pathways are strongly associated with disease progression and poor outcome. This review will address the DNA repair alterations observed in the clinical setting, explore the anticipated molecular and cellular consequence of DNA repair dysfunction, and consider clinical strategies for targeting tumors with altered DNA repair.
    MeSH term(s) Adenocarcinoma/drug therapy ; Adenocarcinoma/metabolism ; Adenocarcinoma/pathology ; Androgen Receptor Antagonists/metabolism ; Androgen Receptor Antagonists/therapeutic use ; Cell Transformation, Neoplastic/genetics ; Cell Transformation, Neoplastic/metabolism ; DNA Damage ; DNA Repair ; Disease Progression ; Gene Expression Regulation, Neoplastic ; Humans ; Male ; Prostatic Neoplasms/drug therapy ; Prostatic Neoplasms/metabolism ; Prostatic Neoplasms/pathology ; Targeted Gene Repair/methods
    Chemical Substances Androgen Receptor Antagonists
    Language English
    Publishing date 2019-01-02
    Publishing country United States
    Document type Journal Article ; Review
    ISSN 2157-1422
    ISSN (online) 2157-1422
    DOI 10.1101/cshperspect.a030486
    Database MEDical Literature Analysis and Retrieval System OnLINE

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