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  1. Article ; Online: Fork restart: unloading FANCD2 to travel ahead.

    Iyer, Divya R / D'Andrea, Alan D

    Molecular cell

    2023  Volume 83, Issue 20, Page(s) 3590–3592

    Abstract: In this issue of Molecular Cell, Brunner et al. ...

    Abstract In this issue of Molecular Cell, Brunner et al.
    MeSH term(s) DNA-Binding Proteins/metabolism ; DNA Replication
    Chemical Substances DNA-Binding Proteins
    Language English
    Publishing date 2023-10-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 1415236-8
    ISSN 1097-4164 ; 1097-2765
    ISSN (online) 1097-4164
    ISSN 1097-2765
    DOI 10.1016/j.molcel.2023.09.027
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5055: Show issues Location:
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  2. Article: Targeting Polymerase Theta (POLθ) for Cancer Therapy.

    Patterson-Fortin, Jeffrey / D'Andrea, Alan D

    Cancer treatment and research

    2023  Volume 186, Page(s) 285–298

    Abstract: Polymerase theta (POLθ) is the critical multi-domain enzyme in microhomology-mediated end-joining DNA double-stranded break repair. POLθ is expressed at low levels in normal tissue but is often overexpressed in cancers, especially in DNA repair deficient ...

    Abstract Polymerase theta (POLθ) is the critical multi-domain enzyme in microhomology-mediated end-joining DNA double-stranded break repair. POLθ is expressed at low levels in normal tissue but is often overexpressed in cancers, especially in DNA repair deficient cancers, such as homologous-recombination cancers, rendering them exquisitely sensitive to POLθ inhibition secondary to synthetic lethality. Development of POLθ inhibitors is an active area of investigation with inhibitors of the N-terminal helicase domain or the C-terminal polymerase domain currently in clinical trial. Here, we review POLθ-mediated microhomology-mediated end-joining, the development of POLθ inhibitors, and the potential clinical uses of POLθ inhibitors.
    MeSH term(s) Humans ; DNA-Directed DNA Polymerase/genetics ; DNA Breaks, Double-Stranded ; Neoplasms/drug therapy ; Neoplasms/genetics
    Chemical Substances DNA-Directed DNA Polymerase (EC 2.7.7.7)
    Language English
    Publishing date 2023-11-17
    Publishing country United States
    Document type Review ; Journal Article
    ISSN 0927-3042
    ISSN 0927-3042
    DOI 10.1007/978-3-031-30065-3_15
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Mechanisms of PARP inhibitor sensitivity and resistance.

    D'Andrea, Alan D

    DNA repair

    2018  Volume 71, Page(s) 172–176

    Abstract: BRCA1 and BRCA2 deficient tumor cells are sensitive to inhibitors of Poly ADP Ribose Polymerase (PARP1) through the mechanism of synthetic lethality. Several PARP inhibitors, which are oral drugs and generally well tolerated, have now received FDA ... ...

    Abstract BRCA1 and BRCA2 deficient tumor cells are sensitive to inhibitors of Poly ADP Ribose Polymerase (PARP1) through the mechanism of synthetic lethality. Several PARP inhibitors, which are oral drugs and generally well tolerated, have now received FDA approval for various ovarian cancer and breast cancer indications. Despite their use in the clinic, PARP inhibitor resistance is common and develops through multiple mechanisms. Broadly speaking, BRCA1/2-deficient tumor cells can become resistant to PARP inhibitors by restoring homologous recombination (HR) repair and/or by stabilizing their replication forks. Here, we review the mechanism of PARP inhibitor resistance.
    MeSH term(s) Animals ; Antineoplastic Agents/pharmacology ; Antineoplastic Agents/therapeutic use ; BRCA1 Protein ; BRCA2 Protein ; Drug Resistance, Neoplasm ; Female ; Homologous Recombination ; Humans ; Male ; Neoplasms/drug therapy ; Neoplasms/metabolism ; Neoplasms/physiopathology ; Poly (ADP-Ribose) Polymerase-1/antagonists & inhibitors ; Poly(ADP-ribose) Polymerase Inhibitors/pharmacology ; Poly(ADP-ribose) Polymerase Inhibitors/therapeutic use
    Chemical Substances Antineoplastic Agents ; BRCA1 Protein ; BRCA2 Protein ; Poly(ADP-ribose) Polymerase Inhibitors ; Poly (ADP-Ribose) Polymerase-1 (EC 2.4.2.30)
    Language English
    Publishing date 2018-08-23
    Publishing country Netherlands
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2071608-4
    ISSN 1568-7856 ; 1568-7864
    ISSN (online) 1568-7856
    ISSN 1568-7864
    DOI 10.1016/j.dnarep.2018.08.021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5555: Show issues Location:
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  4. Article ; Online: REV7 directs DNA repair pathway choice.

    Clairmont, Connor S / D'Andrea, Alan D

    Trends in cell biology

    2021  Volume 31, Issue 12, Page(s) 965–978

    Abstract: REV7 is a small multifunctional protein that participates in multiple DNA repair pathways, most notably translesion DNA synthesis and double-strand break (DSB) repair. While the role of REV7 in translesion synthesis has been known for several decades, ... ...

    Abstract REV7 is a small multifunctional protein that participates in multiple DNA repair pathways, most notably translesion DNA synthesis and double-strand break (DSB) repair. While the role of REV7 in translesion synthesis has been known for several decades, its function in DSB repair is a recent discovery. Investigations into the DSB repair function of REV7 have led to the discovery of a new DNA repair complex known as Shieldin. Recent studies have also highlighted the importance of REV7's HORMA domain, an ancient structural motif, in REV7 function and have identified the HORMA regulators, TRIP13 and p31, as novel DNA repair factors. In this review, we discuss these recent findings and their implications for repair pathway choice, at both DSBs and replication forks. We suggest that REV7, in particular the activation state of its HORMA domain, can act as a critical determinant of mutagenic versus error-free repair in multiple contexts.
    MeSH term(s) ATPases Associated with Diverse Cellular Activities/genetics ; ATPases Associated with Diverse Cellular Activities/metabolism ; Cell Cycle Proteins/genetics ; Cell Cycle Proteins/metabolism ; DNA Repair ; DNA Replication ; Mad2 Proteins/genetics ; Mad2 Proteins/metabolism
    Chemical Substances Cell Cycle Proteins ; Mad2 Proteins ; ATPases Associated with Diverse Cellular Activities (EC 3.6.4.-)
    Language English
    Publishing date 2021-06-16
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 30122-x
    ISSN 1879-3088 ; 0962-8924
    ISSN (online) 1879-3088
    ISSN 0962-8924
    DOI 10.1016/j.tcb.2021.05.009
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 3410: Show issues Location:
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  5. Article ; Online: Disassembly of the Shieldin Complex by TRIP13.

    Sarangi, Prabha / Clairmont, Connor S / D'Andrea, Alan D

    Cell cycle (Georgetown, Tex.)

    2020  Volume 19, Issue 13, Page(s) 1565–1575

    Abstract: In the past decade, the study of the major DNA double strand break (DSB) repair pathways, homologous recombination (HR) and classical non-homologous end joining (C-NHEJ), has revealed a vast and intricate network of regulation.  The choice between HR and ...

    Abstract In the past decade, the study of the major DNA double strand break (DSB) repair pathways, homologous recombination (HR) and classical non-homologous end joining (C-NHEJ), has revealed a vast and intricate network of regulation.  The choice between HR and C-NHEJ is largely controlled at the step of DNA end-resection. A pro-C-NHEJ cascade commencing with 53BP1 and culminating in the newly discovered REV7-Shieldin complex impedes end resection and therefore HR. Importantly, loss of any component of this pathway confers PARP inhibitor resistance in
    MeSH term(s) Amino Acid Sequence ; Animals ; Cell Cycle Proteins/metabolism ; Genomic Instability ; Humans ; Models, Molecular ; Multiprotein Complexes/chemistry ; Multiprotein Complexes/metabolism ; Protein Binding
    Chemical Substances Cell Cycle Proteins ; Multiprotein Complexes
    Language English
    Publishing date 2020-05-18
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2146183-1
    ISSN 1551-4005 ; 1538-4101 ; 1554-8627
    ISSN (online) 1551-4005
    ISSN 1538-4101 ; 1554-8627
    DOI 10.1080/15384101.2020.1758435
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5881: Show issues Location:
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  6. Article ; Online: Exploiting the Microhomology-Mediated End-Joining Pathway in Cancer Therapy.

    Patterson-Fortin, Jeffrey / D'Andrea, Alan D

    Cancer research

    2020  Volume 80, Issue 21, Page(s) 4593–4600

    Abstract: Repair of DNA double-strand breaks (DSB) is performed by two major pathways, homology-dependent repair and classical nonhomologous end-joining. Recent studies have identified a third pathway, microhomology-mediated end-joining (MMEJ). MMEJ has ... ...

    Abstract Repair of DNA double-strand breaks (DSB) is performed by two major pathways, homology-dependent repair and classical nonhomologous end-joining. Recent studies have identified a third pathway, microhomology-mediated end-joining (MMEJ). MMEJ has similarities to homology-dependent repair, in that repair is initiated with end resection, leading to single-stranded 3' ends, which require microhomology upstream and downstream of the DSB. Importantly, the MMEJ pathway is commonly upregulated in cancers, especially in homologous recombination-deficient cancers, which display a distinctive mutational signature. Here, we review the molecular process of MMEJ as well as new targets and approaches exploiting the MMEJ pathway in cancer therapy.
    MeSH term(s) Animals ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; Humans ; Neoplasms
    Language English
    Publishing date 2020-07-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 1432-1
    ISSN 1538-7445 ; 0008-5472
    ISSN (online) 1538-7445
    ISSN 0008-5472
    DOI 10.1158/0008-5472.CAN-20-1672
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  7. Article ; Online: Predictive Potential of Head and Neck Squamous Cell Carcinoma Organoids.

    Hill, Sarah J / D'Andrea, Alan D

    Cancer discovery

    2019  Volume 9, Issue 7, Page(s) 828–830

    Abstract: In this issue ... ...

    Abstract In this issue of
    MeSH term(s) Carcinoma, Squamous Cell ; Head and Neck Neoplasms ; Humans ; Mouth Mucosa ; Organoids ; Squamous Cell Carcinoma of Head and Neck
    Language English
    Publishing date 2019-06-28
    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-19-0527
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    Zs.A 6916: Show issues Location:
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  8. Article ; Online: Genomic Landscape of Primary and Recurrent Anal Squamous Cell Carcinomas in Relation to HPV Integration, Copy-Number Variation, and DNA Damage Response Genes.

    Aldersley, Jordan / Lorenz, David R / Mouw, Kent W / D'Andrea, Alan D / Gabuzda, Dana

    Molecular cancer research : MCR

    2021  Volume 19, Issue 8, Page(s) 1308–1321

    Abstract: The incidence of anal squamous cell carcinoma (ASCC) has been increasing, particularly in populations with HIV. Human papillomavirus (HPV) is the causal factor in 85% to 90% of ASCCs, but few studies evaluated HPV genotypes and integrations in relation ... ...

    Abstract The incidence of anal squamous cell carcinoma (ASCC) has been increasing, particularly in populations with HIV. Human papillomavirus (HPV) is the causal factor in 85% to 90% of ASCCs, but few studies evaluated HPV genotypes and integrations in relation to genomic alterations in ASCC. Using whole-exome sequence data for primary (
    MeSH term(s) Aged ; Alphapapillomavirus/genetics ; Anus Neoplasms/genetics ; Biomarkers, Tumor/genetics ; Carcinoma, Squamous Cell/genetics ; DNA Copy Number Variations/genetics ; DNA Damage/genetics ; Female ; Genomics/methods ; Humans ; Male ; Middle Aged ; Neoplasm Recurrence, Local/genetics ; Papillomavirus Infections/genetics ; Whole Exome Sequencing/methods
    Chemical Substances Biomarkers, Tumor
    Language English
    Publishing date 2021-04-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2098788-2
    ISSN 1557-3125 ; 1541-7786
    ISSN (online) 1557-3125
    ISSN 1541-7786
    DOI 10.1158/1541-7786.MCR-20-0884
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  9. Article: The Fanconi Anemia Pathway in Cancer.

    Niraj, Joshi / Färkkilä, Anniina / D'Andrea, Alan D

    Annual review of cancer biology

    2018  Volume 3, Page(s) 457–478

    Abstract: Fanconi anemia (FA) is a complex genetic disorder characterized by bone marrow failure (BMF), congenital defects, inability to repair DNA interstrand cross-links (ICLs), and cancer predisposition. FA presents two seemingly opposite characteristics: ( ...

    Abstract Fanconi anemia (FA) is a complex genetic disorder characterized by bone marrow failure (BMF), congenital defects, inability to repair DNA interstrand cross-links (ICLs), and cancer predisposition. FA presents two seemingly opposite characteristics: (
    Language English
    Publishing date 2018-12-03
    Publishing country United States
    Document type Journal Article
    ISSN 2472-3428
    ISSN 2472-3428
    DOI 10.1146/annurev-cancerbio-030617-050422
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  10. Article ; Online: DNA Repair Deficiency and Immunotherapy Response.

    Mouw, Kent W / D'Andrea, Alan D

    Journal of clinical oncology : official journal of the American Society of Clinical Oncology

    2018  Volume 36, Issue 17, Page(s) 1710–1713

    MeSH term(s) B7-H1 Antigen ; DNA Damage ; DNA Repair-Deficiency Disorders ; Humans ; Immunotherapy ; Neoplasms ; Programmed Cell Death 1 Receptor
    Chemical Substances B7-H1 Antigen ; Programmed Cell Death 1 Receptor
    Language English
    Publishing date 2018-04-23
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 604914-x
    ISSN 1527-7755 ; 0732-183X
    ISSN (online) 1527-7755
    ISSN 0732-183X
    DOI 10.1200/JCO.2018.78.2425
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