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  1. AU=Skorski Tomasz
  2. AU="Sanayeh, Elie Bou"
  3. AU="Echeverría, J.L."
  4. AU="Balasubramanian, Ramnath"
  5. AU="Adam Orłowski"
  6. AU="Tumanov A"
  7. AU="Hsu, Rafael M C S"
  8. AU=Perfect John R
  9. AU="Francini, Saverio"
  10. AU="Hurley, David"
  11. AU=Thomas L
  12. AU="French, M S"
  13. AU=Bonek Krzysztof
  14. AU="Noviello, Colleen M"
  15. AU="Jill A. Hollenbach"
  16. AU="Bansal, Ramesh C."
  17. AU="Huang, Xuhua"
  18. AU="Latorre, Víctor"
  19. AU="Simon J. Waddell"
  20. AU="Luo, Yueming"

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  1. Artikel ; Online: DNA damage response genes as biomarkers of therapeutic outcomes in acute myeloid leukemia patients.

    Karami, Adam / Skorski, Tomasz

    Leukemia

    2024  

    Sprache Englisch
    Erscheinungsdatum 2024-05-11
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 807030-1
    ISSN 1476-5551 ; 0887-6924
    ISSN (online) 1476-5551
    ISSN 0887-6924
    DOI 10.1038/s41375-024-02269-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Clonal medicine targeting DNA damage response eradicates leukemia.

    Toma, Monika M / Karami, Adam / Nieborowska-Skorska, Margaret / Chirtala, Kumaraswamy Naidu / Pepek, Monika / Hadzijusufovic, Emir / Stoklosa, Tomasz / Valent, Peter / Skorski, Tomasz

    Leukemia

    2024  Band 38, Heft 3, Seite(n) 671–675

    Mesh-Begriff(e) Humans ; Leukemia/genetics ; Clone Cells ; DNA Repair ; DNA Damage
    Sprache Englisch
    Erscheinungsdatum 2024-01-16
    Erscheinungsland England
    Dokumenttyp Journal Article
    ZDB-ID 807030-1
    ISSN 1476-5551 ; 0887-6924
    ISSN (online) 1476-5551
    ISSN 0887-6924
    DOI 10.1038/s41375-024-02138-5
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Verfügbar in ZB MED Köln/Königswinter

    Zs.A 2295: Hefte anzeigen Standort:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Artikel ; Online: Rapid Formation and Hybrid Treatment of a Large Superior Mesenteric Artery Aneurysm.

    Kaszczewski, Piotr / Kozubek, Herbert / Ostrowski, Tomasz / Maciąg, Rafał / Chudziński, Witold / Skórski, Maciej / Gałązka, Zbigniew

    The American journal of case reports

    2023  Band 24, Seite(n) e939558

    Abstract: BACKGROUND Superior mesenteric artery (SMA) aneurysms account for about 5.5% of all visceral aneurysms, and are most commonly secondary to infectious causes or dissection. They tend to expand and rupture. Here, we present our successful diagnosis and ... ...

    Abstract BACKGROUND Superior mesenteric artery (SMA) aneurysms account for about 5.5% of all visceral aneurysms, and are most commonly secondary to infectious causes or dissection. They tend to expand and rupture. Here, we present our successful diagnosis and treatment of a 41-year-old man with asymptomatic coeliac trunk stenosis, in whom the large aneurysm of the branch of the SMA developed in a very short time after conservative treatment of plastron appendicitis. CASE REPORT A 41-year-old man was diagnosed with plastron appendicitis during abdomen ultrasound (US) examination. Following 2 weeks of conservative treatment with intravenous antibiotic therapy, complete resolution of symptoms was obtained and confirmed in the computed tomography (CT) scan, and no other pathologies were diagnosed. Three weeks later, during the US examination, a 33-mm aneurysm of the branch of the SMA was diagnosed. The patient was admitted to the Vascular Surgery Department, where a critical stenosis of the coeliac trunk secondary to the compression by median arcuate ligament and a 33-mm true visceral aneurysm of one of the branches of the SMA were diagnosed. Successful treatment of the aneurysm was performed. Surgical decompression of the coeliac trunk and subsequent elective endovascular embolization of the SMA aneurysm with angioplasty of the coeliac trunk were performed. The postoperative period was uneventful and the patient was released from the hospital and remains asymptomatic. CONCLUSIONS Visceral artery aneurysm can form very quickly. In some of the aneurysms, a combination of open surgical and endovascular methods should be performed.
    Mesh-Begriff(e) Male ; Humans ; Adult ; Mesenteric Artery, Superior/diagnostic imaging ; Mesenteric Artery, Superior/surgery ; Appendicitis ; Constriction, Pathologic/complications ; Treatment Outcome ; Aneurysm/diagnostic imaging ; Aneurysm/surgery ; Endovascular Procedures/adverse effects
    Sprache Englisch
    Erscheinungsdatum 2023-10-29
    Erscheinungsland United States
    Dokumenttyp Case Reports ; Journal Article
    ZDB-ID 2517183-5
    ISSN 1941-5923 ; 1941-5923
    ISSN (online) 1941-5923
    ISSN 1941-5923
    DOI 10.12659/AJCR.939558
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  4. Artikel: Pre-Existing and Acquired Resistance to PARP Inhibitor-Induced Synthetic Lethality.

    Le, Bac Viet / Podszywałow-Bartnicka, Paulina / Piwocka, Katarzyna / Skorski, Tomasz

    Cancers

    2022  Band 14, Heft 23

    Abstract: The advanced development of synthetic lethality has opened the doors for specific anti-cancer medications of personalized medicine and efficient therapies against cancers. One of the most popular approaches being investigated is targeting DNA repair ... ...

    Abstract The advanced development of synthetic lethality has opened the doors for specific anti-cancer medications of personalized medicine and efficient therapies against cancers. One of the most popular approaches being investigated is targeting DNA repair pathways as the implementation of the PARP inhibitor (PARPi) into individual or combinational therapeutic schemes. Such treatment has been effectively employed against homologous recombination-defective solid tumors as well as hematopoietic malignancies. However, the resistance to PARPi has been observed in both preclinical research and clinical treatment. Therefore, elucidating the mechanisms responsible for the resistance to PARPi is pivotal for the further success of this intervention. Apart from mechanisms of acquired resistance, the bone marrow microenvironment provides a pre-existing mechanism to induce the inefficiency of PARPi in leukemic cells. Here, we describe the pre-existing and acquired mechanisms of the resistance to PARPi-induced synthetic lethality. We also discuss the potential rationales for developing effective therapies to prevent/repress the PARPi resistance in cancer cells.
    Sprache Englisch
    Erscheinungsdatum 2022-11-24
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2527080-1
    ISSN 2072-6694
    ISSN 2072-6694
    DOI 10.3390/cancers14235795
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  5. Artikel ; Online: Polθ Inhibition: An Anticancer Therapy for HR-Deficient Tumours.

    Barszczewska-Pietraszek, Gabriela / Drzewiecka, Małgorzata / Czarny, Piotr / Skorski, Tomasz / Śliwiński, Tomasz

    International journal of molecular sciences

    2022  Band 24, Heft 1

    Abstract: DNA polymerase theta (Polθ)-mediated end joining (TMEJ) is, along with homologous recombination (HR) and non-homologous end-joining (NHEJ), one of the most important mechanisms repairing potentially lethal DNA double-strand breaks (DSBs). Polθ is ... ...

    Abstract DNA polymerase theta (Polθ)-mediated end joining (TMEJ) is, along with homologous recombination (HR) and non-homologous end-joining (NHEJ), one of the most important mechanisms repairing potentially lethal DNA double-strand breaks (DSBs). Polθ is becoming a new target in cancer research because it demonstrates numerous synthetically lethal interactions with other DNA repair mechanisms, e.g., those involving PARP1, BRCA1/2, DNA-PK, ATR. Inhibition of Polθ could be achieved with different methods, such as RNA interference (RNAi), CRISPR/Cas9 technology, or using small molecule inhibitors. In the context of this topic, RNAi and CRISPR/Cas9 are still more often applied in the research itself rather than clinical usage, different than small molecule inhibitors. Several Polθ inhibitors have been already generated, and two of them, novobiocin (NVB) and ART812 derivative, are being tested in clinical trials against HR-deficient tumors. In this review, we describe the significance of Polθ and the Polθ-mediated TMEJ pathway. In addition, we summarize the current state of knowledge about Polθ inhibitors and emphasize the promising role of Polθ as a therapeutic target.
    Mesh-Begriff(e) Humans ; DNA/genetics ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA Repair ; Homologous Recombination ; Neoplasms/drug therapy ; Neoplasms/genetics ; Nucleic Acid Synthesis Inhibitors/pharmacology ; DNA Polymerase theta
    Chemische Substanzen DNA (9007-49-2) ; Nucleic Acid Synthesis Inhibitors
    Sprache Englisch
    Erscheinungsdatum 2022-12-24
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms24010319
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  6. Artikel ; Online: Synthetic Lethality Targeting Polθ.

    Drzewiecka, Małgorzata / Barszczewska-Pietraszek, Gabriela / Czarny, Piotr / Skorski, Tomasz / Śliwiński, Tomasz

    Genes

    2022  Band 13, Heft 6

    Abstract: Research studies regarding synthetic lethality (SL) in human cells are primarily motivated by the potential of this phenomenon to be an effective, but at the same time, safe to the patient's anti-cancer chemotherapy. Among the factors that are targets ... ...

    Abstract Research studies regarding synthetic lethality (SL) in human cells are primarily motivated by the potential of this phenomenon to be an effective, but at the same time, safe to the patient's anti-cancer chemotherapy. Among the factors that are targets for the induction of the synthetic lethality effect, those involved in DNA repair seem to be the most relevant. Specifically, when mutation in one of the canonical DNA double-strand break (DSB) repair pathways occurs, which is a frequent event in cancer cells, the alternative pathways may be a promising target for the elimination of abnormal cells. Currently, inhibiting RAD52 and/or PARP1 in the tumor cells that are deficient in the canonical repair pathways has been the potential target for inducing the effect of synthetic lethality. Unfortunately, the development of resistance to commonly used PARP1 inhibitors (PARPi) represents the greatest obstacle to working out a successful treatment protocol. DNA polymerase theta (Polθ), encoded by the POLQ gene, plays a key role in an alternative DSB repair pathway-theta-mediated end joining (TMEJ). Thus, it is a promising target in the treatment of tumors harboring deficiencies in homologous recombination repair (HRR), where its inhibition can induce SL. In this review, the authors discuss the current state of knowledge on Polθ as a potential target for synthetic lethality-based anticancer therapies.
    Mesh-Begriff(e) DNA Breaks, Double-Stranded ; DNA Repair/genetics ; Humans ; Neoplasms/drug therapy ; Neoplasms/genetics ; Recombinational DNA Repair ; Synthetic Lethal Mutations/genetics
    Sprache Englisch
    Erscheinungsdatum 2022-06-20
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Review ; Research Support, Non-U.S. Gov't
    ZDB-ID 2527218-4
    ISSN 2073-4425 ; 2073-4425
    ISSN (online) 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes13061101
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  7. Artikel ; Online: Synthetic Lethality Targeting Polθ

    Małgorzata Drzewiecka / Gabriela Barszczewska-Pietraszek / Piotr Czarny / Tomasz Skorski / Tomasz Śliwiński

    Genes, Vol 13, Iss 1101, p

    2022  Band 1101

    Abstract: Research studies regarding synthetic lethality (SL) in human cells are primarily motivated by the potential of this phenomenon to be an effective, but at the same time, safe to the patient’s anti-cancer chemotherapy. Among the factors that are targets ... ...

    Abstract Research studies regarding synthetic lethality (SL) in human cells are primarily motivated by the potential of this phenomenon to be an effective, but at the same time, safe to the patient’s anti-cancer chemotherapy. Among the factors that are targets for the induction of the synthetic lethality effect, those involved in DNA repair seem to be the most relevant. Specifically, when mutation in one of the canonical DNA double-strand break (DSB) repair pathways occurs, which is a frequent event in cancer cells, the alternative pathways may be a promising target for the elimination of abnormal cells. Currently, inhibiting RAD52 and/or PARP1 in the tumor cells that are deficient in the canonical repair pathways has been the potential target for inducing the effect of synthetic lethality. Unfortunately, the development of resistance to commonly used PARP1 inhibitors (PARPi) represents the greatest obstacle to working out a successful treatment protocol. DNA polymerase theta (Polθ), encoded by the POLQ gene, plays a key role in an alternative DSB repair pathway—theta-mediated end joining (TMEJ). Thus, it is a promising target in the treatment of tumors harboring deficiencies in homologous recombination repair (HRR), where its inhibition can induce SL. In this review, the authors discuss the current state of knowledge on Polθ as a potential target for synthetic lethality-based anticancer therapies.
    Schlagwörter DNA damage ; DNA repair ; personalized medicine ; polymerase theta ; synthetic lethality ; Genetics ; QH426-470
    Sprache Englisch
    Erscheinungsdatum 2022-06-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: Polθ Inhibition

    Gabriela Barszczewska-Pietraszek / Małgorzata Drzewiecka / Piotr Czarny / Tomasz Skorski / Tomasz Śliwiński

    International Journal of Molecular Sciences, Vol 24, Iss 1, p

    An Anticancer Therapy for HR-Deficient Tumours

    2022  Band 319

    Abstract: DNA polymerase theta (Polθ)-mediated end joining (TMEJ) is, along with homologous recombination (HR) and non-homologous end-joining (NHEJ), one of the most important mechanisms repairing potentially lethal DNA double-strand breaks (DSBs). Polθ is ... ...

    Abstract DNA polymerase theta (Polθ)-mediated end joining (TMEJ) is, along with homologous recombination (HR) and non-homologous end-joining (NHEJ), one of the most important mechanisms repairing potentially lethal DNA double-strand breaks (DSBs). Polθ is becoming a new target in cancer research because it demonstrates numerous synthetically lethal interactions with other DNA repair mechanisms, e.g., those involving PARP1, BRCA1/2, DNA-PK, ATR. Inhibition of Polθ could be achieved with different methods, such as RNA interference (RNAi), CRISPR/Cas9 technology, or using small molecule inhibitors. In the context of this topic, RNAi and CRISPR/Cas9 are still more often applied in the research itself rather than clinical usage, different than small molecule inhibitors. Several Polθ inhibitors have been already generated, and two of them, novobiocin (NVB) and ART812 derivative, are being tested in clinical trials against HR-deficient tumors. In this review, we describe the significance of Polθ and the Polθ-mediated TMEJ pathway. In addition, we summarize the current state of knowledge about Polθ inhibitors and emphasize the promising role of Polθ as a therapeutic target.
    Schlagwörter Polθ inhibitors ; anticancer treatment ; DNA double-strand break repair ; DNA repair enzyme ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 616
    Sprache Englisch
    Erscheinungsdatum 2022-12-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel ; Online: Relationship between Oxidative Stress and Imatinib Resistance in Model Chronic Myeloid Leukemia Cells.

    Głowacki, Sylwester / Synowiec, Ewelina / Szwed, Marzena / Toma, Monika / Skorski, Tomasz / Śliwiński, Tomasz

    Biomolecules

    2021  Band 11, Heft 4

    Abstract: Chronic myeloid leukemia (CML) develops due to the presence of the BCR-ABL1 protein, a target of tyrosine kinase inhibitors (TKIs), such as imatinib (IM), used in a CML therapy. CML eradication is a challenge due to developing resistance to TKIs. BCR- ... ...

    Abstract Chronic myeloid leukemia (CML) develops due to the presence of the BCR-ABL1 protein, a target of tyrosine kinase inhibitors (TKIs), such as imatinib (IM), used in a CML therapy. CML eradication is a challenge due to developing resistance to TKIs. BCR-ABL1 induces endogenous oxidative stress leading to genomic instability and development of TKI resistance. Model CML cells susceptible or resistant to IM, as well as wild-type, non-cancer cells without the BCR-ABL1 protein were treated with IM, hydrogen peroxide (H
    Sprache Englisch
    Erscheinungsdatum 2021-04-20
    Erscheinungsland Switzerland
    Dokumenttyp Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2701262-1
    ISSN 2218-273X ; 2218-273X
    ISSN (online) 2218-273X
    ISSN 2218-273X
    DOI 10.3390/biom11040610
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  10. Artikel: Synthetic Lethality Targeting Polθ

    Drzewiecka, Małgorzata / Barszczewska-Pietraszek, Gabriela / Czarny, Piotr / Skorski, Tomasz / Śliwiński, Tomasz

    Genes. 2022 June 20, v. 13, no. 6

    2022  

    Abstract: Research studies regarding synthetic lethality (SL) in human cells are primarily motivated by the potential of this phenomenon to be an effective, but at the same time, safe to the patient’s anti-cancer chemotherapy. Among the factors that are targets ... ...

    Abstract Research studies regarding synthetic lethality (SL) in human cells are primarily motivated by the potential of this phenomenon to be an effective, but at the same time, safe to the patient’s anti-cancer chemotherapy. Among the factors that are targets for the induction of the synthetic lethality effect, those involved in DNA repair seem to be the most relevant. Specifically, when mutation in one of the canonical DNA double-strand break (DSB) repair pathways occurs, which is a frequent event in cancer cells, the alternative pathways may be a promising target for the elimination of abnormal cells. Currently, inhibiting RAD52 and/or PARP1 in the tumor cells that are deficient in the canonical repair pathways has been the potential target for inducing the effect of synthetic lethality. Unfortunately, the development of resistance to commonly used PARP1 inhibitors (PARPi) represents the greatest obstacle to working out a successful treatment protocol. DNA polymerase theta (Polθ), encoded by the POLQ gene, plays a key role in an alternative DSB repair pathway—theta-mediated end joining (TMEJ). Thus, it is a promising target in the treatment of tumors harboring deficiencies in homologous recombination repair (HRR), where its inhibition can induce SL. In this review, the authors discuss the current state of knowledge on Polθ as a potential target for synthetic lethality-based anticancer therapies.
    Schlagwörter DNA ; DNA repair ; DNA-directed DNA polymerase ; death ; drug therapy ; genes ; humans ; mutation ; neoplasms ; patients
    Sprache Englisch
    Erscheinungsverlauf 2022-0620
    Erscheinungsort Multidisciplinary Digital Publishing Institute
    Dokumenttyp Artikel
    ZDB-ID 2527218-4
    ISSN 2073-4425
    ISSN 2073-4425
    DOI 10.3390/genes13061101
    Datenquelle NAL Katalog (AGRICOLA)

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