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  1. AU="Bajtai, Eszter"
  2. AU="Tam, Ka Cheung"
  3. AU="Richardson, Susan E"
  4. AU="Generoso, Erika Marie G"
  5. AU="Moustafa, Ahmed M"
  6. AU="da Cruz, Luciana D"
  7. AU="Ratnayake, Jithendra"
  8. AU="Halesh, L H"
  9. AU=Babajanyan S G
  10. AU="Haruhara, Kotaro"
  11. AU="Wang, Che-Wei"
  12. AU="Eisenberg, Marcia"
  13. AU="Ufnalska, Sylwia"
  14. AU="Leroux, Dominique"
  15. AU="Gallagher, Timothy J"
  16. AU=Baggish Aaron
  17. AU="Bush, Ashley I"
  18. AU="Carr, Kenneth D."
  19. AU="Spiro, Stephen"
  20. AU="Roberts, William Clifford"
  21. AU="Park, Hyungjong"
  22. AU="Das, Debasish"
  23. AU="Sanz-Magro, Adrián"
  24. AU="Fan, Shanhui"
  25. AU="Ellonen, Pekka"
  26. AU="Lambert, T"
  27. AU="Vivekanandan, Rajesh"

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  1. Artikel ; Online: Effective targeting of breast cancer by the inhibition of P-glycoprotein mediated removal of toxic lipid peroxidation byproducts from drug tolerant persister cells.

    Szebényi, Kornélia / Füredi, András / Bajtai, Eszter / Sama, Sai Nagender / Csiszar, Agnes / Gombos, Balázs / Szabó, Pál / Grusch, Michael / Szakács, Gergely

    Drug resistance updates : reviews and commentaries in antimicrobial and anticancer chemotherapy

    2023  Band 71, Seite(n) 101007

    Abstract: Therapy resistance has long been considered to occur through the selection of pre-existing clones equipped to survive and quickly regrow, or through the acquisition of mutations during chemotherapy. Here we show that following in vitro treatment by ... ...

    Abstract Therapy resistance has long been considered to occur through the selection of pre-existing clones equipped to survive and quickly regrow, or through the acquisition of mutations during chemotherapy. Here we show that following in vitro treatment by chemotherapy, epithelial breast cancer cells adopt a transient drug tolerant phenotype characterized by cell cycle arrest, epithelial-to-mesenchymal transition (EMT) and the reversible upregulation of the multidrug resistance (MDR) efflux transporter P-glycoprotein (P-gp). The drug tolerant persister (DTP) state is reversible, as cells eventually resume proliferation, giving rise to a cell population resembling the initial, drug-naïve cell lines. However, recovery after doxorubicin treatment is almost completely eliminated when DTP cells are cultured in the presence of the P-gp inhibitor Tariquidar. Mechanistically, P-gp contributes to the survival of DTP cells by removing reactive oxygen species-induced lipid peroxidation products resulting from doxorubicin exposure. In vivo, prolonged administration of Tariquidar during doxorubicin treatment holidays resulted in a significant increase of the overall survival of Brca1
    Mesh-Begriff(e) Humans ; Animals ; Mice ; Female ; ATP Binding Cassette Transporter, Subfamily B, Member 1/genetics ; Lipid Peroxidation ; Pharmaceutical Preparations ; Breast Neoplasms/drug therapy ; Breast Neoplasms/genetics ; ATP Binding Cassette Transporter, Subfamily B/genetics ; Doxorubicin/pharmacology
    Chemische Substanzen ATP Binding Cassette Transporter, Subfamily B, Member 1 ; Pharmaceutical Preparations ; ATP Binding Cassette Transporter, Subfamily B ; Doxorubicin (80168379AG)
    Sprache Englisch
    Erscheinungsdatum 2023-09-17
    Erscheinungsland Scotland
    Dokumenttyp Journal Article
    ZDB-ID 1474513-6
    ISSN 1532-2084 ; 1368-7646
    ISSN (online) 1532-2084
    ISSN 1368-7646
    DOI 10.1016/j.drup.2023.101007
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Új stratégiák fejlesztése a gyógyszerrezisztens daganatok kezeléséhez.

    Vajda, Flóra / Bajtai, Eszter / Gombos, Balázs / Karai, Edina / Hámori, Lilla / Szakács, Gergely / Füredi, András

    Magyar onkologia

    2021  Band 65, Heft 2, Seite(n) 176–187

    Abstract: There are about 14 million new cancer cases and 8 million deaths every year. Every second man and one in every three women will get cancer during their lifetimes. Following decades of steady increase, death rates have stabilized due to increased ... ...

    Titelübersetzung Development of novel treatment strategies for drug resistant cancer.
    Abstract There are about 14 million new cancer cases and 8 million deaths every year. Every second man and one in every three women will get cancer during their lifetimes. Following decades of steady increase, death rates have stabilized due to increased awareness and prevention, early detection, and the emergence of more effective therapy. Yet despite all the advances cancer remains a major killer. Despite improved therapies, nearly all current treatments face the same problem: for many patients, they ultimately stop working. Therapy resistance is the ultimate challenge facing cancer researchers and patients today. In this review we present an overview of the most important resistance mechanisms, discussing progress in therapies designed to prevent or overcome anticancer therapy resistance. Finally, we present recent findings from our own laboratory on the development of new experimental models and new therapeutic approaches to combat multidrug resistant cancer.
    Mesh-Begriff(e) Drug Resistance, Multiple ; Drug Resistance, Neoplasm ; Female ; Humans ; Male ; Neoplasms/drug therapy ; Pharmaceutical Preparations
    Chemische Substanzen Pharmaceutical Preparations
    Sprache Ungarisch
    Erscheinungsdatum 2021-05-09
    Erscheinungsland Hungary
    Dokumenttyp Journal Article ; Review
    ZDB-ID 414033-3
    ISSN 2060-0399 ; 0025-0244
    ISSN (online) 2060-0399
    ISSN 0025-0244
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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