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Fludarabine nucleoside induces major changes in the p53 interactome in human B-lymphoid cancer cell lines.
Almazi, Juhura G; Alomari, Munther; Belov, Larissa; Best, O Giles; Shen, Yandong; Graham, Mark E; Mulligan, Stephen P; Christopherson, Richard I.
Affiliation
  • Almazi JG; School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, Australia.
  • Alomari M; Respiratory Technology, The Woolcock Institute of Medical Research, University of Sydney, Sydney, NSW, Australia.
  • Belov L; School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, Australia.
  • Best OG; Department of Stem Cell Biology, Institute for Research and Medical Consultations, Imam Abdulrahman Bin Faisal University, Dammam, Saudi Arabia.
  • Shen Y; School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, Australia.
  • Graham ME; Hematology, Kolling Institute for Medical Research, Royal North Shore Hospital, St. Leonards, NSW, Australia.
  • Mulligan SP; School of Life and Environmental Sciences, University of Sydney, Sydney, NSW, Australia.
  • Christopherson RI; Children's Medical Research Institute, University of Sydney, Westmead, NSW, Australia.
Nucleosides Nucleotides Nucleic Acids ; 41(3): 314-320, 2022.
Article in En | MEDLINE | ID: mdl-34886743
ABSTRACT
Triple combination FCR (fludarabine, cyclophosphamide and rituximab) is often used as front-line treatment for chronic lymphocytic leukemia (CLL) and non-Hodgkin's lymphoma. Results from our laboratory indicate that 2-FaraAMP (fludarabine) has multiple mechanisms of cytotoxicity that include accumulation of isoforms and phosphorylated derivatives of p53, and induction of the unfolded protein response (UPR). Using protein pull-downs with Dynabeads coated with p53 antibody, we have found that 2-FaraA (fludarabine nucleoside) induces major changes in the p53 interactome in human Raji lymphoma and IM9 multiple myeloma cells. These changes are likely driven by DNA strand breaks induced by 2-FaraA that activate protein kinases such as ATM, ATR and Chk1.
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Neoplasms / Antineoplastic Agents Limits: Humans Language: En Journal: Nucleosides Nucleotides Nucleic Acids Journal subject: BIOQUIMICA Year: 2022 Document type: Article Affiliation country:
Fulltext
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Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Neoplasms / Antineoplastic Agents Limits: Humans Language: En Journal: Nucleosides Nucleotides Nucleic Acids Journal subject: BIOQUIMICA Year: 2022 Document type: Article Affiliation country: