bims-midomi Biomed News
on MDM2 and mitochondria
Issue of 2026–05–03
three papers selected by
Gavin McStay, Liverpool John Moores University



  1. Malays J Pathol. 2026 Apr;48(1): 21-36
       INTRODUCTION: Cytogenetics analysis of adipocytic tumours revealed varieties of chromosomal translocations beyond MDM2 amplification, so, this report aimed to identify these translocations and recognise the altered genes with their fusion partners.
    MATERIALS AND METHODS: The materials were collected from different databases including PubMed, and Scopus.
    RESULTS: The collected data revealed that HMGA2 gene alteration is the initial finding. In addition, t(9;12)(q33;q14) is a recurring cytogenetic aberration and engenders an HMGA2::GSN chimera. Translocation involving t(3;12)(q28;q14.3) is the most common translocation followed by t(1;12)(p32;q14) in subset of lipomas. Furthermore, three-way translocation t(1;4;12)(q21;q27~28;q14~15) have been reported. In paediatric lipoma, two reports revealed translocations; the first one revealed a translocation involving t(8;13)(q21;q22) and HMGA2::NFIB gene fusion, and in the second report, the translocation t(9;12)(p22;q14) has been identified. Angiolipoma, chondroid lipoma, Myolipoma, hibernoma, spindle cell/pleomorphic lipoma, revealed translocation t(X;2)(p22;p12), t(11;16)(q13;p1213), 46,XX,t(9;12)(p22;q14) t(9;11)(q34;q13), t(4;6)(q25;p23)/46,X,tas(Y;21)(p11;p13), respectively. The presence of PLAG1 alteration is a fundamental oncogenic event that fused with other partners mainly COL1A2 gene and HAS2, and rarely with RAD51L1, and COL1A2, RAB2A, COL3A1, PCMTD1, SRSF3, HNRNPC, YWHAZ, CTDSP2, PPP2R2A, BOC, DDX6,, KLF10, and KANSL1L, SDCBP, HNRNPA2B1, other fusions like EP400::HMGA2 and FGD6::HMGA2 may be found. Myxoid liposarcoma revealed that the incidence of translocation is t(12;16)(q13;p11.2) FUS::DDIT3 is quite common, while t(12;22)(q13;q12) EWSR1::DDIT3 is rare. Recently, t(12;22)(q13;q12) has been described.
    CONCLUSION: HMGA2 and PLAG1 are considered the most important altered genes in most adipocytic tumours subset and lipoblastoma, and identification of their partners is valuable in providing the accurate diagnosis and management especially when the histopathologic diagnosis is unclear.
  2. Nat Prod Res. 2026 Apr 28. 1-14
      In this work, we evaluated the chemical composition and the potential of ethyl acetate fractions of propolis from Babor (EAFPB) and El-Menia (EAFPM) regions against human neuroblastoma SH-SY5Y. The inhibitory of MDM2-P53 interaction by propolis phytochemicals was also evaluated by molecular docking and molecular dynamics simulations. HPLC-DAD revealed the predominance of phenolic acids such as vanillic acid, p-coumaric acid, cynarin; and flavonoids such as naringenin, hesperetin and hesperidin. Besides, fumaric acid and esculetin were detected for the first time in Algerian propolis. In vitro studies validated the selective anticancer and apoptotic properties of propolis fractions, and confirmed the absence of genotoxic effects. Molecular docking and molecular dynamics revealed good binding affinities and stable interactions of Kaempferol, Naringenin, Hesperetin, Apigenin and Luteolin with MDM2. Overall, the findings highlight the potential of Algerian propolis-derived compounds as selective anticancer agents against neuroblastoma.
    Keywords:  MDM2; Propolis; SH-SY5Y; apoptosis; molecular docking; molecular dynamics; neuroblastoma
    DOI:  https://doi.org/10.1080/14786419.2026.2662419
  3. Sci Rep. 2026 Apr 29.
      Ginkgetin, a biflavone isolated from Ginkgo biloba, is a potent Wnt signaling inhibitor that can enhance the pharmacological effects of cisplatin on non-small cell lung cancer (NSCLC) by activating the ferroptosis pathway. However, few studies have examined the role of ginkgetin in regulating ferroptosis in breast cancer cells. In this study, ginkgetin was found to induce ferroptosis by increasing intracellular reactive oxygen species (ROS) accumulation through the downregulation of GPX4, SLC7A11, SLC40A1, and glutathione expression along with the upregulation of transferrin, glutamate, cystine, and cell-free ferroptosis markers. Ferroptotic activity was inhibited using ferrostatin-1, which interfered with ginkgetin-mediated regulation of ferroptosis-related factors, such as GPX4, SLC7A11, SLC40A1, and transferrin, and partially suppressed ginkgetin-induced activation of the ferroptosis pathway. Mechanistically, ginkgetin promoted p53 nuclear translocation and upregulated downstream YAP1 expression by inhibiting the suppressive effect of MDM2 on p53 in breast cancer cells, whereas ferrostatin-1 partially reversed these effects. Consequently, the pharmacological activity of Taxol in breast cancer cells was enhanced. Finally, using a cell line-derived xenograft (CDX) model, we found that ginkgetin induced ferroptosis and suppressed tumor growth, whereas the combined administration of Taxol and ginkgetin produced a synergistic antitumor effect in vivo. Overall, these findings indicate that ginkgetin enhances the tumor-suppressive effect of Taxol by activating ferroptosis through the MDM2-p53-YAP1 axis, suggesting a potential combination therapy for breast cancer treatment.
    Keywords:  Ferroptosis; Ferrostatin-1; Ginkgetin; Luminal-subtype breast cancer; MDM2–p53–YAP1 axis; Taxol
    DOI:  https://doi.org/10.1038/s41598-026-49614-9