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Showing 1–8 of 8 results
Advanced filters: Author: Maja Milanovic Clear advanced filters

  • Cellular senescence plays a crucial role in cancer therapy, influencing how tumours respond to treatment. Here, the authors show that therapy-induced senescence in B-cell lymphoma leads to myeloid-like plasticity, enhancing T-cell recognition and improving patient outcomes.

    • Dimitri Belenki
    • Paulina Richter-Pechanska
    • Clemens A. Schmitt
    ResearchOpen Access
    Nature Communications
    Volume: 16, P: 1-20

  • Therapy-induced senescence reflects a biological effector principle that is underrecognized in lesion-focused cancer precision medicine. Here the authors utilize mouse lymphoma genetics to functionally dissect senescence and cross-species apply a novel senescence-based prognosticator to lymphoma patients.

    • Kolja Schleich
    • Julia Kase
    • Clemens A. Schmitt
    ResearchOpen Access
    Nature Communications
    Volume: 11, P: 1-14

  • Bischof and colleagues report that AP-1 bookmarks prospective senescence enhancers for future activation to achieve a timely execution of the senescence programme.

    • Ricardo Iván Martínez-Zamudio
    • Pierre-François Roux
    • Oliver Bischof
    Research
    Nature Cell Biology
    Volume: 22, P: 842-855

  • Cellular senescence induced by chemotherapy leads to the acquisition of stemness in cancer cells, which results in enhanced tumour-promoting capacity after forced release or spontaneous escape from the senescent cell-cycle arrest.

    • Maja Milanovic
    • Dorothy N. Y. Fan
    • Clemens A. Schmitt
    Research
    Nature
    Volume: 553, P: 96-100

  • In mice with Eµ-myc transgenic lymphomas in which therapy-induced senescence (TIS) depends on the H3K9 histone methyltransferase Suv39h1, TIS-competent lymphomas but not TIS-incompetent Suv39h1– lymphomas show increased glucose utilization and ATP production after senescence-inducing chemotherapy to cope with proteotoxic stress elicited by factors of the senescence-associated secretory phenotype (SASP); senescent cancers are selectively vulnerable to drugs that block glucose utilization or autophagy.

    • Jan R. Dörr
    • Yong Yu
    • Clemens A. Schmitt
    Research
    Nature
    Volume: 501, P: 421-425