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Oncogene-induced senescence as an initial barrier in lymphoma development
H3K9me-mediated senescence is identified as a novel Suv39h1-dependent tumour suppressor mechanism whose inactivation permits the formation of aggressive but apoptosis-competent lymphomas in response to oncogenic Ras.
A Senescence Program Controlled by p53 and p16INK4a Contributes to the Outcome of Cancer Therapy
Synthetic lethal metabolic targeting of cellular senescence in cancer therapy
The hypercatabolic nature of TIS that is therapeutically exploitable by synthetic lethal metabolic targeting is unveiled, which is a consequence of the senescence-associated secretory phenotype (SASP) described previously.
Senescence-associated reprogramming promotes cancer stemness
Senescence-associated stemness is an unexpected, cell-autonomous feature that exerts its detrimental, highly aggressive growth potential upon escape from cell-cycle blockade, and is enriched in relapse tumours.
The dynamic nature of senescence in cancer
Lee and Schmitt discuss how the classical view of senescence as a static, terminally differentiated state has changed to that of a dynamic, reversible condition with diverse roles in tumour biology.
Tumor stroma-derived TGF-beta limits myc-driven lymphomagenesis via Suv39h1-dependent senescence.
FoxO transcription factors suppress Myc-driven lymphomagenesis via direct activation of Arf.
- C. Bouchard, Soyoung Lee, Viola Paulus-Hock, C. Loddenkemper, M. Eilers, C. Schmitt
- BiologyGenes & development
- 1 November 2007
Stable introduction of a dominant-negative FoxO moiety into Emu-myc transgenic hematopoietic stem cells accelerates lymphoma development in recipient mice by attenuating Myc-induced apoptosis and providing direct genetic evidence for their tumor-suppressive capacity.
Aryl hydrocarbon receptor-mediated induction of the microRNA-132/212 cluster promotes interleukin-17–producing T-helper cell differentiation
- T. Nakahama, Hamza Hanieh, T. Kishimoto
- BiologyProceedings of the National Academy of Sciences
- 1 July 2013
It is found that expression of the microRNA (miR)-132/212 cluster is up-regulated by AHR activation under TH17-inducing, but not regulatory T-inducing conditions.
Opposing roles of NF-κB in anti-cancer treatment outcome unveiled by cross-species investigations.
Using a mouse lymphoma model and analyzing transcriptome and clinical data from lymphoma patients, it is shown that therapy-induced senescence presents with and depends on active NF-κB signaling, whereas NF-σB simultaneously promotes resistance to apoptosis.
NF-κB in Cellular Senescence and Cancer Treatment
This review discusses implications of the NF-κB signaling pathway in cancer, and emphasizes the connection of NF-σB with cellular senescence as a response to chemotherapy, and presents examples how distinct oncogenic network contexts surrounding NF-KKB produce fundamentally different treatment outcomes in aggressive B-cell lymphomas.