Tumor stroma-derived TGF-beta limits myc-driven lymphomagenesis via Suv39h1-dependent senescence.

@article{Reimann2010TumorST,
  title={Tumor stroma-derived TGF-beta limits myc-driven lymphomagenesis via Suv39h1-dependent senescence.},
  author={M. Reimann and Soyoung Lee and C. Loddenkemper and J. D{\"o}rr and V. Tabor and P. Aichele and H. Stein and B. Dörken and T. Jenuwein and C. Schmitt},
  journal={Cancer cell},
  year={2010},
  volume={17 3},
  pages={
          262-72
        }
}
Activated RAS/BRAF oncogenes induce cellular senescence as a tumor-suppressive barrier in early cancer development, at least in part, via an oncogene-evoked DNA damage response (DDR). In contrast, Myc activation-although producing a DDR as well-is known to primarily elicit an apoptotic countermeasure. Using the Emu-myc transgenic mouse lymphoma model, we show here in vivo that apoptotic lymphoma cells activate macrophages to secrete transforming growth factor beta (TGF-beta) as a critical non… Expand
The Myc/macrophage tango: oncogene-induced senescence, Myc style.
Non-cell-autonomous tumor suppression: oncogene-provoked apoptosis promotes tumor cell senescence via stromal crosstalk
Novel ARF/p53-independent senescence pathways in cancer repression
Non-Cell-Autonomous Tumor Suppression by p53
Inactivation of MYC reverses tumorigenesis
Oncogene- and tumor suppressor gene-mediated suppression of cellular senescence.
  • L. Larsson
  • Biology, Medicine
  • Seminars in cancer biology
  • 2011
Tipping the balance: Cdk2 enables Myc to suppress senescence.
MYC activation is a hallmark of cancer initiation and maintenance.
...
1
2
3
4
5
...

References

SHOWING 1-10 OF 56 REFERENCES
...
1
2
3
4
5
...