| External factors: | Imatinib(IM) |
| Aging type: | Accelerate |
| Aging characteristic: |
| Category: | Chemical compounds |
| Phenotype: | Fibrosarcoma |
| Experiment: | SA-β-gal activity assay//qRT-PCR//Immunohistochemistry |
| Description: | IM-treated tumors showed a significant up-regulation of the cell-cycle inhibitor p21Cip1 (cyclin-dependent kinase inhibitor (CDKI)1A/CDKN1A) and a marked decrease in cell proliferation, as evidenced by Ki-67 staining.in a subset of IM-treated cases for which material was available, senescence-associated β-galactosidase activity was clearly detectable in the post-IM specimens.Taqman quantitative real-time PCR (Applied Biosystems Division, Foster City, CA) of RNA obtained from macrodissected areas of the post-therapy samples (Pt7 and Pt11) showed a proinflammatory signature characterized by the expression of IL6, TGFB1, PAI1, CXCL1, IL1B, and IL8, which is a cytokine and chemokine profile consistent with the senescence-associated secretory pathway described previously. |
| Regulatory pathway: | -- |
| R-EF-Pathway: | -- |
| Pathway experiment: | -- |
| Pathway description: | -- |
Annotation: