External factors
| External factors: |
Imatinib(IM) |
| Category: |
Chemical compounds |
| Experimental category: |
HL |
| Tissue type: |
Tumor tissue |
| Cell name: |
Primary tumor cell |
| 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. |
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Aging network
Annotation:
The green line represents Upregulation.
The purple line represents Downregulation.
The orange line represents Activation.
The yellow line represents Inhibition.
The gray line represents Unclear.
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