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. Author manuscript; available in PMC: 2020 Jun 1.
Published in final edited form as: Semin Cell Dev Biol. 2018 Jul 27;90:154–160. doi: 10.1016/j.semcdb.2018.07.022

Figure 3.

Figure 3

Nuclear dysmorphism and cytosolic DNA in cancer and senescent cells are precursors to inflammation. Nuclei from cancer and senescent cells share common aberrant nuclear structural properties such as nuclear envelope distensions (blebs) and altered lamin expression. In the cancer nucleus, nuclear blebbing and micronuclei are formed due to genotoxic stresses, lamin A/C (red) or lamin B (blue) dysregulation, and excessive force of perinuclear structural proteins (neon blue). In senescent cells the 3D genome changes represented by dissociation of chromatin (grey) from regions of the nuclear lamina. Lamin B1 (blue) is targeted for degradation with its associated DNA (grey) and is extruded into the cytosol via LC3II (yellow). Detection of aberrant DNA species in the cytosol of cancer and senescent cells by cGAS-STING, propagates a pro-inflammatory type I interferon response.