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. Author manuscript; available in PMC: 2015 Feb 11.
Published in final edited form as: Nat Genet. 2014 Sep 7;46(10):1060–1062. doi: 10.1038/ng.3091

Figure 2.

Figure 2

Ser24Phe kinastrin promotes aneuploidy and enhances tumorigenesis in vivo. (a) Disrupted sister chromatid cohesion in early-passage, primary human keratinocytes pooled from multiple donors and transduced to express wild-type or Ser24Phe kinastrin. Arrowheads mark unpaired chromatids. Scale bars, 5 µm. (b) Quantification of unpaired chromatids (n = 2 biological replicates). *P = 0.0002. (c) Percentage of the genome affected by chromosomal gains and losses in SCC tissues with either wild-type or Ser24Phe mutant kinastrin. Data shown represent means ± s.d.; n = 5 independent primary tumors per group. *P = 0.007. CNVs, copy number variants. (d) Weight of mouse xenograft tumors 23 d after injection. Primary human keratinocytes were transduced to express human Cdk4 and oncogenic Ras as well as LacZ (CTR), wild-type kinastrin or Ser24Phe kinastrin and were injected subcutaneously into NOD SCID mice. Data shown represent means ± s.d.; n = 4 tumors per group. *P = 0.03, **P = 0.04; NS, not significant. (e) Ki-67 immunohistochemistry of the tumors from d. Representative fields are shown. Scale bars, 30 µm. (f) Quantification of the mitotic index for the tumors from d. Two high-power fields each containing an average of 408 cells were quantified per tumor (n = 4 tumors per group). Error bars, s.d. *P = 0.019, **P = 0.002; NS, not significant.