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. Author manuscript; available in PMC: 2021 Jun 22.
Published in final edited form as: Cancer Res. 2020 Sep 16;80(24):5606–5618. doi: 10.1158/0008-5472.CAN-20-0624

Figure 1. Pole mutations confer variable tumorigenic capabilities in vivo and support a genotype-phenotype correlation.

Figure 1.

(A) Kaplan-Meier survival estimates. Mice were followed for long-term survival and observed daily until endpoint. Upper: PoleS459F/S459F (n= 31); PoleS459F/+ (n=33); Pole+/+ (n=16); Lower: PoleP286R/+ (n = 27); Pole+/+ (n=17). One month = 4.3 weeks. Significance are indicated using Log-rank test.

(B) Landscape of germline and somatic POLE driver mutations. Mutations designated as germline were collected from the IRRDC or were previously reported. Mutations designated as “somatic only” are not found in germline cases but were validated drivers as determined by our previous comprehensive characterization[15]. Residues upstream of the exonuclease domains (1–268) and downstream of the polymerase domain (1100 – 2286) are omitted for clarity.

(C) Excision rate constants measured for 7 POLE exonuclease mutants. POLE mutants are indicated on the x-axis. Error fitting for each curve was performed as described previously[37].