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. 2015 Mar 3;12(3):e1001796. doi: 10.1371/journal.pmed.1001796

Table 3. CLL patients with TP53 abnormalities.

Patient Number Del 17p (FISH) P53 Functional Assessment TP53 Mutational Status
25 23% [46/200] Dysfunctional c.536A>G/p.H179R (exon 5)
30 53% [107/200] Dysfunctional c.425C>G/p.P142R (exon 5) + c.665C>T/p.P222L (exon 6)
53 89% [178/200] Dysfunctional Unmutated (exons 5–8)
59 17% [34/200] Dysfunctional c.Del790–792CTA/p.Del264L (exon 8)
62 97% [195/200] Dysfunctional c.417G>T/p.V173L (exon 5)
67 90% [181/200] Dysfunctional c.524G>A/p.R175H (exon 5)
71 96% [193/200] Dysfunctional c.184G>T, p.E62X (exon 4)
72 93% [186/200] Dysfunctional p.R273H (exon 8)
73 97% [195/200] Dysfunctional c.818G>A, p.R273H (exon 8)
74 16% [33/200] Dysfunctional c.536C>T/p.H179Y (exon 5)
79 0% [0/200] Dysfunctional IVS9+2A>G (intron 9) (homozygous)

The assessment of the functional status of P53 in CLL cells was based on induction of P21 and P53 protein expression using etoposide and nutlin-3a [39]. The detection of TP53 mutations was performed as described in Methods. FISH: score of interphasic cells with an abnormality. Del, deletion.