Figure 6
Figure 6. Patients with Burkitt lymphoma and DLBCL with deregulated MYC but high BCL-2 expression show increased disease latency. (A) IHC staining of tumors from patients with DLBCL with MYC translocations. One representative example of a TP53 mutation (patient #1; n = 11) and one example of a tumor with a BCL-2 overexpression because of t(14;18) translocation (patient #2; n = 10) is shown. (B) Kaplan-Meier plot; 4 different groups are shown: (1) patients showing wild-type p53 and regular BCL-2 expression [lack of t(14;18), n = 31; “no t(14;18); no p53 signaling disrupted”], (2) patients showing TP53 mutation or deletion alone (n = 14, “p53 signaling disrupted”), (3) patients showing high BCL-2 expression because of t(14;18) alone [n = 10 “t(14;18”)], and (4) patients showing both second hits [“t(14,18) and p53 signaling disrupted,” n = 4]. Patients with both second hits display an evident trend for an increase in survival time compared with patients with disrupted p53 signaling pathway alone. (P = .152).

Patients with Burkitt lymphoma and DLBCL with deregulated MYC but high BCL-2 expression show increased disease latency. (A) IHC staining of tumors from patients with DLBCL with MYC translocations. One representative example of a TP53 mutation (patient #1; n = 11) and one example of a tumor with a BCL-2 overexpression because of t(14;18) translocation (patient #2; n = 10) is shown. (B) Kaplan-Meier plot; 4 different groups are shown: (1) patients showing wild-type p53 and regular BCL-2 expression [lack of t(14;18), n = 31; “no t(14;18); no p53 signaling disrupted”], (2) patients showing TP53 mutation or deletion alone (n = 14, “p53 signaling disrupted”), (3) patients showing high BCL-2 expression because of t(14;18) alone [n = 10 “t(14;18”)], and (4) patients showing both second hits [“t(14,18) and p53 signaling disrupted,” n = 4]. Patients with both second hits display an evident trend for an increase in survival time compared with patients with disrupted p53 signaling pathway alone. (P = .152).

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