Table 1

Response of Eμ-Myc lymphomas of different genotypes to DNA-damaging drugs in vitro and in vivo

Etoposide response in vitro*Cyclophosphamide response in vivo
Pre-B lymphomas
B-cell lymphomas
200 mg/kg300 mg/kg200 mg/kg300 mg/kg
Noxa−/− 
Puma−/− S 
Noxa−/−Puma+/− 
Noxa−/−Puma−/− S 
Bim−/− (M) 
p53−/− 
Etoposide response in vitro*Cyclophosphamide response in vivo
Pre-B lymphomas
B-cell lymphomas
200 mg/kg300 mg/kg200 mg/kg300 mg/kg
Noxa−/− 
Puma−/− S 
Noxa−/−Puma+/− 
Noxa−/−Puma−/− S 
Bim−/− (M) 
p53−/− 

S indicates similar sensitivity to that seen for control (wild-type) Eμ-Myc lymphomas; M, midresistant, compared with control Eμ-Myc lymphomas; R, resistant, as seen for p53 loss. See Figures 2A-E, 3C-E, and supplemental Figure 3A-D.

*

Similar responses were observed in vitro for lymphoma cell lines of Pre-B and B-cell phenotype.

Significant resistance (P < .05 relative to control Eμ-Myc lymphomas) was observed with the loss of Puma; however, even with a concomitant loss of Noxa, this was not as severe as the resistance seen with the loss of p53. Pre-B lymphomas were more dependent on Puma, whereas B-cell lymphomas showed a trend toward dependence on Bim for optimal drug response (P < .08).

Relative to Eμ-Myc lymphomas lacking Puma, those lacking both Puma and Noxa were relatively more sensitive to CTX in vivo when treated with 300 mg/kg (see also Figure 2D; ordinal regression, P = .04).

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