Fig. 1.
Fig. 1. BAL expression in DLB-CLs (primary tumors and cell lines) and normal human tissues. / (A) Northern blot analysis of primary DLB-CLs from patients with known clinical characteristics, well-defined IPI risk profiles, and mature follow-up whose specimens were analyzed in initial differential display. The filter was hybridized with the differential display product equivalent to the 3′ end of BAL cDNA. The approximately 3.2-kb BAL transcript is more abundant in high risk (HR) than in low risk (LR) primary DLB-CLs. The filters were also hybridized with β-actin to confirm equal loading. (B) Semiquantitative duplex RT-PCR analysis of BAL expression in an additional series of primary DLB-CLs from patients with well-characterized IPI risk profiles, long-term follow-up, and aggressive B-cell lymphoma cell lines (DHL-4, DHL-7, DHL-8, and DHL-10). (C) Densitometric analysis ofBAL expression in the expanded series of primary DLB-CLs (shown in B). The abundance of BAL in a given sample was determined by comparing the intensity of coamplified BAL and internal control signals via scanning densitometry. Thereafter, a ratio of the intensity of the 2 bands was generated to reflect BAL expression. Densitometric profiles of BAL expression in tumors from patients with low/low-intermediate–risk and high-intermediate/high–risk (IPI) disease are shown and demonstrated to be significantly different (P = .0023, 1-sided Student t test). (D) Northern blot analysis of BAL transcripts in the aggressive B-cell lymphoma cell lines (DHL-4, DHL-7, DHL-8, and DHL-10). The filters were also hybridized with β-actin to confirm equal loading. (E) Northern blot analysis of BAL transcripts in multiple normal human tissues.

BAL expression in DLB-CLs (primary tumors and cell lines) and normal human tissues.

(A) Northern blot analysis of primary DLB-CLs from patients with known clinical characteristics, well-defined IPI risk profiles, and mature follow-up whose specimens were analyzed in initial differential display. The filter was hybridized with the differential display product equivalent to the 3′ end of BAL cDNA. The approximately 3.2-kb BAL transcript is more abundant in high risk (HR) than in low risk (LR) primary DLB-CLs. The filters were also hybridized with β-actin to confirm equal loading. (B) Semiquantitative duplex RT-PCR analysis of BAL expression in an additional series of primary DLB-CLs from patients with well-characterized IPI risk profiles, long-term follow-up, and aggressive B-cell lymphoma cell lines (DHL-4, DHL-7, DHL-8, and DHL-10). (C) Densitometric analysis ofBAL expression in the expanded series of primary DLB-CLs (shown in B). The abundance of BAL in a given sample was determined by comparing the intensity of coamplified BAL and internal control signals via scanning densitometry. Thereafter, a ratio of the intensity of the 2 bands was generated to reflect BAL expression. Densitometric profiles of BAL expression in tumors from patients with low/low-intermediate–risk and high-intermediate/high–risk (IPI) disease are shown and demonstrated to be significantly different (P = .0023, 1-sided Student t test). (D) Northern blot analysis of BAL transcripts in the aggressive B-cell lymphoma cell lines (DHL-4, DHL-7, DHL-8, and DHL-10). The filters were also hybridized with β-actin to confirm equal loading. (E) Northern blot analysis of BAL transcripts in multiple normal human tissues.

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