Fig. 1.
Fig. 1. Southern blot analysis of 10 indolent (A) and 13 aggressive (B) NHLs. The indolent lymphoid neoplasms 321b (CLL), 577 (CLL), and 291 (FCL) in A have their subsequent sample of the progressed lymphoma in B, cases 321 (Richter's syndrome), 8324 (Richter's syndrome), and 1106 (transformed FCL), respectively. Genomic DNA was digested with HindIII restriction enzyme and hybridized with the exon 2 of p16INK4a and β-actin probes. (A) Indolent lymphomas showed germline configuration except cases 291 (FCL) and 8216 (typical MCL), which had a homozygous deletion of the p16INK4a gene. (B) Analyses of transformed and aggressive variants of NHLs showed homozygous deletions of both p15INK4b and p16INK4a genes in cases 321 and 8324 (Richter's syndrome), 1106 (transformed FCL), and 9630 (diffuse LCL). Case 2286 (lymphoblastic lymphoma) showed a homozygous deletion of p16INK4a but no p15INK4b. The identification number of these cases is the same as that in Figs 2, 3, and 4.

Southern blot analysis of 10 indolent (A) and 13 aggressive (B) NHLs. The indolent lymphoid neoplasms 321b (CLL), 577 (CLL), and 291 (FCL) in A have their subsequent sample of the progressed lymphoma in B, cases 321 (Richter's syndrome), 8324 (Richter's syndrome), and 1106 (transformed FCL), respectively. Genomic DNA was digested with HindIII restriction enzyme and hybridized with the exon 2 of p16INK4a and β-actin probes. (A) Indolent lymphomas showed germline configuration except cases 291 (FCL) and 8216 (typical MCL), which had a homozygous deletion of the p16INK4a gene. (B) Analyses of transformed and aggressive variants of NHLs showed homozygous deletions of both p15INK4b and p16INK4a genes in cases 321 and 8324 (Richter's syndrome), 1106 (transformed FCL), and 9630 (diffuse LCL). Case 2286 (lymphoblastic lymphoma) showed a homozygous deletion of p16INK4a but no p15INK4b. The identification number of these cases is the same as that in Figs 2, 3, and 4.

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