In Response to Fakruddin et al. and Apostolou et al Martin J.S Dyer, Helen P Price, Dalal M Jadayel, Milena Gasco, Amanda R Perry, Rifat A Hamoudi, Tony G Willis, Huaizheng Peng, Ming-Qing Du, Peter G Isaacson  Cell  Volume 97, Issue 6, Pages 686-688 (June 1999) DOI: 10.1016/S0092-8674(02)09766-0

Figure 1 Reverse BCL10 cDNA Sequences Showing Presence of Alterations within both Homopolymeric Runs (A) Clone from normal lymphocytes showing 8 A’s. (B) Direct sequencing of cDNA from patient with B cell precursor acute leukemia showing complex aberrations within the 8 A’s including deletion of two adenines and A→G point mutation. (C) Direct sequencing of cDNA from myeloma cell line showing normal run of 7 T’s. (D) Direct sequence of cDNA from normal human fetal brain mRNA (Clontech) showing presence of additional thymidine in about 50% of the transcripts (arrow). Note loss of readable sequence in lanes B and D subsequent to inserted or deleted nucleotides. RT and PCR reactions performed as described (Willis et al. 1999). Poly(A)+ RNA was reverse transcribed using Superscript II (GIBCO–BRL) or rTth (Amersham) and random hexamers and the BCL10 open reading frame amplified using either Taq or Pfu polymerase with forward primer: 5′-CCTCCTCTCCTTCTTCCCCATTACC-3′ and reverse primer 5′-GCAATAAAGTGTCATTGTCTGGAAACAGT-3′. RT-PCR products were either sequenced directly or cloned into pCR2.1 (Invitrogen). Clones were sequenced in both directions using either Licor (MWG-Biotech, Germany) or ABI-377 (Applied Biosystems) automated sequencers. Cell 1999 97, 686-688DOI: (10.1016/S0092-8674(02)09766-0)