Randerson J, Cawkwell L, Jack A S, Child A J, Shiach C R, Lewis F, Johnson P, Evans P, Barrans S, Morgan G J
Institute of Pathology, University of Leeds, West Yorkshire, England, UK.
Leuk Lymphoma. 1996 Jun;22(1-2):113-7, follow. 186, color plate X. doi: 10.3109/10428199609051737.
We have examined 41 cases of follicle centre cell lymphoma with fluorescent PCR of microsatellite repeats closely linked to or within six tumour suppressor gene loci (APC, DCC, P53, RB1, WT1 and NM23). These probes are highly informative with heterozygousity rates in the range of 57%-90%. In addition we have used four loci from chromosome 6 (D6S260, TNFa, D6S281 and D6S262) as control loci which are unlikely to be involved in the pathogenesis of lymphoma. Of 369 informative PCR reactions allele imbalance was identified in 38 (10%) and this was seen in 23 of the 41 cases. Looking at individual loci allele imbalance was seen in APC(1) 11%, APC(2) 12%, P53(1) 5%, P53 (2) 7%, WT1 5%, RB1 13%, DCC 18% and NM23 0%. This frequency of change was no different from that seen at the control loci D6S260 16%, TNFa 20%, D6S281 4% and D6S262 9%. In the indolent phase of germinal centre cell lymphoma there is therefore quite a high rate of allele imbalance at all loci but this is no higher in those loci linked to tumour suppressor genes.
我们采用荧光PCR技术，检测了41例滤泡中心细胞淋巴瘤，该技术针对与6个肿瘤抑制基因位点（APC、DCC、P53、RB1、WT1和NM23）紧密连锁或位于其内部的微卫星重复序列。这些探针具有高度信息性，杂合率在57%-90%范围内。此外，我们使用了来自6号染色体的4个位点（D6S260、TNFa、D6S281和D6S262）作为对照位点，这些位点不太可能参与淋巴瘤的发病机制。在369次信息性PCR反应中，有38次（10%）检测到等位基因失衡，41例中有23例出现这种情况。观察各个位点，发现APC(1)等位基因失衡率为11%，APC(2)为12%，P53(1)为5%，P53(2)为7%，WT1为5%，RB1为13%，DCC为18%，NM23为0%。这种变化频率与对照位点D6S260的16%、TNFa的20%、D6S281的4%和D6S262的9%没有差异。因此，在生发中心细胞淋巴瘤的惰性期，所有位点的等位基因失衡率相当高，但与肿瘤抑制基因相关的位点并不更高。
