Abstract
Jaskowski et al1 have confirmed our previous paper2 reporting an association between BAT26 stability and germline MSH2 deletion. Among seven highly unstable tumours with MSH2 deletion spanning exon 5 they found normal BAT26 sequences in 4. Although their analysis was based on a small number of tumours, they observed this phenomenon in 57% of cases, a percentage very close to the 68% we obtained in the analysis of 19 tumour DNAs.2 It is reasonable to suppose that the molecular mechanism leading to somatic loss of BAT26 sequences, as we described previously,2 is responsible for the observed BAT26 stability in both subsets of MSH2 deleted tumours.
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