Barrois M, Eychenne M K, Terrier-Lacombe M J, Duarte N, Dubourg C, Douc-Rasy S, Chompret A, Khagad M, Hartmann O, Caput D, Bénard J
Department of Clinical Biology, Institut Gustave Roussy, Villejuif, France.
Med Pediatr Oncol. 2001 Jan;36(1):45-7. doi: 10.1002/1096-911X(20010101)36:1<45::AID-MPO1012>3.0.CO;2-E.
The p53 gene homologue, p73, is located on the 1p36-3 locus, which is frequently deleted in human neuroblastoma (NB). A survey of 61 NB showed that among 33% of informative cases, p73 loss of heterozygosity (LOH) occurred in 7 of 20 (35%).
LOH pattern of vicinal markers suggested that the p73 gene could not be considered as the candidate NB suppressor gene. Moreover, comparative measurements of allelic expression in tumors and corresponding patient lymphocytes indicate that pure biallelism is much more frequent in lymphocytes than in tumors (71% vs 30%, P= 0.05), which suggests that disequilibrated allelic expression is associated with NB disease.
Therefore, in the p73 LOH NBs, the p73 gene could be altered in the maintained allele not by mutations [Ishimiya et al.: Med Pediatr Oncol, this issue], but rather by an abnormal transcription.
