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N Terada, J Miyoshi, K Kawa-Ha, H Sasai, S Orita, K Yumura-Yagi, J Hara, A Fujinami and T Kakunaga
Department of Oncogene Research, Osaka University, Japan.
We investigated N-ras activation in childhood acute lymphoblastic leukemia
(dALL) by the polymerase chain reaction (PCR) and the oligonucleotide
hybridization method. The frequency of point-mutation of the N-ras gene was
not high (2 of 15), and one positive case who relapsed was analyzed in
detail. Although N-ras gene activation was detected at both onset and
relapse, the mutation sites were different. At onset, Gly (GGT) was changed
to Ser (AGT) at codon 12, and at relapse, Gly (GGT) to Asp (GAT) was
observed at the same codon. In addition, the DNA at relapse showed a
remarkably higher transforming activity than the DNA at onset on two
independent recipient cell lines. The identical cell surface phenotype and
the same rearrangement patterns of both the immunoglobulin (Ig) heavy chain
and T-cell receptor (TCR) gamma chain genes indicated that the leukemic
cells at onset and those at relapse were derived from the same precursor
cell. Therefore, this case supports the concept that ras activation is not
the event initiating leukemogenesis, but may be involved in leukemic
progression.
This article has been cited by other articles:
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| Copyright © 1990 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
