Relapse cell population differs from acute onset clone as shown by absence
of the initially activated N-ras oncogene in a patient with acute
myelomonocytic leukemia
HP Senn, J Jiricny, M Fopp, L Schmid and C Moroni
Friedrich Miescher-Institut, Basel, Switzerland.
We have conducted a follow-up study of a patient with myelomonocytic
leukemia exhibiting an N-ras mutation (Gln61----Lys61) using the polymerase
chain reaction method and synthetic oligonucleotide hybridization probes.
This method allowed us to detect as little as 3% of N-ras-mutated cells
within a population. When the patient went into clinical remission, the
mutation became undetectable. When a relapse occurred, the blasts did not
carry the N-ras mutation. Analysis of M13 cloned amplified N-ras sequences
from relapse DNA revealed exclusively the wild type allele of the N-ras
gene. These findings suggest that the relapse cell population is derived
from a different clone than the acute phase population. Furthermore, the
data argue that N-ras mutation is not an initiating lesion in this case of
acute myelomonocytic leukemia (AMML).
Volume 72,
Issue 3,
pp. 931-935,
09/01/1988
Copyright © 1988 by The American Society of Hematology
