TY - JOUR
T1 - Clonal Analysis of Multiple Point Mutations in the N‐ras Gene in Patients with Acute Myeloid Leukemia
AU - Kubo, Kazuaki
AU - Naoe, Tomoki
AU - Kiyoi, Hitoshi
AU - Fukutani, Hisashi
AU - Kato, Yoshiro
AU - Oguri, Takashi
AU - Yamamori, Shunji
AU - Akatsuka, Yoshiki
AU - Kodera, Yoshihisa
AU - Ohno, Ryuzo
PY - 1993/4
Y1 - 1993/4
N2 - We have screened mutations of the N‐ras gene at codons 12, 13, and 61 in leukemia cells obtained from 100 patients with acute myeloid leukemia (AMD, and found mutated N‐ras alleles in 9 patients. We further analyzed the polyclonality of multiple N‐ras gene mutations in 4 AML patients. One patient, who had the monoclonal karyotype, t(11;17), had two types of double missense mutations at codons 13 and 61 in the same allele. Each of the remaining three patients, one of whom had t(15;17) with a monoclonal rearrangement of the retinoic acid receptor alpha and PML genes, carried two missense mutations in a relatively small population of leukemia cells. We have demonstrated that multiple clonality of the N‐ras gene is occasionally observed in leukemia with a monoclonal karyotype. These findings indicate that the N‐ras mutations may not always be characterized simply by an accumulative process and that the activated N‐ras gene alone is not sufficient to cause leukemia.
AB - We have screened mutations of the N‐ras gene at codons 12, 13, and 61 in leukemia cells obtained from 100 patients with acute myeloid leukemia (AMD, and found mutated N‐ras alleles in 9 patients. We further analyzed the polyclonality of multiple N‐ras gene mutations in 4 AML patients. One patient, who had the monoclonal karyotype, t(11;17), had two types of double missense mutations at codons 13 and 61 in the same allele. Each of the remaining three patients, one of whom had t(15;17) with a monoclonal rearrangement of the retinoic acid receptor alpha and PML genes, carried two missense mutations in a relatively small population of leukemia cells. We have demonstrated that multiple clonality of the N‐ras gene is occasionally observed in leukemia with a monoclonal karyotype. These findings indicate that the N‐ras mutations may not always be characterized simply by an accumulative process and that the activated N‐ras gene alone is not sufficient to cause leukemia.
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U2 - 10.1111/j.1349-7006.1993.tb00147.x
DO - 10.1111/j.1349-7006.1993.tb00147.x
M3 - Article
C2 - 8514604
AN - SCOPUS:0027155193
SN - 0910-5050
VL - 84
SP - 379
EP - 387
JO - Japanese Journal of Cancer Research
JF - Japanese Journal of Cancer Research
IS - 4
ER -