
Clonal Analysis of Multiple Point Mutations in the N‐ ras Gene in Patients with Acute Myeloid Leukemia
Author(s) -
Kubo Kazuaki,
Naoe Tomoki,
Kiyoi Hitoshi,
Fukutani Hisashi,
Kato Yoshiro,
Oguri Takashi,
Yamamori Shunji,
Akatsuka Yoshiki,
Kodera Yoshihisa,
Ohno Ryuzo
Publication year - 1993
Publication title -
japanese journal of cancer research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.035
H-Index - 141
eISSN - 1349-7006
pISSN - 0910-5050
DOI - 10.1111/j.1349-7006.1993.tb00147.x
Subject(s) - missense mutation , myeloid leukemia , leukemia , point mutation , biology , cancer research , monoclonal , microbiology and biotechnology , myeloid , mutation , gene , genetics , monoclonal antibody , antibody
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.