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N‐ras and p53 gene mutations in Japanese patients with myeloproliferative disorders
Author(s) -
Tsurumi Shigeharu,
Nakamura Yuichi,
Maki Kazuhiro,
Omine Mitsuhiro,
Fujita Kazuhiro,
Okamura Takashi,
Niho Yoshiyuki,
Hashimoto Sachiko,
Kanno Keiko,
Suzuki Kenshi,
Hangaishi Akira,
Ogawa Seishi,
Hirai Hisamaru,
Mitani Kinuko
Publication year - 2002
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.10188
Subject(s) - essential thrombocythemia , polycythemia vera , myelofibrosis , exon , missense mutation , gene , myeloproliferative disorders , cancer research , mutation , leukemia , pathogenesis , tumor suppressor gene , bone marrow , biology , gene mutation , medicine , genetics , immunology , carcinogenesis
Alterations of the N‐ras oncogene and p53 tumor suppressor gene have been demonstrated to play an important role in pathogenesis of hematological malignancies. We simultaneously investigated genetic lesions of both genes in bone marrow cells from 64 Japanese patients with myeloproliferative disorders (MPD), including polycythemia vera (PV), essential thrombocythemia (ET), and idiopathic myelofibrosis (MF), by direct sequencing analysis. No mutations of the N‐ras gene were detected in any cases. Two patients, one with chronic neutrophilic leukemia derived from PV and one with acute mylogenous leukemia derived from ET, exhibited three mutations of the p53 gene. Among them, two were missense mutations in exon 5 or 7 and one was a deletion in exon 5. All samples in chronic phase or from MF were devoid of mutations in both genes. These data suggested that disruptions of both genes are extremely rare in MPD in chronic phase and that loss of functions in the p53 gene could be involved in progression of MPD such as PV and ET. Am. J. Hematol. 71:131–133, 2002. © 2002 Wiley‐Liss, Inc.