@article{oai:soar-ir.repo.nii.ac.jp:00008010,
 author = {Matsuda,  K and Nakazawa,  Y and Iwashita,  C and Kurata,  T and Hirabayashi,  K and Saito,  S and Tanaka,  M and Yoshikawa,  K and Yanagisawa,  R and Sakashita,  K and Sasaki,  S and Honda,  T and Koike,  K},
 issue = {7},
 journal = {LEUKEMIA},
 month = {Jul},
 note = {advance online publication, February 25, 2014, Juvenile myelomonocytic leukemia (JMML) is a fatal, mixed myeloproliferative and myelodysplastic disorder occurring in infancy and early childhood. Children with JMML have mutually exclusive genetic abnormalities in granulocyte-macrophage colony-stimulating factor (GM-CSF) signaling pathways, inactivation of the NF1 or mutations in PTPN11, NRAS, KRAS and CBL. A whole-exome sequencing study, performed by Sakaguchi et al.,3 has recently demonstrated that in addition to the high frequency of RAS pathway mutations, mutations in SETBP1 and JAK3 are common recurrent secondary events, and that these events may be involved in tumor progression, and are associated with poor clinical outcomes., Article, LEUKEMIA. 28(7):1545-1548 (2014)},
 pages = {1545--1548},
 title = {Myeloid progenitors with PTPN11 and nonRAS pathway gene mutations are refractory to treatment with 6-mercaptopurine in juvenile myelomonocytic leukemia},
 volume = {28},
 year = {2014}
}