@article{oai:miyazaki-u.repo.nii.ac.jp:00004590,
 author = {Kameda, Takuro and 亀田, 拓郎 and Shide, Kotaro and 幣, 光太郎 and 山路, 卓巳 and Yamaji, Takumi and 上運天, 綾子 and Kamiunten, Ayako and 関根, 雅明 and Sekine, Masaaki and Taniguchi, Yasuhiro and 日髙, 智徳 and Hidaka, Tomonori and Kubuki, Yoko and 久冨木, 庸子 and 下田, 晴子 and Shimoda, Haruko and 丸塚, 浩助 and Marutsuka, Kousuke and Sashida, Goro and Aoyama, Kazumasa and Yoshimitsu, Makoto and 原田, 拓 and Harada, Taku and Abe, Hiroo and 安倍, 弘生 and 三池, 忠 and Miike, Tadashi and Iwakiri, Hisayoshi and 岩切, 久芳 and 田原, 良博 and Tahara, Yoshihiro and Sueta, Mitsue and 末田, 光恵 and Yamamoto, Shojiro and 山本, 章二朗 and Hasuike, Satoru and 蓮池, 悟 and Nagata, Kenji and 永田, 賢治 and Iwama, Atsushi and Kitanaka, Akira and 北中, 明 and Shimoda, Kazuya and 下田, 和哉},
 issue = {2},
 journal = {Blood},
 month = {Jan},
 note = {Acquired mutations of JAK2 and TET2 are frequent in myeloproliferative neoplasms (MPNs). We examined the individual and cooperative effects of these mutations on MPN development. Recipients of JAK2V617F cells developed primary myelofibrosis-like features; the addition of loss of TET2 worsened this JAK2V617F-induced disease, causing prolonged leukocytosis, splenomegaly, extramedullary hematopoiesis, and modestly shorter survival. Double-mutant (JAK2V617F plus loss of TET2) myeloid cells were more likely to be in a proliferative state than JAK2V617F single-mutant myeloid cells. In a serial competitive transplantation assay, JAK2V617F cells resulted in decreased chimerism in the second recipients, which did not develop MPNs. In marked contrast, cooperation between JAK2V617F and loss of TET2 developed and maintained MPNs in the second recipients by compensating for impaired hematopoietic stem cell (HSC) functioning. In-vitro sequential colony formation assays also supported the observation that JAK2V617F did not maintain HSC functioning over the long-term, but concurrent loss of TET2 mutation restored it. Transcriptional profiling revealed that loss of TET2 affected the expression of many HSC signature genes. We conclude that loss of TET2 has two different roles in MPNs: disease accelerator and disease initiator and sustainer in combination with JAK2V617F., Citation:
Kameda T, Shide K, Yamaji T, Kamiunten A, Sekine M, Taniguchi Y, Hidaka T, Kubuki Y, Shimoda H, Marutsuka K, Sashida G, Aoyama K, Yoshimitsu M, Harada T, Abe H, Miike T, Iwakiri H, Tahara Y, Sueta M, Yamamoto S, Hasuike S, Nagata K, Iwama A, Kitanaka A, Shimoda K. Loss of TET2 has dual roles in murine myeloproliferative neoplasms: disease sustainer and disease accelerator. Blood. 2015 Jan 8;125(2):304-15. doi: 10.1182/blood-2014-04-555508. Epub 2014 Nov 13. PMID: 25395421.},
 pages = {304--315},
 title = {Loss of TET2 has dual roles in murine myeloproliferative neoplasms: disease sustainer and disease accelerator},
 volume = {125},
 year = {2015},
 yomi = {カメダ, タクロウ and シデ, コウタロウ and ヤマジ, タクミ and カミウンテン, アヤコ and セキネ, マサアキ and ヒダカ, トモノリ and クブキ, ヨウコ and シモダ, ハルコ and マルツカ, コウスケ and ハラダ, タク and アベ, ヒロオ and ミイケ, タダシ and イワキリ, ヒサヨシ and タハラ, ヨシヒロ and スエタ, ミツエ and ヤマモト, ショウジロウ and ハスイケ, サトル and ナガタ, ケンジ and キタナカ, アキラ and シモダ, カズヤ}
}