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3. Integrin-α9 overexpression underlies the niche-independent maintenance of leukemia stem cells in acute myeloid leukemia

Author

Niibori-Nambu, Akiko, Wang, Chelsia Qiuxia, Chin, Desmond Wai Loon, Chooi, Jing Yuan, Hosoi, Hiroki, Sonoki, Takashi, Tham, Cheng-Yong, Nah, Giselle Sek Suan, Cirovic, Branko, Tan, Darren Qiancheng, Takizawa, Hitoshi, Sashida, Goro, Goh, Yufen, Tng, Jiaqi, Fam, Wee Nih, Fullwood, Melissa Jane, Suda, Toshio, Yang, Henry, Tergaonkar, Vinay, Taniuchi, Ichiro, Li, Shang, Chng, Wee Joo, and Osato, Motomi

Published
2024
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6. Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes.

Author

Hayashi, Yoshihiro, Zhang, Yue, Yokota, Asumi, Yan, Xiaomei, Liu, Jinqin, Choi, Kwangmin, Li, Bing, Sashida, Goro, Peng, Yanyan, Xu, Zefeng, Huang, Rui, Zhang, Lulu, Freudiger, George M, Wang, Jingya, Dong, Yunzhu, Zhou, Yile, Wang, Jieyu, Wu, Lingyun, Bu, Jiachen, Chen, Aili, Zhao, Xinghui, Sun, Xiujuan, Chetal, Kashish, Olsson, Andre, Watanabe, Miki, Romick-Rosendale, Lindsey E, Harada, Hironori, Shih, Lee-Yung, Tse, William, Bridges, James P, Caligiuri, Michael A, Huang, Taosheng, Zheng, Yi, Witte, David P, Wang, Qian-Fei, Qu, Cheng-Kui, Salomonis, Nathan, Grimes, H Leighton, Nimer, Stephen D, Xiao, Zhijian, and Huang, Gang

Subjects
Animals, Mice, Knockout, Humans, Mice, Myelodysplastic Syndromes, Histone-Lysine N-Methyltransferase, Gene Expression Regulation, Neoplastic, Core Binding Factor Alpha 2 Subunit, Myeloid-Lymphoid Leukemia Protein, Hypoxia-Inducible Factor 1, alpha Subunit, Metabolome, Hypoxia, Rare Diseases, Hematology, Genetics, Cancer, Stem Cell Research, Aging, 2.1 Biological and endogenous factors, Aetiology, Oncology and Carcinogenesis
Abstract

Myelodysplastic syndromes (MDS) are heterogeneous hematopoietic disorders that are incurable with conventional therapy. Their incidence is increasing with global population aging. Although many genetic, epigenetic, splicing, and metabolic aberrations have been identified in patients with MDS, their clinical features are quite similar. Here, we show that hypoxia-independent activation of hypoxia-inducible factor 1α (HIF1A) signaling is both necessary and sufficient to induce dysplastic and cytopenic MDS phenotypes. The HIF1A transcriptional signature is generally activated in MDS patient bone marrow stem/progenitors. Major MDS-associated mutations (Dnmt3a, Tet2, Asxl1, Runx1, and Mll1) activate the HIF1A signature. Although inducible activation of HIF1A signaling in hematopoietic cells is sufficient to induce MDS phenotypes, both genetic and chemical inhibition of HIF1A signaling rescues MDS phenotypes in a mouse model of MDS. These findings reveal HIF1A as a central pathobiologic mediator of MDS and as an effective therapeutic target for a broad spectrum of patients with MDS.Significance: We showed that dysregulation of HIF1A signaling could generate the clinically relevant diversity of MDS phenotypes by functioning as a signaling funnel for MDS driver mutations. This could resolve the disconnection between genotypes and phenotypes and provide a new clue as to how a variety of driver mutations cause common MDS phenotypes. Cancer Discov; 8(11); 1438-57. ©2018 AACR. See related commentary by Chen and Steidl, p. 1355 This article is highlighted in the In This Issue feature, p. 1333.

Published
2018

9. CARD11 mutation and HBZ expression induce lymphoproliferative disease and adult T-cell leukemia/lymphoma

Author

Kameda, Takuro, Shide, Kotaro, Kamiunten, Ayako, Kogure, Yasunori, Morishita, Daisuke, Koya, Junji, Tahira, Yuki, Akizuki, Keiichi, Yokomizo-Nakano, Takako, Kubota, Sho, Marutsuka, Kosuke, Sekine, Masaaki, Hidaka, Tomonori, Kubuki, Yoko, Kitai, Yuichi, Matsuda, Tadashi, Yoda, Akinori, Ohshima, Takayuki, Sugiyama, Midori, Sashida, Goro, Kataoka, Keisuke, Ogawa, Seishi, and Shimoda, Kazuya

Published
2022
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10. RUNX1-ETO (RUNX1-RUNX1T1) induces myeloid leukemia in mice in an age-dependent manner

Author

Abdallah, Mohamed Gaber, Niibori-Nambu, Akiko, Morii, Mariko, Yokomizo, Takako, Yokomizo, Tomomasa, Ideue, Takako, Kubota, Sho, Teoh, Vania Swee Imm, Mok, Michelle Meng Huang, Wang, Chelsia Qiuxia, Omar, Abdellah Ali, Tokunaga, Kenji, Iwanaga, Eisaku, Matsuoka, Masao, Asou, Norio, Nakagata, Naomi, Araki, Kimi, AboElenin, Mabrouk, Madboly, Sayed Hamada, Sashida, Goro, and Osato, Motomi

Published
2021
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20. Ezh2 loss propagates hypermethylation at T cell differentiation-regulating genes to promote leukemic transformation

Author

Wang, Changshan, Oshima, Motohiko, Sato, Daisuke, Matsui, Hirotaka, Kubota, Sho, Aoyama, Kazumasa, Nakajima-Takagi, Yaeko, Koide, Shuhei, Matsubayashi, Jun, Mochizuki-Kashio, Makiko, Nakano-Yokomizo, Takako, Bai, Jie, Nagao, Toshitaka, Kanai, Akinori, Iwama, Atsushi, and Sashida, Goro

Subjects
Cell differentiation -- Genetic aspects -- Health aspects, Transcription factors -- Health aspects, Acute lymphocytic leukemia -- Genetic aspects -- Development and progression -- Care and treatment, T cells -- Genetic aspects -- Health aspects, Health care industry
Abstract

Early T cell precursor acute lymphoblastic leukemia (ETP-ALL) is a new pathological entity with poor outcomes in T cell ALL (T-ALL) that is characterized by a high incidence of loss-of-function mutations in polycomb repressive complex 2 (PRC2) genes. We generated a mouse model of ETP-ALL by deleting Ezh2, one of the PRC2 genes, in p53-null hematopoietic cells. The loss of Ezh2 in p53-null hematopoietic cells impeded the differentiation of ETPs and eventually induced ETP-ALL-like disease in mice, indicating that PRC2 functions as a bona fide tumor suppressor in ETPs. A large portion of PRC2 target genes acquired DNA hypermethylation of their promoters following reductions in H3K27me3 levels upon the loss of Ezh2, which included pivotal T cell differentiation-regulating genes. The reactivation of a set of regulators by a DNA-demethylating agent, but not the transduction of single regulator genes, effectively induced the differentiation of ETP-ALL cells. Thus, PRC2 protects key T cell developmental regulators from DNA hypermethylation in order to keep them primed for activation upon subsequent differentiation phases, while its insufficiency predisposes ETPs to leukemic transformation. These results revealed a previously unrecognized epigenetic switch in response to PRC2 dysfunction and provide the basis for specific rational epigenetic therapy for ETP-ALL with PRC2 insufficiency., Introduction Early T cell precursor acute lymphoblastic leukemia (ETP-ALL) has been identified as a new pathological entity of T cell ALL (T-ALL) that shows resistance to conventional chemotherapies and has [...]

Published
2018
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21. Exposure to microbial products followed by loss of Tet2 promotes myelodysplastic syndrome via remodeling HSCs

Author

Yokomizo-Nakano, Takako, primary, Hamashima, Ai, additional, Kubota, Sho, additional, Bai, Jie, additional, Sorin, Supannika, additional, Sun, Yuqi, additional, Kikuchi, Kenta, additional, Iimori, Mihoko, additional, Morii, Mariko, additional, Kanai, Akinori, additional, Iwama, Atsushi, additional, Huang, Gang, additional, Kurotaki, Daisuke, additional, Takizawa, Hitoshi, additional, Matsui, Hirotaka, additional, and Sashida, Goro, additional

Published
2023
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22. Data from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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23. Supplementary Methods from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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24. Supplementary Table S2 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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25. Supplementary Figure S1-13 and Supplementary Table S1,3 from Pathobiological Pseudohypoxia as a Putative Mechanism Underlying Myelodysplastic Syndromes

Author

Hayashi, Yoshihiro, primary, Zhang, Yue, primary, Yokota, Asumi, primary, Yan, Xiaomei, primary, Liu, Jinqin, primary, Choi, Kwangmin, primary, Li, Bing, primary, Sashida, Goro, primary, Peng, Yanyan, primary, Xu, Zefeng, primary, Huang, Rui, primary, Zhang, Lulu, primary, Freudiger, George M., primary, Wang, Jingya, primary, Dong, Yunzhu, primary, Zhou, Yile, primary, Wang, Jieyu, primary, Wu, Lingyun, primary, Bu, Jiachen, primary, Chen, Aili, primary, Zhao, Xinghui, primary, Sun, Xiujuan, primary, Chetal, Kashish, primary, Olsson, Andre, primary, Watanabe, Miki, primary, Romick-Rosendale, Lindsey E., primary, Harada, Hironori, primary, Shih, Lee-Yung, primary, Tse, William, primary, Bridges, James P., primary, Caligiuri, Michael A., primary, Huang, Taosheng, primary, Zheng, Yi, primary, Witte, David P., primary, Wang, Qian-fei, primary, Qu, Cheng-Kui, primary, Salomonis, Nathan, primary, Grimes, H. Leighton, primary, Nimer, Stephen D., primary, Xiao, Zhijian, primary, and Huang, Gang, primary

Published
2023
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26. Data from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome

Author

Yokomizo-Nakano, Takako, primary, Kubota, Sho, primary, Bai, Jie, primary, Hamashima, Ai, primary, Morii, Mariko, primary, Sun, Yuqi, primary, Katagiri, Seiichiro, primary, Iimori, Mihoko, primary, Kanai, Akinori, primary, Tanaka, Daiki, primary, Oshima, Motohiko, primary, Harada, Yuka, primary, Ohyashiki, Kazuma, primary, Iwama, Atsushi, primary, Harada, Hironori, primary, Osato, Motomi, primary, and Sashida, Goro, primary

Published
2023
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27. Supplementary Data 4 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome

Author

Yokomizo-Nakano, Takako, primary, Kubota, Sho, primary, Bai, Jie, primary, Hamashima, Ai, primary, Morii, Mariko, primary, Sun, Yuqi, primary, Katagiri, Seiichiro, primary, Iimori, Mihoko, primary, Kanai, Akinori, primary, Tanaka, Daiki, primary, Oshima, Motohiko, primary, Harada, Yuka, primary, Ohyashiki, Kazuma, primary, Iwama, Atsushi, primary, Harada, Hironori, primary, Osato, Motomi, primary, and Sashida, Goro, primary

Published
2023
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28. Supplementary Table 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome

Author

Yokomizo-Nakano, Takako, primary, Kubota, Sho, primary, Bai, Jie, primary, Hamashima, Ai, primary, Morii, Mariko, primary, Sun, Yuqi, primary, Katagiri, Seiichiro, primary, Iimori, Mihoko, primary, Kanai, Akinori, primary, Tanaka, Daiki, primary, Oshima, Motohiko, primary, Harada, Yuka, primary, Ohyashiki, Kazuma, primary, Iwama, Atsushi, primary, Harada, Hironori, primary, Osato, Motomi, primary, and Sashida, Goro, primary

Published
2023
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29. Supplementary Figure 1-11 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome

Author

Yokomizo-Nakano, Takako, primary, Kubota, Sho, primary, Bai, Jie, primary, Hamashima, Ai, primary, Morii, Mariko, primary, Sun, Yuqi, primary, Katagiri, Seiichiro, primary, Iimori, Mihoko, primary, Kanai, Akinori, primary, Tanaka, Daiki, primary, Oshima, Motohiko, primary, Harada, Yuka, primary, Ohyashiki, Kazuma, primary, Iwama, Atsushi, primary, Harada, Hironori, primary, Osato, Motomi, primary, and Sashida, Goro, primary

Published
2023
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30. Supplementary Data 2 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome

Author

Yokomizo-Nakano, Takako, primary, Kubota, Sho, primary, Bai, Jie, primary, Hamashima, Ai, primary, Morii, Mariko, primary, Sun, Yuqi, primary, Katagiri, Seiichiro, primary, Iimori, Mihoko, primary, Kanai, Akinori, primary, Tanaka, Daiki, primary, Oshima, Motohiko, primary, Harada, Yuka, primary, Ohyashiki, Kazuma, primary, Iwama, Atsushi, primary, Harada, Hironori, primary, Osato, Motomi, primary, and Sashida, Goro, primary

Published
2023
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31. Supplementary Data 1 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome

Author

Yokomizo-Nakano, Takako, primary, Kubota, Sho, primary, Bai, Jie, primary, Hamashima, Ai, primary, Morii, Mariko, primary, Sun, Yuqi, primary, Katagiri, Seiichiro, primary, Iimori, Mihoko, primary, Kanai, Akinori, primary, Tanaka, Daiki, primary, Oshima, Motohiko, primary, Harada, Yuka, primary, Ohyashiki, Kazuma, primary, Iwama, Atsushi, primary, Harada, Hironori, primary, Osato, Motomi, primary, and Sashida, Goro, primary

Published
2023
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32. Supplementary Table 2 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome

Author

Yokomizo-Nakano, Takako, primary, Kubota, Sho, primary, Bai, Jie, primary, Hamashima, Ai, primary, Morii, Mariko, primary, Sun, Yuqi, primary, Katagiri, Seiichiro, primary, Iimori, Mihoko, primary, Kanai, Akinori, primary, Tanaka, Daiki, primary, Oshima, Motohiko, primary, Harada, Yuka, primary, Ohyashiki, Kazuma, primary, Iwama, Atsushi, primary, Harada, Hironori, primary, Osato, Motomi, primary, and Sashida, Goro, primary

Published
2023
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33. Supplementary Data 3 from Overexpression of RUNX3 Represses RUNX1 to Drive Transformation of Myelodysplastic Syndrome

Author

Yokomizo-Nakano, Takako, primary, Kubota, Sho, primary, Bai, Jie, primary, Hamashima, Ai, primary, Morii, Mariko, primary, Sun, Yuqi, primary, Katagiri, Seiichiro, primary, Iimori, Mihoko, primary, Kanai, Akinori, primary, Tanaka, Daiki, primary, Oshima, Motohiko, primary, Harada, Yuka, primary, Ohyashiki, Kazuma, primary, Iwama, Atsushi, primary, Harada, Hironori, primary, Osato, Motomi, primary, and Sashida, Goro, primary

Published
2023
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36. A gain‐of‐function mutation in micro‐RNA ‐142 is sufficient to cause the development of T‐cell leukemia in mice

Author

Kawano, Shingo, primary, Araki, Kimi, additional, Bai, Jie, additional, Furukawa, Imari, additional, Tateishi, Keigo, additional, Yoshinobu, Kumiko, additional, Usuki, Shingo, additional, Nimmo, Rachael A., additional, Kaname, Tadashi, additional, Yoshihara, Masaharu, additional, Takahashi, Satoru, additional, Sashida, Goro, additional, and Araki, Masatake, additional

Published
2023
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42. Loss of TET2 has dual roles in murine myeloproliferative neoplasms: disease sustainer and disease accelerator

Author

Kameda, Takuro, Shide, Kotaro, Yamaji, Takumi, Kamiunten, Ayako, Sekine, Masaaki, Taniguchi, Yasuhiro, Hidaka, Tomonori, Kubuki, Yoko, Shimoda, Haruko, Marutsuka, Kousuke, Sashida, Goro, Aoyama, Kazumasa, Yoshimitsu, Makoto, Harada, Taku, Abe, Hiroo, Miike, Tadashi, Iwakiri, Hisayoshi, Tahara, Yoshihiro, Sueta, Mitsue, Yamamoto, Shojiro, Hasuike, Satoru, Nagata, Kenji, Iwama, Atsushi, Kitanaka, Akira, and Shimoda, Kazuya

Published
2015
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45. A gain‐of‐function mutation in microRNA 142 is sufficient to cause the development of T‐cell leukemia in mice.

Author

Kawano, Shingo, Araki, Kimi, Bai, Jie, Furukawa, Imari, Tateishi, Keigo, Yoshinobu, Kumiko, Usuki, Shingo, Nimmo, Rachael A., Kaname, Tadashi, Yoshihara, Masaharu, Takahashi, Satoru, Sashida, Goro, and Araki, Masatake

Abstract

MicroRNAs (miRNAs) play a crucial role in regulating gene expression. MicroRNA expression levels fluctuate, and point mutations and methylation occur in cancer cells; however, to date, there have been no reports of carcinogenic point mutations in miRNAs. MicroRNA 142 (miR‐142) is frequently mutated in patients with follicular lymphoma, diffuse large B‐cell lymphoma, chronic lymphocytic leukemia (CLL), and acute myeloid leukemia/myelodysplastic syndrome (AML/MDS). To understand the role of miR‐142 mutation in blood cancers, the CRISPR‐Cas9 system was utilized to successfully generate miR‐142‐55A>G mutant knock‐in (Ki) mice, simulating the most frequent mutation in patients with miR‐142 mutated AML/MDS. Bone marrow cells from miR‐142 mutant heterozygous Ki mice were transplanted, and we found that the miR‐142 mutant/wild‐type cells were sufficient for the development of CD8+ T‐cell leukemia in mice post‐transplantation. RNA‐sequencing analysis in hematopoietic stem/progenitor cells and CD8+ T‐cells revealed that miR‐142‐Ki/+ cells had increased expression of the mTORC1 activator, a potential target of wild‐type miR‐142‐3p. Notably, the expression of genes involved in apoptosis, differentiation, and the inhibition of the Akt–mTOR pathway was suppressed in miR‐142‐55A>G heterozygous cells, indicating that these genes are repressed by the mutant miR‐142‐3p. Thus, in addition to the loss of function due to the halving of wild‐type miR‐142‐3p alleles, mutated miR‐142‐3p gained the function to suppress the expression of distinct target genes, sufficient to cause leukemogenesis in mice. [ABSTRACT FROM AUTHOR]

Published
2023
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46. HMGN3 represses transcription of epithelial regulators to promote migration of cholangiocarcinoma in a SNAI2‐dependent manner

Author

Sorin, Supannika, primary, Kubota, Sho, additional, Hamidi, Sofiane, additional, Yokomizo‐Nakano, Takako, additional, Vaeteewoottacharn, Kulthida, additional, Wongkham, Sopit, additional, Waraasawapati, Sakda, additional, Pairojkul, Chawalit, additional, Bai, Jie, additional, Morii, Mariko, additional, Sheng, Guojun, additional, Sawanyawisuth, Kanlayanee, additional, and Sashida, Goro, additional

Published
2022
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49. Stress hematopoiesis reveals abnormal control of self-renewal, lineage bias, and myeloid differentiation in Mll partial tandem duplication (Mll-PTD) hematopoietic stem/progenitor cells

Author

Zhang, Yue, Yan, Xiaomei, Sashida, Goro, Zhao, Xinghui, Rao, Yalan, Goyama, Susumu, Whitman, Susan P., Zorko, Nicholas, Bernot, Kelsie, Conway, Rajeana M., Witte, David, Wang, Qian-fei, Tenen, Daniel G., Xiao, Zhijian, Marcucci, Guido, Mulloy, James C., Grimes, H. Leighton, Caligiuri, Michael A., and Huang, Gang

Published
2012
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