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2. Chromatin regulator Asxl1 loss and Nf1 haploinsufficiency cooperate to accelerate myeloid malignancy

Author

Zhang, Peng, He, Fuhong, Bai, Jie, Yamamoto, Shohei, Chen, Shi, Zhang, Lin, Sheng, Mengyao, Zhang, Lei, Guo, Ying, Man, Na, Yang, Hui, Wang, Suyun, Cheng, Tao, Nimer, Stephen D., Zhou, Yuan, Xu, Mingjiang, Wang, Qian-Fei, and Yang, Feng-Chun

Subjects
Cellular signal transduction -- Research, Chromatin -- Research, Gene mutation -- Research, Myeloid leukemia -- Genetic aspects -- Development and progression -- Care and treatment, Neurofibromatosis -- Genetic aspects, Cancer, Hematopoietic stem cells, Epigenetic inheritance, Genes, Transcription (Genetics), Medical research, Genetic research, Health care industry
Abstract

ASXL1 is frequently mutated in myeloid malignancies and is known to co-occur with other gene mutations. However, the molecular mechanisms underlying the leukemogenesis associated with ASXL1 and cooperating mutations remain to be elucidated. Here, we report that Asxl1 loss cooperated with haploinsufficiency of Nf1, a negative regulator of the RAS signaling pathway, to accelerate the development of myeloid leukemia in mice. Loss of Asxl1 and Nf1 in hematopoietic stem and progenitor cells resulted in a gain-of-function transcriptional activation of multiple pathways such as MYC, NRAS, and BRD4 that are critical for leukemogenesis. The hyperactive MYC and BRD9 transcription programs were correlated with elevated H3K4 trimethylation at the promoter regions of genes involving these pathways. Furthermore, pharmacological inhibition of both the MAPK pathway and BET bromodomain prevented leukemia initiation and inhibited disease progression in [Asxl.sup.1[DELTA]/[DELTA]][Nf1.sup.[DELTA]1/[DELTA]] mice. Concomitant mutations of ASXL1 and RAS pathway genes were associated with aggressive progression of myeloid malignancies in patients. This study sheds light on the effect of cooperation between epigenetic alterations and signaling pathways on accelerating the progression of myeloid malignancies and provides a rational therapeutic strategy for the treatment of myeloid malignancies with ASXL1 and RAS pathway gene mutations., IntroductionAlteration of epigenetic regulation provides a critical mechanism in the development of myeloid leukemia (1-3). Recent genomic studies have resulted in an emerging understanding of the significance of chromatin regulators [...]

Published
2018
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7. Loss of Asxl2 leads to myeloid malignancies in mice

Author

Li, Jianping, He, Fuhong, Zhang, Peng, Chen, Shi, Shi, Hui, Sun, Yanling, Guo, Ying, Yang, Hui, Man, Na, Greenblatt, Sarah, Li, Zhaomin, Guo, Zhengyu, Zhou, Yuan, Wang, Lan, Morey, Lluis, Williams, Sion, Chen, Xi, Wang, Qun-Tian, Nimer, Stephen D., Yu, Peng, Wang, Qian-Fei, Xu, Mingjiang, and Yang, Feng-Chun

Published
2017
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10. Identification of Chemo-Resistant Residual Cell Population in Pediatric AML of Complete Remission By Single Cell RNA Sequencing

Author

Jiang, Shuting, primary, He, Fuhong, additional, Gao, Li, additional, Chen, Aili, additional, Hu, Yixin, additional, Fan, Liyan, additional, Zhang, Lin, additional, Zhang, Yongping, additional, Hu, Haiyang, additional, Liu, Dan, additional, Zhou, Zihan, additional, Su, Yanxun, additional, Qin, Lei, additional, Lu, Jun, additional, Xiao, Peifang, additional, Ribeiro, Raul, additional, Hu, Shaoyan, additional, and Wang, Qian-fei, additional

Published
2020
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13. Ecological principle meets cancer treatment: treating children with acute myeloid leukemia with low-dose chemotherapy

Author

Hu, Yixin, primary, Chen, Aili, additional, Zheng, Xinchang, additional, Lu, Jun, additional, He, Hailong, additional, Yang, Jin, additional, Zhang, Ya, additional, Sui, Pinpin, additional, Yang, Jingyi, additional, He, Fuhong, additional, Wang, Yi, additional, Xiao, Peifang, additional, Liu, Xin, additional, Zhou, Yinmei, additional, Pei, Deqing, additional, Cheng, Cheng, additional, Ribeiro, Raul C, additional, Hu, Shaoyan, additional, and Wang, Qian-fei, additional

Published
2019
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16. How many human genes can be defined as housekeeping with current expression data?

Author

Song Shuhui, He Fuhong, Zhu Jiang, Wang Jing, and Yu Jun

Subjects
Biotechnology, TP248.13-248.65, Genetics, QH426-470
Abstract

Abstract Background Housekeeping (HK) genes are ubiquitously expressed in all tissue/cell types and constitute a basal transcriptome for the maintenance of basic cellular functions. Partitioning transcriptomes into HK and tissue-specific (TS) genes relatively is fundamental for studying gene expression and cellular differentiation. Although many studies have aimed at large-scale and thorough categorization of human HK genes, a meaningful consensus has yet to be reached. Results We collected two latest gene expression datasets (both EST and microarray data) from public databases and analyzed the gene expression profiles in 18 human tissues that have been well-documented by both two data types. Benchmarked by a manually-curated HK gene collection (HK408), we demonstrated that present data from EST sampling was far from saturated, and the inadequacy has limited the gene detectability and our understanding of TS expressions. Due to a likely over-stringent threshold, microarray data showed higher false negative rate compared with EST data, leading to a significant underestimation of HK genes. Based on EST data, we found that 40.0% of the currently annotated human genes were universally expressed in at least 16 of 18 tissues, as compared to only 5.1% specifically expressed in a single tissue. Our current EST-based estimate on human HK genes ranged from 3,140 to 6,909 in number, a ten-fold increase in comparison with previous microarray-based estimates. Conclusion We concluded that a significant fraction of human genes, at least in the currently annotated data depositories, was broadly expressed. Our understanding of tissue-specific expression was still preliminary and required much more large-scale and high-quality transcriptomic data in future studies. The new HK gene list categorized in this study will be useful for genome-wide analyses on structural and functional features of HK genes.

Published
2008
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20. Clinical Outcome and Non-Synonymous Mutation Clearance in Chinese Children with Acute Myeloid Leukemia Treated with a Low-Intensity Induction Chemotherapy Regimen

Author

Chen, Aili, primary, Hu, Yixin, additional, Liu, Xin, additional, Lu, Jun, additional, Xiao, Peifang, additional, Zheng, Xinchang, additional, Yang, Jin, additional, Zhang, Ya, additional, Yang, Jingyi, additional, He, Fuhong, additional, Sui, Pinpin, additional, He, Hailong, additional, Wang, Yi, additional, Cheng, Cheng, additional, Ribeiro, Raul C., additional, Hu, Shaoyan, additional, and Wang, Qianfei, additional

Published
2016
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24. Analysis of saline groundwater infiltration into two loam soils.

Author

He, Fuhong, Zhang, Zhenhua, Pan, Yinghua, Li, Wenxue, Li, Peng, Sun, Junna, Yang, Runya, Zheng, Mengzhu, and Shao, Hongbo

Subjects
SALINITY & the environment, GROUNDWATER analysis, LOAM soils, SOIL infiltration, SALINE water conversion
Abstract

Irrigation with saline groundwater may cause salt accumulation in the soil and even land degradation in coastal areas. The aim of this study was to reveal how the changes in groundwater salinity affect the infiltration characteristics under controlled conditions. One‐dimensional vertical infiltration experiments were conducted in uniform columns of silty clay‐loam and sandy‐loam under different salinity levels of irrigation groundwater (0, 1, 2, 3, 6, 9, and 12 g L−1 NaCl). The results showed that as groundwater salinity increased, the infiltration capacity of the silty clay‐loam increased under low salinity levels but decreased under higher salinity levels, with a turning point at the salinity of 6 g L−1 NaCl. However, there were no significant differences in the infiltration capacity of the sandy‐loam under salinity levels of 1–9 g L−1 NaCl, whereas a significant increase was found under 12 g L−1 NaCl. The infiltration capacity of the sandy‐loam was consistently higher compared with the silty clay‐loam under different salinity levels. Under short‐term irrigation with a conventional amount of 750–900 m3 ha−1, extracting groundwater with the salinity of <6 g L−1 NaCl obtained higher desalination efficiency in the silty clay‐loam and resulted in less salt accumulation in the surface soil (0–20 cm). Under the same amount of irrigation with groundwater containing 1–12 g L−1 NaCl, the increase of soil salt content was relatively small in the sandy‐loam and might not significantly affect crop growth. [ABSTRACT FROM AUTHOR]

Published
2018
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25. Loss of Asxl1 Alters Self-Renewal and Cell Fate of Bone Marrow Stromal Cells, Leading to Bohring-Opitz-like Syndrome in Mice

Author

Zhang, Peng, primary, Xing, Caihong, additional, Rhodes, Steven D., additional, He, Yongzheng, additional, Deng, Kai, additional, Li, Zhaomin, additional, He, Fuhong, additional, Zhu, Caiying, additional, Nguyen, Lihn, additional, Zhou, Yuan, additional, Chen, Shi, additional, Mohammad, Khalid S., additional, Guise, Theresa A., additional, Abdel-Wahab, Omar, additional, Xu, Mingjiang, additional, Wang, Qian-Fei, additional, and Yang, Feng-Chun, additional

Published
2016
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28. RUNX1/CBFβ Dosage Is Critical for MLL Leukemias Development

Author

Yan, Xiaomei, primary, Hayashi, Yoshihiro, additional, Zhao, Xinghui, additional, Chen, Aili, additional, Zhang, Yue, additional, He, Fuhong, additional, Dong, Yunzhu, additional, Rao, Yalan, additional, Li, Bo, additional, Conway, Rajeana, additional, Maiques-Díaz, Alba, additional, Huang, Nuomin, additional, Elf, Shannon E, additional, Zuber, Johannes, additional, Xiao, Zhijian, additional, Tse, William, additional, Tenen, Daniel G., additional, Wang, Qianfei, additional, Chen, Wei, additional, Mulloy, James C., additional, Nimer, Stephen D, additional, and Huang, Gang, additional

Published
2014
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29. Effects of pyrolysis temperature and residence time on physicochemical properties of different biochar types.

Author

Sun, Junna, He, Fuhong, Pan, Yinghua, and Zhang, Zhenhua

Subjects
*BIOCHAR, *PYROLYSIS, *FUNCTIONAL groups, *TEMPERATURE effect, *PH effect
Abstract

Here we selected eight types of feedstocks to assess the effects of pyrolysis temperature (300°C, 400°C, 500°C and 600°C) and residence time (0.5, 1, 2, 4, 8 and 24 h), respectively, on the physicochemical properties. The fixed-carbon content, pH value and amount of basic functional groups in biochars increased as the pyrolysis temperature increased from 300°C to 600°C; the opposite trend was found in the biochar yield, adsorption capacity and amount of acidic functional groups. Increasing the residence time at low pyrolysis temperature (300°C) resulted in a gradual reduction in the biochar yield and progressive increase in the pH and iodine adsorption number of biochars. However, increasing the residence time at high pyrolysis temperature (600°C) had little effect on the biochar yield or pH, while it decreased the iodine adsorption number of biochars. Given the effects of pyrolysis conditions on the pH and iodine adsorption number of biochars, low-ash agricultural wastes (e.g. wheat straw) can be pyrolysed at 300°C, 2 h to produce biochar for improving alkaline soils; high-ash agricultural wastes (e.g. sweet potato vine) and forest litter (e.g. fresh leaves of apricot tree) are preferably pyrolysed at 300°C, 4 h to produce biochar for use in acidic soils. [ABSTRACT FROM PUBLISHER]

Published
2017
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30. Identification of functional cooperative mutations of SETD2 in human acute leukemia

Author

Zhu, Xiaofan, primary, He, Fuhong, additional, Zeng, Huimin, additional, Ling, Shaoping, additional, Chen, Aili, additional, Wang, Yaqin, additional, Yan, Xiaomei, additional, Wei, Wei, additional, Pang, Yakun, additional, Cheng, Hui, additional, Hua, Chunlan, additional, Zhang, Yue, additional, Yang, Xuejing, additional, Lu, Xin, additional, Cao, Lihua, additional, Hao, Lingtong, additional, Dong, Lili, additional, Zou, Wei, additional, Wu, Jun, additional, Li, Xia, additional, Zheng, Si, additional, Yan, Jin, additional, Zhou, Jing, additional, Zhang, Lixia, additional, Mi, Shuangli, additional, Wang, Xiaojuan, additional, Zhang, Li, additional, Zou, Yao, additional, Chen, Yumei, additional, Geng, Zhe, additional, Wang, Jianmin, additional, Zhou, Jianfeng, additional, Liu, Xin, additional, Wang, Jianxiang, additional, Yuan, Weiping, additional, Huang, Gang, additional, Cheng, Tao, additional, and Wang, Qian-fei, additional

Published
2014
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33. PDGFRBmutation and tyrosine kinase inhibitor resistance in Ph-like acute lymphoblastic leukemia

Author

Zhang, Yingchi, Gao, Yufeng, Zhang, Hui, Zhang, Jingliao, He, Fuhong, Hnízda, Aleš, Qian, Maoxiang, Liu, Xiaoming, Gocho, Yoshihiro, Pui, Ching-Hon, Cheng, Tao, Wang, Qianfei, Yang, Jun J., Zhu, Xiaofan, and Liu, Xin

Abstract

Philadelphia chromosome (Ph)-like acute lymphoblastic leukemia (ALL) comprises ∼10% to 15% of childhood ALL cases, many of which respond exquisitely to tyrosine kinase inhibitors (TKIs), for example, imatinib in PDGFRB-rearranged ALL. However, some cases developed drug resistance to TKIs and the mechanisms are poorly understood. In this study, we identified a novel PDGFRBfusion gene, namely AGGF1-PDGFRB, and functionally characterized its oncogenic potential in vitro. Further genomic profiling of longitudinally collected samples during treatment revealed the emergence of a mutation, PDGFRBC843G, which directly conferred resistance to all generations of ABL TKIs, including imatinib, dasatinib, nilotinib, and ponatinib. PDGFRB-mutant leukemia cells are highly sensitive to multitarget kinase inhibitor CHZ868, suggesting potential therapeutic options for some patients resistant to ABL TKIs. In summary, we describe a complex clonal evolution pattern in Ph-like ALL and identified a novel PDGFRBpoint mutation that drives leukemia relapse after ABL TKI treatment.

Published
2018
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34. PU.1 Is Essential For MLL Leukemia Via Activation Of The Meis/HOX Pathway and A Monocytic Cytokine Mediated Anti-Apoptotic Inflammatory Program

Author

Zhou, Jing, primary, Wu, Jun, additional, Li, Bo, additional, Liu, Dan, additional, Yu, Jian, additional, Yan, Xiaomei, additional, Zheng, Si, additional, Wang, Jiguang, additional, Zhang, Lixia, additional, Zhang, Lin, additional, He, Fuhong, additional, Li, Qiang, additional, Chen, Aili, additional, Zhang, Yue, additional, Zhao, Xinghui, additional, Guan, Yinghui, additional, Zhao, Xiaohong, additional, Yan, Jin, additional, Ni, Jun, additional, Nobrega, Marcelo, additional, Löwenberg, Bob, additional, Delwel, Ruud, additional, Valk, Peter J., additional, Kumar, Ashish, additional, Lu, Xie, additional, Tenen, Daniel G., additional, Huang, Gang, additional, and Wang, Qian-fei, additional

Published
2013
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35. Whole-Genome Sequencing of a Monozygotic Twin Pair Reveals Functional Cooperative Mutations of SETD2 in Acute Leukemia

Author

Zhu, Xiaofan, primary, He, Fuhong, additional, Zeng, Huimin, additional, Ling, Shaoping, additional, Yan, Xiaomei, additional, Wang, Yaqin, additional, Chen, Aili, additional, Wei, Wei, additional, Zhang, Yue, additional, Cheng, Hui, additional, Wu, Jun, additional, Li, Xia, additional, Hao, Lingtong, additional, Cao, Lihua, additional, Dong, Lili, additional, Zou, Wei, additional, Yang, Xuejing, additional, Lu, Xin, additional, Zheng, Si, additional, Yan, Jin, additional, Zhou, Jing, additional, Zhang, Lixia, additional, Mi, Shuangli, additional, Wang, Xiaojuan, additional, Zhang, Li, additional, Zou, Yao, additional, Chen, Yumei, additional, Geng, Zhe, additional, Zhou, Jianfeng, additional, Wang, Jianmin, additional, Liu, Xin, additional, Wang, Jianxiang, additional, Huang, Gang, additional, Yuan, Weiping, additional, Cheng, Tao, additional, and Wang, Qian-fei, additional

Published
2012
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37. Essential Role for PU.1 in MEIS1 Activation and MLL Fusion Leukemia,

Author

Zhou, Jing, primary, Li, Bo, additional, Wu, Jun, additional, He, Fuhong, additional, Li, Qiang, additional, Yan, Xiaomei, additional, Zhang, Yue, additional, Zhang, Lixia, additional, Zhao, Xinghui, additional, Yan, Jin, additional, Nobrega, Marcelo, additional, Tenen, Daniel G., additional, Huang, Gang, additional, and Wang, Qian-fei, additional

Published
2011
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45. Cooperative Epigenetic Regulation By ASXL1and NF1Loss on Leukemogenesis

Author

Zhang, Peng, He, Fuhong, Bai, Jie, Chen, Shi, Nimer, Stephen D., Zhou, Yuan, Xu, Mingjiang, Wang, Qianfei, and Yang, Feng-Chun

Abstract

Introduction:Additional sex combs-like 1(ASXL1) is frequently mutated in a wide range of myeloid malignancies, including myelodysplastic syndrome (MDS), myeloproliferative neoplasm, chronic myelomonocytic leukemia, and acute myeloid leukemia (AML). Notably, ASXL1mutations are generally associated with the poor clinical outcomes. We and others have established Asxl1mouse models and demonstrated that loss of Asxl1leads to MDS-like disease, which can transform to myeloid leukemia in aged mice. These studies suggest that additional mutations may cooperate with Asxl1loss to induce the leukemia transformation. However, the molecular mechanisms underlying the leukemogenesis associated with ASXL1and cooperating mutations remain to be elucidated.

Published
2018
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46. Identification of APPAs a Novel Candidate Familial Eosinophilia Predisposition Gene

Author

Liu, Dan, Zhang, Peiling, He, Fuhong, Li, Yueying, Liu, Wenbing, Liu, Xin, Wang, Qianfei, and Zhou, Jianfeng

Abstract

Eosinophilia, such as familial eosinophilia (FE), idiopathic eosinophilia and reactive eosinophilia, is characterized by a sustained overproduction of peripheral blood eosinophils with or without end-organ damage. Germline variants in cytokine and eosinophil function genes are known to contribute to the development of the disease, suggesting common genetic basis may be shared among FE and sporadic eosinophilia. For example, FE is a rare autosomal dominant disorder with susceptible locus mapped to the chromosome 5q region in one American famliy (Rioux et al., 1998). This region (5q31-33) contains several cytokine genes which play functional roles in the development of eosinophils. Germline mutation in JAK1, which is involved in cytokine signaling, has been found in inherited eosinophilia (Kate et al., 2016). Furthermore, genetic variants in genes associated with eosinophilopoietic function (CCR3,CCL5 etc) have been identified in several idiopathic eosinophilia (Lee et al.,2017). Despite of these findings, most cases of eosinophilia have no identifiable mutations. In this new study, we collected a Chinese three-generation pedigree with documented FE. We aimed to investigate novel genetic variants of FE in this pedigree, and found that APP(amyloid-β precursor protein) might be a novel predisposition gene associated with FE.

Published
2018
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47. ASXL2 Is Required for Normal Hematopoiesis and Loss of asxl2Leads to Myeloid Malignancies in Mice

Author

Li, Jianping, He, Fuhong, Zhang, Peng, Chen, Shi, Shi, Hui, Sun, Yanling, Ying, Guo, Yang, Hui, Nimer, Stephen D., Wang, Qian-Fei, Xu, Mingjiang, and Yang, Feng-Chun

Abstract

Somatic mutations and chromosomal translocations of genes have emerged as major drivers in a range of hematopoietic malignancies. While ASXL1is mutated in all forms of myeloid malignancies, ASXL2is specifically mutated in t(8;21) AML patients. ASXL1and ASXL2mutations are mutually exclusive in t(8;21) AML. Despite the importance of ASXL2mutations in clinical, it's role in leukemogenesis remain unknown. In the current study, we sought to dissect the role of ASXL2 in normal hematopoiesis and to identify the molecular mechanisms by which Asxl2loss contributes to myeloid malignancies.

Published
2016
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48. Downregulation of SETD2-H3K36me3 Tumor Suppression Axis Promotes MLLLeukemia through Activation of DOT1L-H3K79me2 Axis

Author

Bu, Jiachen, Chen, Aili, Dong, Yunzhu, He, Fuhong, Yan, Xiaomei, Zhou, Yile, Zhan, Di, Hayashi, Yoshihiro, Wang, Qianfei, and Huang, Gang

Abstract

SET domain containing 2 (SETD2) gene encodes the sole methyltransferase that is specific for histone H3 lysine 36 trimethylation (H3K36me3) in mammals. Previously we identified somatic SETD2loss-of-function (LOF) mutations in both acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL) patients. Interestingly, SETD2mutations were identified in over 20% of leukemia patients with MLLgene rearrangement. Using an Mll-Af9(MA9) knock-in AML mouse model, we found that downregulation of Setd2by shRNA or genetic knock-out/knock-in strategies significantly accelerated disease development. However, the contribution of SETD2-H3K36me3 axis downregulation to MLLleukemia progression has not yet been fully understood. In MLLleukemia, high expression levels of MLLtargets, driven by aberrant histone H3 lysine 79 dimethylation (H3K79me2), have been reported. Both H3K36me3 and H3K79me2 are enriched within the body of transcriptionally active genes and are associated with phosphorylated RNA Polymerase II. Whether H3K36me3 also contributes to gene dysregulation in MLLleukemia, whether SETD2-H3K36me3 downregulation has impacts on DOT1L-H3K79me2 axis, and how it promotes MLLleukemia progression are unclear. More importantly, SETD2mutations were enriched in relapsed B-cell ALL patients. SETD2LOF mutation could cause chemotherapy resistance or relapse after bone marrow transplantation. Thus, mechanistic-driven novel therapies are urgently needed for leukemia with SETD2mutation.

Published
2016
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50. Chromatin regulator Asxl1 loss and Nf1 haploinsufficiency cooperate to accelerate myeloid malignancy.

Author

Peng Zhang, Fuhong He, Jie Bai, Shohei Yamamoto, Shi Chen, Lin Zhang, Mengyao Sheng, Lei Zhang, Ying Guo, Na Man, Hui Yang, Suyun Wang, Tao Cheng, Nimer, Stephen D., Yuan Zhou, Mingjiang Xu, Qian-Fei Wang, Feng-Chun Yang, Zhang, Peng, and He, Fuhong

Subjects
*CHROMATIN, *LEUKEMIA etiology, *MYELOID leukemia, *NEGATIVE regulatory factor, *HEMATOPOIETIC stem cells, *PROGENITOR cells, *DISEASE progression
Abstract

ASXL1 is frequently mutated in myeloid malignancies and is known to co-occur with other gene mutations. However, the molecular mechanisms underlying the leukemogenesis associated with ASXL1 and cooperating mutations remain to be elucidated. Here, we report that Asxl1 loss cooperated with haploinsufficiency of Nf1, a negative regulator of the RAS signaling pathway, to accelerate the development of myeloid leukemia in mice. Loss of Asxl1 and Nf1 in hematopoietic stem and progenitor cells resulted in a gain-of-function transcriptional activation of multiple pathways such as MYC, NRAS, and BRD4 that are critical for leukemogenesis. The hyperactive MYC and BRD9 transcription programs were correlated with elevated H3K4 trimethylation at the promoter regions of genes involving these pathways. Furthermore, pharmacological inhibition of both the MAPK pathway and BET bromodomain prevented leukemia initiation and inhibited disease progression in Asxl1Δ/Δ Nf1Δ/Δ mice. Concomitant mutations of ASXL1 and RAS pathway genes were associated with aggressive progression of myeloid malignancies in patients. This study sheds light on the effect of cooperation between epigenetic alterations and signaling pathways on accelerating the progression of myeloid malignancies and provides a rational therapeutic strategy for the treatment of myeloid malignancies with ASXL1 and RAS pathway gene mutations. [ABSTRACT FROM AUTHOR]

Published
2018
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