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《医学前沿(英文)》 2011年 第5卷 第1期 页码 45-52 doi: 10.1007/s11684-011-0117-y
Acute promyelocytic leukemia (APL) is a subtype of acute myeloid leukemia. In past decades, intensive studies on the biology and treatment of this disease have resulted in a remarkably thorough understanding of its pathogenesis and improvement of treatment outcomes. In particular, the introduction of all-trans retinoic acid to conventional chemotherapy improved dramatically the remission and survival rates of APL patients and consequently became the major treatment modality for it. In the last decade, the groundbreaking development of arsenic further improved the survival rate of APL patients. As the most active agent in APL, arsenic directly degrades the PML-RARα fusion transcript, leading to the differentiation and apoptosis of leukemia cells and the potential eradication of APL leukemia-initiating cells (LICs), thus making the disease a potentially curable type of leukemia. More notably, the recent development of oral arsenic compounds may further enhance not only clinical outcomes but also the convenience of patients, which may dramatically change the APL clinical scenario in the near future.
关键词: acute promyelocytic leukemia arsenic all-trans retinoic acid survival
《医学前沿(英文)》 2022年 第16卷 第6期 页码 909-918 doi: 10.1007/s11684-021-0890-1
关键词: acute promyelocytic leukemia intracranial hemorrhage cytokines biomarker
Current treatment strategy of acute promyelocytic leukemia
Jianqing Mi
《医学前沿(英文)》 2011年 第5卷 第4期 页码 341-347 doi: 10.1007/s11684-011-0169-z
关键词:
acute promyelocytic leukemia
all-
《医学前沿(英文)》 doi: 10.1007/s11684-023-1022-x
关键词: acute promyelocytic leukemia plasma proteomics plasma metabolomics cross-sectional correlation network pathogenesis treatment
null
《医学前沿(英文)》 2016年 第10卷 第4期 页码 420-429 doi: 10.1007/s11684-016-0478-3
Inappropriate cell proliferation during oncogenesis is often accompanied by inactivation of components involved in the cell cycle machinery. Here, we report that cyclin-dependent kinase inhibitor 2C (CDKN2C) as a member of the cyclin-dependent kinase inhibitors is a target of the PML/RARα oncofusion protein in leukemogenesis of acute promyelocytic leukemia (APL). We found that CDKN2C was markedly downregulated in APL blasts compared with normal promyelocytes. Chromatin immunoprecipitation combined with quantitative polymerase chain reaction demonstrated that PML/RARα directly bound to the CDKN2C promoter in the APL patient-derived cell line NB4. Luciferase assays indicated that PML/RARα inhibited the CDKN2C promoter activity in a dose-dependent manner. Furthermore, all-trans retinoic acid treatment induced CDKN2C expression by releasing the PML/RARα binding on chromatin in NB4 cells. Functional studies showed that ectopic expression of CDKN2C induced a cell cycle arrest at the G0/G1 phase and a partial differentiation in NB4 cells. Finally, the transcriptional regulation of CDKN2C was validated in primary APL patient samples. Collectively, this study highlights the importance of CDKN2C inactivation in the abnormal cell cycle progression and differentiation block of APL cells and may provide new insights into the study of pathogenesis and targeted therapy of APL.
关键词: CDKN2C acute promyelocytic leukemia cell cycle arrest differentiation
null
《医学前沿(英文)》 2017年 第11卷 第3期 页码 410-422 doi: 10.1007/s11684-017-0527-6
Aberrant expression of annexin A2-S100A10 heterotetramer (AIIt) associated with PML/RARα fusion protein causes lethal hyperfibrinolysis in acute promyelocytic leukemia (APL), but the mechanism is unclear. To facilitate the investigation of regulatory association between ANXA2 and promyelocytic leukemia/retinoic acid receptor a (PML/RARα) fusion protein, this work was performed to determine the transcription start site of ANXA2 promoter with rapid amplification of 5′-cDNA ends analysis. Zinc-induced U937/PR9 cells expressed PML/RARα fusion protein, and resultant increases in ANXA2 transcripts and translational expressions of both ANXA2 and S100A10, while S100A10 transcripts remained constitutive. The transactivation of ANXA2 promoter by PML/RARα fusion protein was 3.29±0.13 fold higher than that by control pSG5 vector or wild-type RARα. The overexpression of ANXA2 in U937 transfected with full-length ANXA2 cDNA was associated with increased S100A10 subunit, although S100A10 transcripts remained constitutive. The tPA-dependent initial rate of plasmin generation (IRPG) in zinc-treated U937/PR9 increased by 2.13-fold, and cell invasiveness increased by 27.6%. Antibodies against ANXA2, S100A10, or combination of both all remarkably inhibited the IRPG and invasiveness in U937/PR9 and NB4. Treatment of zinc-induced U937/PR9 or circulating APL blasts with all-trans retinoic acid (ATRA) significantly reduced cell surface ANXA2 and S100A10 and associated reductions in IRPG and invasiveness. Thus, PML/RARα fusion protein transactivated the ANXA2 promoter to upregulate ANXA2 and accumulate S100A10. Increased AIIt promoted IRPG and invasiveness, both of which were partly abolished by antibodies against ANXA2 and S100A10 or by ATRA.
关键词: annexin A2-S100A10 heterotetramer PML/RARα fusion protein plasmin cell invasion acute promyelocytic leukemia
Molecular pathogenesis of acute myeloid leukemia: A diverse disease with new perspectives
Felicitas THOL, Arnold GANSER
《医学前沿(英文)》 2010年 第4卷 第4期 页码 356-362 doi: 10.1007/s11684-010-0220-5
BRD4 interacts with PML/RARα in acute promyelocytic leukemia
Qun Luo, Wanglong Deng, Haiwei Wang, Huiyong Fan, Ji Zhang
《医学前沿(英文)》 2018年 第12卷 第6期 页码 726-734 doi: 10.1007/s11684-017-0604-x
关键词: BRD4 PML/RARα APL interaction
FGF13 suppresses acute myeloid leukemia by regulating bone marrow niches
《医学前沿(英文)》 2022年 第16卷 第6期 页码 896-908 doi: 10.1007/s11684-022-0944-z
关键词: acute myeloid leukemia FGF13 prognosis immune-related genes bone marrow niches
《医学前沿(英文)》 2023年 第17卷 第3期 页码 518-526 doi: 10.1007/s11684-022-0958-6
关键词: acute lymphoblastic leukemia child venous thromboembolism epidemiology clinical characteristic risk factor
《医学前沿(英文)》 2022年 第16卷 第4期 页码 627-636 doi: 10.1007/s11684-020-0815-4
关键词: RUNX1 gene mutation acute myeloid leukemia transcriptional repression DNA methylation
Early T-cell precursor leukemia: a subtype of high risk childhood acute lymphoblastic leukemia
null
《医学前沿(英文)》 2012年 第6卷 第4期 页码 416-420 doi: 10.1007/s11684-012-0224-4
Acute lymphoblastic leukemia includes T-cell acute lymphoblastic leukemia (T-ALL) and B-cell acute lymphoblastic leukemia (B-ALL). In children, T-ALL usually has a worse prognosis than B-ALL, although childhood T-ALL prognoses have improved remarkably. The varying outcomes among T-ALL cases suggest that an unrecognized biological heterogeneity may contribute to chemo-resistance. Deep exploration of T-lymphocyte development in recent years has found a subgroup of patients with a phenotype that resembles early T-cell precursor, which confers a much poorer prognosis than any other form of T-ALL. This novel subtype of T-ALL was called early T-cell precursor acute lymphoblastic leukemia (ETP-ALL). Flow cytometry data from T-ALL patients enrolled in Shanghai Children’s Medical Center between July 2002 and October 2010 were assessed according to Dr. Campana’s protocol. Among total 89 T-ALL cases, 74 cases had enough immunophenotype data available to differentiate between ETP (CD1a-, CD8-, CD5dim, at least one marker of stem cell or myeloid lineage) and non-ETP. From these 74 subjects, 12 ETP-ALL cases (16.2%) were identified. The event-free survival (EFS) rate at 66.8 months was 11.1%±10.1% for ETP-ALL and 57.6%±5.6% for non-ETP-ALL (P=0.003). The overall survival rates were 13.3%±11.0% for ETP-ALL and 64.7%±6.3% for non-ETP-ALL (P=0.002). Our findings demonstrate that early T-cell precursor leukemia is a very high-risk subtype of acute lymphoblastic leukemia with poor prognosis.
关键词: acute lymphoblastic leukemia early T precursor prognosis
《医学前沿(英文)》 2023年 第17卷 第4期 页码 685-698 doi: 10.1007/s11684-022-0942-1
关键词: acute myeloid leukemia acyl-CoA synthetase long chain family member 5 Wnt3a palmitoylation ABT-199
Zhi-Ruo ZHANG PhD, Jian-Qing MI MD, Zhao-Jun WEN MA, Sai-Juan CHEN MD, PhD, Zhu CHEN PhD, Long-Jun GU MD, Jing-Yan TANG MD, PhD, Shu-Hong SHEN MD, PhD,
《医学前沿(英文)》 2010年 第4卷 第1期 页码 8-15 doi: 10.1007/s11684-010-0018-5
关键词: healthcare reform diagnosis-related groups clinical paths comparative effectiveness analysis acute promyelocytic leukemia childhood acute lymphoblastic leukemia
《医学前沿(英文)》 2022年 第16卷 第1期 页码 139-149 doi: 10.1007/s11684-021-0835-8
关键词: B-cell acute lymphoblastic leukemia bispecific antibody trispecific antibody CD19 CD20
标题 作者 时间 类型 操作
Arsenic in the treatment of newly diagnosed acute promyelocytic leukemia: current status and future research
null
期刊论文
Predictive values of plasma TNFα and IL-8 for intracranial hemorrhage in patients with acute promyelocyticleukemia
期刊论文
network analysis of plasma proteins/metabolites correlated with pathogenesis and therapeutic response in acutepromyelocytic leukemia
期刊论文
Repression of CDKN2C caused by PML/RARα binding promotes the proliferation and differentiation block in acutepromyelocytic leukemia
null
期刊论文
upregulated by PML/RARα fusion protein and promotes plasminogen-dependent fibrinolysis and matrix invasion in acutepromyelocytic leukemia
null
期刊论文
Molecular pathogenesis of acute myeloid leukemia: A diverse disease with new perspectives
Felicitas THOL, Arnold GANSER
期刊论文
BRD4 interacts with PML/RARα in acute promyelocytic leukemia
Qun Luo, Wanglong Deng, Haiwei Wang, Huiyong Fan, Ji Zhang
期刊论文
Venous thromboembolism in children with acute lymphoblastic leukemia in China: a report from the Chinese
期刊论文
expression pattern of mutations coordinated by target repression and promoter hypermethylation in acutemyeloid leukemia
期刊论文
Early T-cell precursor leukemia: a subtype of high risk childhood acute lymphoblastic leukemia
null
期刊论文
ACSL5, a prognostic factor in acute myeloid leukemia, modulates the activity of Wnt/-catenin signaling
期刊论文
Diagnosis-related Groups (DRGs)-based payment reform to bring benefits to patient care: A case study of leukemia
Zhi-Ruo ZHANG PhD, Jian-Qing MI MD, Zhao-Jun WEN MA, Sai-Juan CHEN MD, PhD, Zhu CHEN PhD, Long-Jun GU MD, Jing-Yan TANG MD, PhD, Shu-Hong SHEN MD, PhD,
期刊论文