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Prognostic analysis of chronic myeloid leukemia in Chinese population in an imatinib era
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《医学前沿(英文)》 2012年 第6卷 第2期 页码 204-211 doi: 10.1007/s11684-012-0202-x
We evaluated the outcomes of chronic myeloid leukemia (CML) patients in three clinical phases, namely, chronic (CP), accelerated (AP), and blast (BP) phases, receiving imatinib treatment. The single-institution treatment experiences of Chinese patients with CML were presented. A total of 275 CML patients (CP, 210; AP, 24; and BP, 41) who received imatinib between February 2001 and April 2008 were enrolled in this study. We evaluated the responses (hematologic, cytogenetic, and molecular), overall survival (OS), treatment event-free survival (EFS), and prognostic factors of outcome. At the cut-off point, the complete cytogenetic response (CCyR) and complete molecular response rates of patients in the CP were 84.7% and 61.9%, respectively, which were significantly higher than those of patients in the AP (50% and 29.1%, respectively, both P<0.001) and BP (24.3% and 9.7%, respectively, both P<0.001). The estimated five-year OS and five-year EFS rates were 93.2% and 86.4% for CP patients, as well as 64.5% and 50.9% for AP patients, which were significantly higher than those for BP patients (P<0.001). In CP patients, univariate analysis revealed that early treatment with imatinib, achieving CCyR within 12 months, additional cytogenetic abnormalities, and kinase domain mutations were associated with the treatment outcome. More patients are needed to carry out multivariate analysis.
关键词: imatinib chronic myeloid leukemia complete cytogenetic response
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《医学前沿(英文)》 2015年 第9卷 第3期 页码 304-311 doi: 10.1007/s11684-015-0400-4
In the tyrosine kinase inhibitor (TKI) era, imatinib is the first-line therapy for patients with chronic myeloid leukemia (CML) in chronic or accelerated phase. Although second-generation TKIs (TKI2), including dasatinib and nilotinib, are appropriate treatment regimens for patients with disease that progressed to accelerated phase following imatinib therapy, allogeneic hematopoietic stem cell transplantation (allo-HSCT) is the only curative therapy. This study retrospectively analyzed the efficacy of TKI2 and HSCT for treatment of CML in accelerated phase. Ninety-three patients with CML registered in the Chinese CML alliance database from February 2001 to February 2014 were enrolled and divided into the TKI2 (n?=?33) and allo-HSCT (n?=?60) groups. In the TKI2 group, 26 and 7 patients received nilotinib and dasatinib, respectively, as initial TKI2 and 11 patients transferred to the alternative TKI2 after failure to one TKI2. In the allo-HSCT group, 22 (36.7%), 35 (58.3%), and 3 (10%) patients underwent allo-HSCT from an HLA-matched sibling donor, HLA mismatched/haploidentical donor, and unrelated donor, respectively. All patients in the HSCT group were engrafted. Overall, 69.7%, 48.5%, and 45.5% of patients presented hematological, cytogenetic, and major molecular responses, respectively, to at least one of TKI2. All 60 patients (100%) achieved CHR and cytogenetic response in the HSCT group. Patients in the TKI2 group exhibited lower 5-year overall survival rate (42.9% vs. 86.4%, P = 0.002), 5-year event-free survival rate (14.3% vs. 76.1%, P<0.001), and 5-year progression-free survival (28.6% vs. 78.1%, P<0.001) than those in the allo-HSCT group. Multivariate analysis showed that male sex and TKI2therapy were predictors of poor overall survival, whereas hemoglobin<100 g/L and TKI2 therapy were predictors of poor event-free survival and progression-free survival. These results indicated that allo-HSCT may be superior to nilotinib and dasatinib for adult patients with CML in accelerated phase.
关键词: chronic myeloid leukemia imatinib dasatinib nilotinib allogeneic hematopoietic stem cell transplantation
Xiaojun Huang, Qian Jiang, Jianda Hu, Jianyong Li, Jie Jin, Fanyi Meng, Zhixiang Shen, Ting Liu, Depei Wu, Jianmin Wang, Jianxiang Wang
《医学前沿(英文)》 2019年 第13卷 第3期 页码 344-353 doi: 10.1007/s11684-018-0639-7
关键词: chronic myeloid leukemia (CML) dasatinib tyrosine kinase inhibitor long-term follow-up
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
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
《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
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《医学前沿(英文)》 2017年 第11卷 第3期 页码 440-444 doi: 10.1007/s11684-017-0523-x
Philadelphia chromosome-positive acute myeloid leukemia is controversial and difficult to distinguish from the blast phase of chronic myeloid leukemia. As a myeloid neoplasm, rare cases of this leukemia manifest multiple soft-tissue tumors or bone lytic lesions. In this paper, we describe a 49-year-old male patient who had an abrupt onset with sharp chest pain, fever, fatigue, emaciation, and splenomegaly. 18F-fluoro-deoxy-glucose positron emission tomography/computed tomography (18F-FDG PET/CT) result showed diffuse and uneven hypermetabolic lesions in the bone marrow with peripheral bone marrow expansion, multiple soft tissue neoplasms with high 18F-FDG uptake, and lytic bone lesions. Bone marrow smear and biopsy detected aberrant blast cells expressing myeloid rather than lymphoid immunophenotype marker. For the existence of Philadelphia chromosome and BCR-ABL1 fusion gene together with complex chromosome abnormalities, a diagnosis of Philadelphia-positive acute myeloid leukemia was made, although the type (de novo or blast crisis) remained unclear.
关键词: Philadelphia chromosome acute myeloid leukemia mass osteolysis positron emission tomography
Meng Lv, Xiaohui Zhang, Lanping Xu, Yu Wang, Chenhua Yan, Huan Chen, Yuhong Chen, Wei Han, Fengrong Wang, Jingzhi Wang, Kaiyan Liu, Xiaojun Huang, Xiaodong Mo
《医学前沿(英文)》 2019年 第13卷 第6期 页码 667-679 doi: 10.1007/s11684-019-0702-z
关键词: acute graft-versus-host disease chronic graft-versus-host disease National Institutes of Health consensus criteria acute myeloid leukemia anti-thymocyte globulin
Chimeric antigen receptor T cell therapies for acute myeloid leukemia
Bin Gu, Jianhong Chu, Depei Wu
《医学前沿(英文)》 2020年 第14卷 第6期 页码 701-710 doi: 10.1007/s11684-020-0763-z
Bingshan Liu, Roshni Narurkar, Madhura Hanmantgad, Wahib Zafar, Yongping Song, Delong Liu
《医学前沿(英文)》 2018年 第12卷 第5期 页码 593-599 doi: 10.1007/s11684-018-0635-y
Conventional combination therapies have not resulted in considerable progress in the treatment of acute myeloid leukemia (AML). Elderly patients with AML and poor risk factors have grave prognosis. Midostaurin has been recently approved for the treatment of FLT-3-mutated AML. Venetoclax, a BCL-2 inhibitor, has been approved for the treatment of relapsed and/or refractory chronic lymphoid leukemia. Clinical trials on applying venetoclax in combination with cytarabine and other agents to treat various hematological malignancies are currently underway. Here, we present a case of a male patient with poor performance status and who developed AML following allogeneic hematopoietic stem cell transplant for high-risk myelodysplasia. The patient with high risk AML achieved complete response to the combined treatment regimen of low-dose cytarabine and venetoclax. Furthermore, we reviewed current clinical trials on the use of venetoclax for hematological malignancies.
关键词: venetoclax cytarabine AML leukemia
The role of RAS effectors in BCR/ABL induced chronic myelogenous leukemia
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《医学前沿(英文)》 2013年 第7卷 第4期 页码 452-461 doi: 10.1007/s11684-013-0304-0
BCR/ABL is the causative agent of chronic myelogenous leukemia (CML). Through structure/function analysis, several protein motifs have been determined to be important for the development of leukemogenesis. Tyrosine177 of BCR is a Grb2 binding site required for BCR/ABL-induced CML in mice. In the current study, we use a mouse bone marrow transduction/transplantation system to demonstrate that addition of oncogenic NRAS (NRASG12D) to a vector containing a BCR/ABLY177F mutant “rescues” the CML phenotype rapidly and efficiently. To further narrow down the pathways downstream of RAS that are responsible for this rescue effect, we utilize well-characterized RAS effector loop mutants and determine that the RAL pathway is important for rapid induction of CML. Inhibition of this pathway by a dominant negative RAL is capable of delaying disease progression. Results from the present study support the notion of RAL inhibition as a potential therapy for BCR/ABL-induced CML.
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《医学前沿(英文)》 2015年 第9卷 第4期 页码 412-420 doi: 10.1007/s11684-015-0423-x
Genetic mutations are considered to drive the development of acute myeloid leukemia (AML). With the rapid progress in sequencing technologies, many newly reported genes that are recurrently mutated in AML have been found to govern the initiation and relapse of AML. These findings suggest the need to distinguish the driver mutations, especially the most primitive single mutation, from the subsequent passenger mutations. Recent research on DNA methyltransferase 3A (DNMT3A) mutations provides the first proof-of-principle investigation on the identification of preleukemic stem cells (pre-LSCs) in AML patients. Although DNMT3A mutations alone may only transform hematopoietic stem cells into pre-LSCs without causing the full-blown leukemia, the function of this driver mutation appear to persist from AML initiation up to relapse. Therefore, identifying and targeting preleukemic mutations, such as DNMT3A mutations, in AML is a promising strategy for treatment and reduction of relapse risk.
关键词: preleukemic stem cell acute myeloid leukemia relapse DNMT3A
Xiaoxiao Chen, Yanjing Tang, Jing Chen, Ru Chen, Longjun Gu, Huiliang Xue, Ci Pan, Jingyan Tang, Shuhong Shen
《医学前沿(英文)》 2019年 第13卷 第3期 页码 378-387 doi: 10.1007/s11684-018-0658-4
Mutation profiling of 16 candidate genes in
Yang Zhang, Fang Wang, Xue Chen, Wenjing Liu, Jiancheng Fang, Mingyu Wang, Wen Teng, Panxiang Cao, Hongxing Liu
《医学前沿(英文)》 2019年 第13卷 第2期 页码 229-237 doi: 10.1007/s11684-018-0616-1
标题 作者 时间 类型 操作
allogeneic hematopoietic stem cell transplantation to nilotinib and dasatinib for adult patients with chronicmyelogenous leukemia in the accelerated phase
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期刊论文
Four-year follow-up of patients with imatinib-resistant or intolerant chronic myeloid leukemia receiving
Xiaojun Huang, Qian Jiang, Jianda Hu, Jianyong Li, Jie Jin, Fanyi Meng, Zhixiang Shen, Ting Liu, Depei Wu, Jianmin Wang, Jianxiang Wang
期刊论文
Molecular pathogenesis of acute myeloid leukemia: A diverse disease with new perspectives
Felicitas THOL, Arnold GANSER
期刊论文
ACSL5, a prognostic factor in acute myeloid leukemia, modulates the activity of Wnt/-catenin signaling
期刊论文
expression pattern of mutations coordinated by target repression and promoter hypermethylation in acute myeloidleukemia
期刊论文
Philadelphia chromosome-positive acute myeloid leukemia with masses and osteolytic lesions: finding of
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期刊论文
Risk factors for chronic graft-versus-host disease after anti-thymocyte globulin-based haploidenticalhematopoietic stem cell transplantation in acute myeloid leukemia
Meng Lv, Xiaohui Zhang, Lanping Xu, Yu Wang, Chenhua Yan, Huan Chen, Yuhong Chen, Wei Han, Fengrong Wang, Jingzhi Wang, Kaiyan Liu, Xiaojun Huang, Xiaodong Mo
期刊论文
Chimeric antigen receptor T cell therapies for acute myeloid leukemia
Bin Gu, Jianhong Chu, Depei Wu
期刊论文
Venetoclax and low-dose cytarabine induced complete remission in a patient with high-risk acute myeloidleukemia: a case report
Bingshan Liu, Roshni Narurkar, Madhura Hanmantgad, Wahib Zafar, Yongping Song, Delong Liu
期刊论文
methylation regulators endow hematopoietic stem cells with the preleukemic stem cell property, a requisite of leukemia
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期刊论文
a safe and effective substitute for anthracyclines in children younger than 2 years old with acute myeloidleukemia
Xiaoxiao Chen, Yanjing Tang, Jing Chen, Ru Chen, Longjun Gu, Huiliang Xue, Ci Pan, Jingyan Tang, Shuhong Shen
期刊论文