Home / Advanced Search

  • Title/Keywords

  • Author/Affliations

  • Journal

  • Article Type

  • Start Year

  • End Year

Update SearchingClear
  • Articles
  • Online
Search Results (12)
  • Open Access


    Induction of Multidrug Resistance of Acute Myeloid Leukemia Cells by Cocultured Stromal Cells via Upregulation of the PI3K/Akt Signaling Pathway

    Ping Chen*, Qing Jin*, Qiang Fu*, Peidong You*, Xi Jiang*, Qin Yuan*, Huifang Huang

    Oncology Research, Vol.24, No.4, pp. 215-223, 2016, DOI:10.3727/096504016X14634208143021

    Abstract This study aimed to investigate the role of the PI3K/Akt signaling pathway in multidrug resistance of acute myeloid leukemia (AML) cells induced by cocultured stromal cells. Human AML cell lines HL-60 and U937 were adhesion cocultured with human bone marrow stromal cell line HS-5 cells. Such coculturing induced HL-60 and U937 cells resistant to chemotherapeutic drugs including daunorubicin (DNR), homoharringtonine (HHT), and cytosine arabinoside (Ara-C). The coculturing-induced resistance of AML cells to DNR, HHT, and Ara-C can be partially reversed by inhibition of the PI3K/Akt signaling pathway. Clinically, AML patients with a low level of More >

  • Open Access


    miR-34b Targets HSF1 to Suppress Cell Survival in Acute Myeloid Leukemia

    Gangcan Li, Yanping Song, Yunjie Zhang, Hao Wang, Jia Xie

    Oncology Research, Vol.24, No.2, pp. 109-116, 2016, DOI:10.3727/096504016X14611963142254

    Abstract Acute myeloid leukemia (AML) is the most lethal hematological malignancy, and the occurrence of chemoresistance prevents the achievement of complete remission following the standard therapy. MicroRNAs have been extensively investigated as critical regulators of hematopoiesis and leukemogenesis, and they represent a promising strategy for AML therapy. In this study, we identified miR-34b as a novel regulator in myeloid proliferation and apoptosis of leukemic cells. We found that miR-34b was developmentally upregulated in plasma and myeloid cells of healthy subjects, while it was significantly reduced in blood samples of patients with AML and AML cell lines.… More >

  • Open Access


    Mitoxantrone and Etoposide for the Treatment of Acute Myeloid Leukemia Patients in First Relapse

    Annie Im, Ali Amjad, Mounzer Agha, Anastasios Raptis, Jing-Zhou Hou, Rafic Farah, Seah Lim, Alison Sehgal, Kathleen A. Dorritie, Robert L. Redner, Brian McLaughlin, Yongli Shuai, Shrina Duggal, Michael Boyiadzis

    Oncology Research, Vol.24, No.2, pp. 73-80, 2016, DOI:10.3727/096504016X14586627440156

    Abstract Relapsed acute myeloid leukemia (AML) represents a major therapeutic challenge. Achieving complete remission (CR) with salvage chemotherapy is the first goal of therapy for relapsed AML. However, there is no standard salvage chemotherapy. The current study evaluated outcomes and prognostic factors for achievement of CR in 91 AML patients in first relapse who were treated with the mitoxantrone–etoposide combination regimen. The overall response rate (CR and CRi) was 25%. Factors that were associated with a lower rate of CR included older age, shorter duration of first CR, low hemoglobin, and low platelet count. The median… More >

  • Open Access


    miR-92a Inhibits Proliferation and Induces Apoptosis by Regulating Methylenetetrahydrofolate Dehydrogenase 2 (MTHFD2) Expression in Acute Myeloid Leukemia

    Yueli Gu*, Jinchun Si, Xichun Xiao*, Ying Tian*, Shuo Yang*

    Oncology Research, Vol.25, No.7, pp. 1069-1079, 2017, DOI:10.3727/096504016X14829256525028

    Abstract Aberrant expression of microRNA-92a (miR-92a) has been investigated in various cancers. However, the function and mechanism of miR-92a in acute myeloid leukemia (AML) remain to be elucidated. Our data showed that miR-92a was evidently downregulated and methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) was remarkably upregulated in AML cell lines HL-60 and THP-1. Dual luciferase reporter assay revealed that MTHFD2 was a direct target of miR-92a. Gain- and loss-of-function analysis demonstrated that MTHFD2 knockdown or miR-92a overexpression notably inhibited proliferation and promoted apoptosis of AML cell lines. Restoration of MTHFD2 expression reversed proliferation inhibition and apoptosis induction of More >

  • Open Access


    A Construction of Object Detection Model for Acute Myeloid Leukemia

    K. Venkatesh1,*, S. Pasupathy1, S. P. Raja2

    Intelligent Automation & Soft Computing, Vol.36, No.1, pp. 543-560, 2023, DOI:10.32604/iasc.2023.030701

    Abstract The evolution of bone marrow morphology is necessary in Acute Myeloid Leukemia (AML) prediction. It takes an enormous number of times to analyze with the standardization and inter-observer variability. Here, we proposed a novel AML detection model using a Deep Convolutional Neural Network (D-CNN). The proposed Faster R-CNN (Faster Region-Based CNN) models are trained with Morphological Dataset. The proposed Faster R-CNN model is trained using the augmented dataset. For overcoming the Imbalanced Data problem, data augmentation techniques are imposed. The Faster R-CNN performance was compared with existing transfer learning techniques. The results show that the More >

  • Open Access


    MicroRNA-204 Potentiates the Sensitivity of Acute Myeloid Leukemia Cells to Arsenic Trioxide

    Zhiguo Wang*†1, Zehui Fang‡1, Runzhang Lu, Hongli Zhao, Tiejun Gong, Dong Liu, Luojia Hong, Jun Ma, Mei Zhang*

    Oncology Research, Vol.27, No.9, pp. 1035-1042, 2019, DOI:10.3727/096504019X15528367532612

    Abstract Although arsenic trioxide (ATO) is a well-known antileukemic drug used for acute promyelocytic leukemia treatment, the development of ATO resistance is still a big challenge. We previously reported that microRNA- 204 (miR-204) was involved in the regulation of acute myeloid leukemia (AML) cell apoptosis, but its role in chemoresistance is poorly understood. In the present study, we showed that miR-204 was significantly increased in AML cells after ATO treatment. Interestingly, the increased miR-204 level that was negatively correlated with ATO induced the decrease in cell viability and baculoviral inhibition of apoptosis protein repeatcontaining 6 (BIRC6)… More >

  • Open Access


    RAS-Responsive Element-Binding Protein 1 Blocks the Granulocytic Differentiation of Myeloid Leukemia Cells

    Juanjuan Yao*, Liang Zhong, Pengqiang Zhong*, Dongdong Liu, Zhen Yuan, Junmei Liu*, Shifei Yao*, Yi Zhao*, Min Chen*, Lianwen Li*, Lu Liu, Beizhong Liu*†

    Oncology Research, Vol.27, No.7, pp. 809-818, 2019, DOI:10.3727/096504018X15451301487729

    Abstract RAS-responsive element-binding protein 1 (RREB1) is a transcription factor that is implicated in RAS signaling and multiple tumors. However, the role of RREB1 in acute myeloid leukemia has not been studied. We found that RREB1 is overexpressed in AML patients and myeloid leukemia cell lines (NB4 and HL-60), and RREB1 expression was significantly decreased during granulocytic differentiation of myeloid leukemia cells induced by all-trans retinoic acid (ATRA). Then we performed a RREB1 knockdown assay in NB4 and HL-60 cells; the results showed that knockdown of RREB1 upregulated expression of CD11b, CEBP , and microRNA-145 (miR-145), More >

  • Open Access


    Knockdown of IARS2 Inhibited Proliferation of Acute Myeloid Leukemia Cells by Regulating p53/p21/PCNA/eIF4E Pathway

    Hong Li*1, Yaning Tian*1, Xiang Li*, Bin Wang, Dongzhi Zhai*, Yingying Bai*, Changhu Dong*, Xu Chao*‡

    Oncology Research, Vol.27, No.6, pp. 673-680, 2019, DOI:10.3727/096504018X15426261956343

    Abstract IARS2 encodes mitochondrial isoleucine-tRNA synthetase, which mutation may cause multiple diseases. However, the biological function of IARS2 on acute myeloid leukemia (AML) has not yet been identified. In the present study, qRT-PCR was used to determine the expression of IARS2 in K562, THP1, and HL-60 leukemia cells. Additionally the mRNA levels of IARS2 in CD34 cells and AML cells obtained from patients were detected by qRT-PCR. IARS2-shRNA lentiviral vector was established and used to infect acute myeloid leukemia HL-60 cells. qRT-PCR and Western blot analysis were employed to assess the knockdown effect of IARS2. The… More >

  • Open Access


    miRNA–mRNA Profiling Reveals Prognostic Impact of SMC1A Expression in Acute Myeloid Leukemia

    Nikhil Gadewal*1, Rohit Kumar†1, Swapnil Aher, Anagha Gardane, Tarang Gaur, Ashok K. Varma*‡§, Navin Khattry, Syed K. Hasan†§¶

    Oncology Research, Vol.28, No.3, pp. 321-330, 2020, DOI:10.3727/096504020X15816752427321

    Abstract Acute myeloid leukemia (AML) with NPM1 mutation is a disease driving genetic alteration with good prognosis. Although it has been suggested that NPM1 mutation induces chemosensitivity in leukemic cells, the underlying cause for the better survival of NPM1 mutated patients is still not clear. Mutant NPM1 AML has a unique microRNA and their target gene (mRNA) signature compared to wild-type NPM1. Dynamic regulation of miRNA–mRNA has been reported to influence the prognostic outcome. In the present study, in silico expression data of miRNA and mRNA in AML patients was retrieved from genome data commons, and differentially expressed miRNA… More >

  • Open Access


    miR-4792 Inhibits Acute Myeloid Leukemia Cell Proliferation and Invasion and Promotes Cell Apoptosis by Targeting Kindlin-3

    Yun Qin*, Yu Wang†‡§, Dongbo Liu

    Oncology Research, Vol.28, No.4, pp. 357-369, 2020, DOI:10.3727/096504020X15844389264424

    Abstract It has been reported that kindlin-3 expression is closely associated with progression of many cancers and microRNA (miRNA) processing. However, the effects and precise mechanisms of kindlin-3 in acute myeloid leukemia (AML) have not been well clarified. Our study aimed to explore the interaction between kindlin-3 and miR-4792 in AML. In our study, we found that the expression of kindlin-3 was dramatically increased in AML samples and cell lines, and the miR-4792 level was significantly downregulated. Interestingly, the low miR-4792 level was closely associated with upregulated kindlin-3 expression in AML samples. Moreover, introduction of miR-4792 More >

Displaying 1-10 on page 1 of 12. Per Page