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  1. Article ; Online: Unveiling myeloid transformation: T-LGLL with eosinophilia masking myeloid-associated STAT5B mutation culminating in AML.

    Dong, Qianze / Wang, Yang / Xiu, Yan / Wu, Xiaogang / O'Neill, Stacey / Meyerson, Howard / Tobias, Suske / Moriggl, Richard / Hu, Shimin / Wang, Wei / Zhao, Chen

    British journal of haematology

    2024  

    Language English
    Publishing date 2024-03-20
    Publishing country England
    Document type Letter
    ZDB-ID 80077-6
    ISSN 1365-2141 ; 0007-1048
    ISSN (online) 1365-2141
    ISSN 0007-1048
    DOI 10.1111/bjh.19421
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Philadelphia chromosome-positive T-cell acute lymphoblastic leukemia: a case report.

    Dong, Qianze / Darwish, Tarneem / Howard, Meyerson / Shetty, Shashirekha / Wang, Yang / Xiu, Yan / Gallogly, Molly / Zhao, Chen

    The Journal of international medical research

    2024  Volume 52, Issue 2, Page(s) 3000605231156757

    Abstract: Philadelphia chromosome-positive (Ph+) T-cell acute lymphoblastic leukemia (T-ALL) is a rare and aggressive type of acute leukemia. The Philadelphia chromosome is the hallmark of chronic myeloid leukemia (CML). The differentiation between Ph+ T-ALL and T- ...

    Abstract Philadelphia chromosome-positive (Ph+) T-cell acute lymphoblastic leukemia (T-ALL) is a rare and aggressive type of acute leukemia. The Philadelphia chromosome is the hallmark of chronic myeloid leukemia (CML). The differentiation between Ph+ T-ALL and T-cell lymphoblastic crisis of CML may be problematic in some cases. Here, we report a rare case of de novo Ph+ T-ALL that presented a diagnostic challenge. The overall clinical, immunophenotypic, cytogenetic, and xenotransplantation results suggest a diagnosis of Ph+ T-ALL. The patient was treated with induction chemotherapy including imatinib followed by haploidentical stem cell transplantation and achieved complete remission.
    MeSH term(s) Humans ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/diagnosis ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor T-Cell Lymphoblastic Leukemia-Lymphoma/therapy ; T-Lymphocytes ; Philadelphia Chromosome ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/diagnosis ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/genetics ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/therapy ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive
    Language English
    Publishing date 2024-02-29
    Publishing country England
    Document type Case Reports ; Journal Article
    ZDB-ID 184023-x
    ISSN 1473-2300 ; 0300-0605 ; 0142-2596
    ISSN (online) 1473-2300
    ISSN 0300-0605 ; 0142-2596
    DOI 10.1177/03000605231156757
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: AATF is Overexpressed in Human Bladder Cancer and Regulates Chemo-Sensitivity Through Survivin.

    Tan, Shutao / Fu, Lin / Dong, Qianze

    OncoTargets and therapy

    2021  Volume 14, Page(s) 5493–5505

    Abstract: Objective: Dysregulation of apoptosis antagonizing transcription factor (AATF) has been reported to be closely associated with human cancers. However, its involvement in human bladder cancer (BC) remains unexplored. This study aimed to investigate the ... ...

    Abstract Objective: Dysregulation of apoptosis antagonizing transcription factor (AATF) has been reported to be closely associated with human cancers. However, its involvement in human bladder cancer (BC) remains unexplored. This study aimed to investigate the clinical significance and biological roles of AATF in human bladder cancers.
    Methods: AATF protein expression was examined in 107 cases of bladder cancer tissues using immunohistochemistry. AATF plasmid transfection and small interfering RNA (siRNA) knockdown were performed in T24 and 5637 cell lines. CCK-8, colony formation, annexin V/PI, JC-1 staining, and Western blotting were carried out to investigate the biological roles and underlying mechanisms of AATF in bladder cancer cells.
    Results: Our results showed that AATF expression was upregulated in human bladder cancer specimens and correlated with T stage. Analysis of the Oncomine database showed elevation of AATF mRNA in BC tissues. The Cancer Genome Atlas (TCGA) data suggested that high AATF expression correlated with poor patient survival. Western blotting showed that AATF protein expression was higher in BC cell lines compared to normal bladder transitional epithelial cell line SV-HUC-1. CCK-8 and colony assays showed that ectopic AATF expression upregulated cell growth rate and colony numbers. CCK-8, annexin V/propidium iodide (PI), JC-1 assays and Western blotting showed that AATF overexpression decreased cisplatin sensitivity, downregulated cisplatin-induced apoptosis and upregulated mitochondrial membrane potential, with decreased cytochrome c and cleaved-PARP expression. AATF siRNA knockdown showed the opposite effects. Mechanistically, AATF overexpression upregulated cyclin E and Survivin at both mRNA and protein levels. The decreased cisplatin sensitivity/apoptosis induced by ectopic AATF were reversed after treatment with Survivin inhibitor YM155.
    Conclusion: Our results showed that AATF was overexpressed in human bladder cancers and promoted malignant behavior by regulating cyclin E and Survivin, indicating AATF could serve as a malignant biomarker and potential therapeutic target in BC.
    Language English
    Publishing date 2021-12-29
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2495130-4
    ISSN 1178-6930
    ISSN 1178-6930
    DOI 10.2147/OTT.S319734
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: AATF is Overexpressed in Human Head and Neck Squamous Cell Carcinoma and Regulates STAT3/Survivin Signaling.

    Fu, Lin / Jin, Quanxiu / Dong, Qianze / Li, Qingchang

    OncoTargets and therapy

    2021  Volume 14, Page(s) 5237–5248

    Abstract: Objective: Dysregulation of apoptosis antagonizing transcription factor (AATF) has been implicated in several cancers. However, its involvement in human head and neck squamous cell carcinoma (HNSCC) remains unclear. This study aimed to explore the ... ...

    Abstract Objective: Dysregulation of apoptosis antagonizing transcription factor (AATF) has been implicated in several cancers. However, its involvement in human head and neck squamous cell carcinoma (HNSCC) remains unclear. This study aimed to explore the expression pattern and biological roles of AATF in head and neck squamous cell carcinoma tissues and cell lines.
    Methods: Immunohistochemistry was used to detect the level of AATF protein in 119 cases of HNSCC samples. CCK-8, colony formation, Annexin V/PI staining, Western blotting and RNA-sequencing were carried out to examine the change of proliferation, apoptosis and potential underlying mechanisms.
    Results: Immunohistochemical staining showed that AATF was elevated in HNSCC, and high AATF level correlated with higher stage. The Cancer Genome Atlas (TCGA) and Oncomine data showed upregulated AATF expression in HNSCC compared with normal tissues. TCGA data also suggested that high AATF expression correlated with poor patient survival. Ectopic AATF expression upregulated the cell growth and colony formation ability in both FaDu and Detroit 562 cell lines, while AATF siRNA decreased the cell proliferation rate and colony numbers. AATF overexpression also decreased cisplatin sensitivity, downregulated cisplatin-induced apoptosis. Mechanistically, AATF overexpression upregulated survivin, while AATF knockdown downregulated survivin. RNA-sequencing (RNA-seq) and Gene Set Enrichment Analysis (GSEA) suggested that AATF knockdown decreased STAT3 signaling. Western blotting showed that AATF overexpression upregulated while AATF knockdown downregulated STAT3 phosphorylation. There was a positive correlation between AATF and survivin mRNA based on TCGA data analysis. Blockage of STAT3 signaling using inhibitor downregulated survivin expression and largely abolished the effects of AATF on survivin.
    Conclusion: Our results showed that AATF was overexpressed in human HNSCC. AATF promoted cisplatin resistance and reduced apoptosis possibly through regulation of STAT3/survivin signaling. AATF could serve as a potential therapeutic target in HNSCC.
    Language English
    Publishing date 2021-11-09
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2495130-4
    ISSN 1178-6930
    ISSN 1178-6930
    DOI 10.2147/OTT.S333134
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article: N1, N12-Diacetylspermine Is Elevated in Colorectal Cancer and Promotes Proliferation through the miR-559/CBS Axis in Cancer Cell Lines.

    Mu, Teng / Chu, Tingguang / Li, Wenxin / Dong, Qianze / Liu, Yong

    Journal of oncology

    2021  Volume 2021, Page(s) 6665704

    Abstract: N1, N12-Diacetylspermine (DiAcSpm) has been reported to be upregulated in the urine of cancer patients. Mass spectrometry has shown elevated DiAcSpm expressions in colorectal cancer (CRC) tissues. However, the diagnostic application of DiAcSpm is not ... ...

    Abstract N1, N12-Diacetylspermine (DiAcSpm) has been reported to be upregulated in the urine of cancer patients. Mass spectrometry has shown elevated DiAcSpm expressions in colorectal cancer (CRC) tissues. However, the diagnostic application of DiAcSpm is not available due to a lack of diagnostic grade antibodies. Also, its biological roles in CRC cells remain unexplored. In the present study, we developed an antibody that directly detected DiAcSpm expression in paraffin-embedded tissues. We also characterized its biological characteristics and underlying mechanisms. Polyclonal antibodies were generated by immunizing animals with a synthetic product of DiAcSpm. Antibody DAS AB016 showed strong sensitivity against DiAcSpm in CRC tissues. Immunohistochemistry results showed that DiAcSpm expression was significantly elevated in CRC tissues. High levels of DiAcSpm correlated with the clinical stage and Ki67 index. DiAcSpm treatment increased levels of proliferation, cell cycle progression, and cyclin D1 and cyclin E proteins in CRC cell lines, SW480 and Caco-2. DiAcSpm also upregulated ATP production in these two cell lines. RNA-sequencing showed that DiAcSpm downregulated miR-559, which was confirmed using RT-qPCR. The luciferase reporter assay, western blotting, and RT-qPCR showed that
    Language English
    Publishing date 2021-09-24
    Publishing country Egypt
    Document type Journal Article
    ZDB-ID 2461349-6
    ISSN 1687-8469 ; 1687-8450
    ISSN (online) 1687-8469
    ISSN 1687-8450
    DOI 10.1155/2021/6665704
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article: BCAT1 Overexpression Promotes Proliferation, Invasion, and Wnt Signaling in Non-Small Cell Lung Cancers.

    Lin, Xiumin / Tan, Shutao / Fu, Lin / Dong, Qianze

    OncoTargets and therapy

    2020  Volume 13, Page(s) 3583–3594

    Abstract: Introduction: Dysregulation of BCAT1 has been implicated in carcinogenesis. However, its clinical significance and biological roles in human non-small cell lung cancer (NSCLC) are not clear.: Methods: Immunohistochemistry was used to examine the ... ...

    Abstract Introduction: Dysregulation of BCAT1 has been implicated in carcinogenesis. However, its clinical significance and biological roles in human non-small cell lung cancer (NSCLC) are not clear.
    Methods: Immunohistochemistry was used to examine the protein expression of BCAT1 in 107 cases of lung cancer tissues. Biological roles and potential mechanisms of BCAT1 were examined using MTT, colony formation assay, Matrigel invasion assay, Western blot, RNA-sequencing, and luciferase reporter assay.
    Results: We found BCAT1 was upregulated in 60 of 107 lung cancer tissues and correlated with nodal metastasis, advanced stages and short overall survival. The Cancer Genome Atlas (TCGA) and ONCOMINE data analyses also indicated that BCAT1 was elevated in human NSCLC tissues. BCAT1 protein was higher in lung cancer cell lines than in normal bronchial epithelial cell line. BCAT1 overexpression increased the cell growth rate, colony numbers and invasion abilities in both BEAS-2B and H1299 cell lines, while BCAT1 siRNA decreased the cell proliferation rate, colony numbers, and inhibited invasion. RNA-sequencing (RNA-seq) and Gene Set Enrichment Analysis (GSEA) analyses indicated that BCAT1 overexpression activated Wnt/Myc signaling. Western blot revealed that BCAT1 increased protein expression of MMP7, cyclin D1, c-Myc, and decreased E-cadherin and p27 in the BEAS-2B and H1299 cell lines. Further experiments showed that BCAT1 overexpression elevated Wnt reporter luciferase activity and increased activate β-catenin protein while downregulating p-β-catenin protein expression. BCAT1 knockdown showed the opposite effects. TCGA data analysis suggested positive correlations between BCAT1 and c-Myc, cyclin D1, and MMP7 mRNA. Blockage of Wnt signaling using an inhibitor (ICG-001) downregulated c-Myc, cyclin D1, MMP7 expressions and abolished the upregulating effects of BCAT1 on these proteins.
    Conclusion: In summary, our data showed that BCAT1 was overexpressed in human NSCLCs. BCAT1 facilitated cell proliferation and invasion possibly through regulation of the Wnt signaling pathway.
    Language English
    Publishing date 2020-04-29
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2495130-4
    ISSN 1178-6930
    ISSN 1178-6930
    DOI 10.2147/OTT.S237306
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  7. Article ; Online: Clonally related composite chronic lymphocytic leukaemia and mantle cell lymphoma.

    Dong, Qianze / Wang, Yang / Xiu, Yan / Sakr, Hany / Burnworth, Bettina / Xu, Dongbin / O'Brien, Timothy / Burke, Juanita / Hu, Shimin / Zeng, Gang / Zhao, Chen

    British journal of haematology

    2022  Volume 200, Issue 5, Page(s) 660–664

    MeSH term(s) Humans ; Adult ; Lymphoma, Mantle-Cell/genetics ; Lymphoma, Mantle-Cell/pathology ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Leukemia, Lymphocytic, Chronic, B-Cell/pathology ; Immunophenotyping
    Language English
    Publishing date 2022-11-14
    Publishing country England
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80077-6
    ISSN 1365-2141 ; 0007-1048
    ISSN (online) 1365-2141
    ISSN 0007-1048
    DOI 10.1111/bjh.18565
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  8. Article: Rab11a Is Overexpressed in Gastric Cancer and Regulates FAK/AKT Signaling.

    Du, Jiang / Fu, Lin / Hao, Jie / Lin, Xiumin / Dong, Qianze

    Journal of oncology

    2020  Volume 2020, Page(s) 3494396

    Abstract: Dysregulation of Rab11a has been implicated in the progression of several cancers. However, there have been no such studies for human gastric cancers. In the current study, we examined Rab11a protein expression and found it was upregulated in 49 of 108 ... ...

    Abstract Dysregulation of Rab11a has been implicated in the progression of several cancers. However, there have been no such studies for human gastric cancers. In the current study, we examined Rab11a protein expression and found it was upregulated in 49 of 108 gastric cancer tissues and correlated with local invasion, nodal metastasis, and advanced stage. Rab11a protein was higher in gastric cancer cell lines than normal gastric cell line. We transfected Rab11a plasmid and siRNA in both MGC803 and AGS cell lines. Rab11a overexpression increased the cell growth rate, colony numbers, and invasion ability in both MGC803 and AGS cell lines. Downregulation of Rab11a using siRNA decreased the cell proliferation rate, colony numbers, and inhibited invasion. Rab11a overexpression also conferred cisplatin resistance. Annexin V/PI staining showed that Rab11a overexpression suppressed cisplatin-induced apoptosis, while Rab11a depletion promoted cell apoptosis. We also showed that Rab11a overexpression maintained mitochondrial membrane potential. Western blot analysis revealed that Rab11a increased protein expression of MMP2, cyclin D1, Bcl-2, p-FAK, and p-AKT, while Rab11a depletion showed the opposite effects. Blockage of FAK using inhibitor downregulated Bcl-2, cyclin D1, MMP2, and p-AKT expression and abolished the effects of Rab11a on these proteins. In summary, our data demonstrated that Rab11a is upregulated in human gastric cancers. Rab11a facilitated cell proliferation and invasion, as well as cisplatin sensitivity and mitochondrial membrane potential, possibly via the FAK/AKT signaling pathway.
    Language English
    Publishing date 2020-10-31
    Publishing country Egypt
    Document type Journal Article
    ZDB-ID 2461349-6
    ISSN 1687-8469 ; 1687-8450
    ISSN (online) 1687-8469
    ISSN 1687-8450
    DOI 10.1155/2020/3494396
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article: MicroRNA-320 inhibits invasion and induces apoptosis by targeting CRKL and inhibiting ERK and AKT signaling in gastric cancer cells.

    Zhao, Yue / Dong, Qianze / Wang, Enhua

    OncoTargets and therapy

    2017  Volume 10, Page(s) 1049–1058

    Abstract: MicroRNA-320 (miR-320) downregulation has been reported in several human cancers. Until now, its expression pattern and biological roles in human cancer remain unknown. This study aims to clarify its clinical expression pattern and biological function in ...

    Abstract MicroRNA-320 (miR-320) downregulation has been reported in several human cancers. Until now, its expression pattern and biological roles in human cancer remain unknown. This study aims to clarify its clinical expression pattern and biological function in gastric cancers. We found miR-320 level was downregulated in gastric cancer tissues. miR-320 mimic was transfected in SGC-7901 cells with low endogenous expression. miR-320 inhibitor was used in BGC-823 cells with high endogenous expression. We found that miR-320 inhibited SGC-7901 proliferation and invasion, with decreased expression of cyclin D1 and MMP9 at both mRNA and protein levels. We also found that miR-320 mimic downregulated chemoresistance and cell survival of gastric cancer cells when treated with 5-fluorouracil. miR-320 inhibitor displayed the opposite effects in BGC-823 cell line. In addition, we discovered that miR-320 mimic could inhibit AKT and ERK activity. By using luciferase reporter assay, we found that CRKL serves as the target of miR-320. miR-320 mimic downregulated CRKL expression, whereas miR-320 inhibitor upregulated CRKL expression. miR-320 suppressed CRKL-3'-untranslated region reporter intensity in SGC-7901 cells. Furthermore, CRKL depletion abrogated the effects of miR-320. In gastric cancer tissues, we observed a negative correlation between CRKL and miR-320. In conclusion, our study demonstrated that downregulation of miR-320 was closely related with malignant progression of gastric cancer. miR-320 inhibits proliferation, invasion, and chemoresistance through ERK and AKT signaling by targeting CRKL.
    Language English
    Publishing date 2017-02-20
    Publishing country New Zealand
    Document type Journal Article
    ZDB-ID 2495130-4
    ISSN 1178-6930
    ISSN 1178-6930
    DOI 10.2147/OTT.S123324
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: CLL dedifferentiation to clonally related myeloid cells.

    Dong, Qianze / Xiu, Yan / Bossler, Aaron / Syrbu, Sergei / Wang, Hongming / Xue, Weishuang / Zhao, Jinming / Li, Qingchang / Jin, Meiling / Wang, Lili / Boyce, Brendan / Sakr, Hany / Ansari, Mohammad Q / Zhao, Chen

    Blood advances

    2020  Volume 4, Issue 24, Page(s) 6169–6174

    MeSH term(s) Cell Transformation, Neoplastic ; Humans ; Leukemia, Lymphocytic, Chronic, B-Cell/genetics ; Myeloid Cells
    Language English
    Publishing date 2020-12-22
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2915908-8
    ISSN 2473-9537 ; 2473-9529
    ISSN (online) 2473-9537
    ISSN 2473-9529
    DOI 10.1182/bloodadvances.2020002726
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