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Alteration of gene expression profile following PPP2R5C knockdown may be associated with proliferation suppression and increased apoptosis of K562 cells
In this study, we further characterized the gene expression profiles after PPP2R5C suppression by microarray analysis. Genes which participate in the MAPK, PI3K/AKT, and JAK/STAT pathways, were mainly altered in the K562 cells. We propose that the mechanism for proliferation inhibition and increased apoptosis of K562 cells following PPP2R5C suppression may be related to the alteration of expression profiles of BRAF, AKT2, AKT3, NFKB2 and STAT3 genes.
Source: Journal of Hematology and Oncology - April 12, 2015 Category: Hematology Authors: Sichu LiuQi ShenYu ChenChengwu ZengChangshu CaoLijiang YangShaohua ChenXiuli WuBo LiYangqiu Li Source Type: research

ATP directed agent, 8-chloro-adenosine, induces AMP activated protein kinase activity, leading to autophagic cell death in breast cancer cells
Conclusions: Our data demonstrates that 8-Cl-Ado treatment activates the AMPK pathway leading to autophagy induction of in breast cancer cells, eliciting, in part, its tumoricidal effects. Additionally, 8-Cl-Ado effectively inhibited in vivo tumor growth in mice. Based on this biological activity, we are planning to test 8-Cl-Ado in the clinic for patients with breast cancer.
Source: Journal of Hematology and Oncology - March 14, 2014 Category: Hematology Authors: Christine StellrechtHima VangapanduXiao-Feng LeWeiqun MaoShujun Shentu Source Type: research

Interferon-¿-induced upregulation of immunoproteasome subunit assembly overcomes bortezomib resistance in human hematological cell lines
Conclusion: Downregulation of β5i subunit expression is a major determinant in acquisition of bortezomib-resistance and enhancement of its proteasomal assembly after induction by interferon-γ facilitates restoration of sensitivity in bortezomib-resistant leukemia cells towards bortezomib and next generation (immuno) proteasome inhibitors.
Source: Journal of Hematology and Oncology - January 13, 2014 Category: Hematology Authors: Denise NiewerthGertjan KaspersYehuda AssarafJohan van MeerlooChristopher KirkJanet AnderlJonathan BlankPeter van de VenSonja ZweegmanGerrit JansenJacqueline Cloos Source Type: research

Interferon-gamma-induced upregulation of immunoproteasome subunit assembly overcomes bortezomib resistance in human hematological cell lines
Conclusion: Downregulation of beta5i subunit expression is a major determinant in acquisition of bortezomib-resistance and enhancement of its proteasomal assembly after induction by interferon-gamma facilitates restoration of sensitivity in bortezomib-resistant leukemia cells towards bortezomib and next generation (immuno) proteasome inhibitors.
Source: Journal of Hematology and Oncology - January 13, 2014 Category: Hematology Authors: Denise NiewerthGertjan KaspersYehuda AssarafJohan van MeerlooChristopher KirkJanet AnderlJonathan BlankPeter van de VenSonja ZweegmanGerrit JansenJacqueline Cloos Source Type: research

Genomic amplification and high expression of EGFR are key targetable oncogenic events in malignant peripheral nerve sheath tumor
Conclusion: These results suggest that EGFR is a potential therapeutic target for MPNST.
Source: Journal of Hematology and Oncology - December 17, 2013 Category: Hematology Authors: Xiaoling DuJilong YangAntti YlipääZe Zhu Source Type: research

Inhibition of Hedgehog signaling sensitizes NSCLC cells to standard therapies through modulation of EMT-regulating miRNAs
Conclusions: We demonstrate that Hh pathway, through EMT-induction, leads to reduced sensitivity to EGFR-TKIs in NSCLCs. Therefore, targeting Hh pathway may lead to the reversal of EMT phenotype and improve the therapeutic efficacy of EGFR-TKIs in NSCLC patients.
Source: Journal of Hematology and Oncology - October 7, 2013 Category: Hematology Authors: Aamir AhmadMa¿in MaitahKevin GinnebaughYiwei LiBin BaoShirish GadgeelFazlul Sarkar Source Type: research

Proliferation inhibition and apoptosis induction of imatinib-resistant chronic myeloid leukemia cells via PPP2R5C down-regulation
In conclusion, the suppression of PPP2R5C by RNA interference could inhibit proliferation and effectively induce apoptosis in CML cells that were either imatinib sensitive or resistant. Down-regulating PPP2R5C gene expression might be considered as a new therapeutic target strategy for CML, particularly for imatinib-resistant CML.
Source: Journal of Hematology and Oncology - September 3, 2013 Category: Hematology Authors: Qi ShenSichu LiuYu ChenLijian YangShaohua ChenXiuli WuBo LiYuhong LuKanger ZhuYangqiu Li Source Type: research

Histone deacetylase inhibitor potentiated the ability of MTOR inhibitor to induce autophagic cell death in Burkitt leukemia/lymphoma
Conclusions: These findings confirmed the synergistic effect of the HDAC and MTOR inhibitors on Burkitt leukemia/lymphoma, and provided an insight into clinical application of targeting autophagy in treating MYC-associated lymphoid malignancies.
Source: Journal of Hematology and Oncology - July 18, 2013 Category: Hematology Authors: Li Hua DongShu ChengZhong ZhengLi WangYang ShenZhi Xiang ShenSai Juan ChenWei Li Zhao Source Type: research

Sodium selenite alters microtubule assembly and induces apoptosis in vitro and in vivo
Conclusions: Taken together, the results from our study indicate that microtubules are novel targets of selenite in leukemic HL60 cells.
Source: Journal of Hematology and Oncology - January 17, 2013 Category: Hematology Authors: Kejian ShiQian JiangZhushi LiLei ShanFeng LiJiaJia AnYang YangCaimin Xu Source Type: research

Notch1 is required for hypoxia-induced proliferation, invasion and chemoresistance of T-cell acute lymphoblastic leukemia cells
Conclusions: Notch1 signalling is required for hypoxia/HIF-1alpha-induced proliferation, invasion and chemoresistance in T-ALL. Pharmacological inhibitors of HIF-1alpha or Notch1 signalling may be attractive interventions for T-ALL treatment.
Source: Journal of Hematology and Oncology - January 5, 2013 Category: Hematology Authors: Jie ZouPeng LiFei LuNa LiuJianjian DaiJingjing YeXun QuXiulian SunDaoxin MaJino ParkChunyan Ji Source Type: research