Research Topics
Genomes and Genes | Yun DaiSummaryAffiliation: Massey Cancer Center, Virginia Commonwealth University Location: Richmond, USA Summary: Department of Medicine 内科, Massey Cancer Center 梅西癌症中心, School of Medicine 弗吉尼亚医学院, VCU 弗吉尼亚联邦大学, Richmond, Virginia, USA Jul 2010 - present Associate Professor (副教授) Jul 2003 – Jul 2010 Assistant Professor (助理教授) Mar 2002 - Jun 2003 Instructor (讲师) Jan 2000 – Mar 2002 Post-Doc Research Associate (博士后) Jun. 17, 2005-Present Active Member 正式会员, American Society of Hematology (ASH, 美国血液学会) Dec. 16, 2002-Present Active Member 正式会员, American Association for Cancer Research (AACR, 美国癌症研究协会) PEER-REVIEWED JOURNALS 学术期刊的同行主审 Cancer Research, 2009- Journal of Cellular and Molecular Medicine, 2009- Cancer Biology & Therapy, 2008- Molecular Cancer Therapeutics, 2010- Molecular Pharmacology, 2010- PLoS ONE, 2011- Cell Proliferation, 2011- Food and Chemical Toxicology, 2011- Grants: Project Title: Checkpoint abrogation and MEK1/2 inhibition in myeloma (CA100866-05) Source: NIH RO1 Period of Support: 07/01/09-06/30/14 Project Title: NF-kB and HDAC inhibition in leukemia (CA93738-05) Source: NIH RO1 Period of Support: 3/01/07-2/28/12 Project Title: Aurora-Bcr/abl kinase and HDAC inhibition in refractory Bcr/abl+ leukemias Source: Leukemia and Lymphoma Society Period of Support: 10/01/09-09/30/12 Project Title: Lymphoma SPORE (P50 CA130805; Project #3: Improving proteasome inhibitor activity in NHL) Source: NCI/NIH P50 Period of Support: 11/01/08-10/30/13 Project Title: M. D. Anderson Cancer Center SPORE in Multiple Myeloma (P50 CA142509; Project 4: Targeting multiple myeloma by combining CDK inhibitors and Bcl-2 antagonists) Source: NCI/NIH P50 Period of Support: 09/22/10 to 08/31/15 Project Title: M. D. Anderson Cancer Center SPORE in Multiple Myeloma (P50 CA142509; DRP Project: Cdk9/P-TEFb inhibitors against bortezomib-resistant multiple myeloma) Source: NCI/NIH P50 Period of Support: 09/22/10 to 08/31/11 Project Title: HDAC inhibitors and BH3 mimetics in resistant/refractory multiple myeloma Source: Multiple Myeloma Research Foundation Period of Support: 07/01/10 to 06/30/12 Project Title: Promotion of Bcl-2 antagonist activity in myeloma by flavopiridol Source: Multiple Myeloma Research Foundation Period of Support: 12/30/07-12/30/09 Project Title: Checkpoint abrogation and MEK1/2 inhibition in myeloma (CA 100866-01) Source: NIH RO1 Period of Support: 07/01/03-12/30/08 Project Title: MEK1/2 inhibition and checkpoint abrogation: a novel therapeutic strategy in multiple myeloma Source: Multiple Myeloma Research Foundation Period of Support: 9/1/01-8/31/02 Project Title: Potentiation of taxane activity by MEK/MAPK inhibitors (CA83705-01) Source: NIH/NCI RO1 Period of Support: 12/1/99-11/31/03 Project Title: Mechanisms for transformation of vascular smooth muscle cells to synthetic phenotype (39400069) Source: National Natural Science Foundation of China (project of free application) Period of Support: 05/01/1995-12/31/1997 Project Title: Hypersensitive status of platelets in human coronary heart disease: mechanisms and clinical significance (38970431) Source: National Natural Science Foundation of China (project of free application) Period of Support: 01/01/1990-12/31/1992 Publications
| Collaborators
|
Detail Information
Publications
LBH-589 (panobinostat) potentiates fludarabine anti-leukemic activity through a JNK- and XIAP-dependent mechanismRoberto Rosato
Division of Hematology Oncology, Department of Medicine, Virginia Commonwealth University and the Massey Cancer Center, Richmond, VA 23298, USA
Leuk Res 36:491-8. 2012..These studies highlight the interplay between NF-κB activation, XIAP down-regulation, and JNK activation in anti-leukemic synergism between fludarabine and LBH-589...
Synergistic interactions between vorinostat and sorafenib in chronic myelogenous leukemia cells involve Mcl-1 and p21CIP1 down-regulationGirija Dasmahapatra
Department of Medicine, Massey Cancer Center, Virginia Commonwealth University, Richmond, Virginia 23298, USA
Clin Cancer Res 13:4280-90. 2007..Interactions between the multikinase inhibitor sorafenib (Bay 43-9006) and the histone deacetylase inhibitor vorinostat were examined in chronic myelogenous leukemia (CML) cells sensitive and resistant to imatinib mesylate...
MEK1/2 inhibitors potentiate UCN-01 lethality in human multiple myeloma cells through a Bim-dependent mechanismXin Yan Pei
Departments of Medicine, Virginia Commonwealth University Massey Cancer Center, Richmond, VA 23298, USA
Blood 110:2092-101. 2007....
Targeting multiple arms of the apoptotic regulatory machineryYun Dai
Department of Medicine, Virginia Commonwealth University and Massey Cancer Center, Richmond, Virginia, USA
Cancer Res 67:2908-11. 2007..Collectively, these findings suggest a novel therapeutic strategy targeting multiple arms of the apoptotic machinery...
Statins synergistically potentiate 7-hydroxystaurosporine (UCN-01) lethality in human leukemia and myeloma cells by disrupting Ras farnesylation and activationYun Dai
Department of Medicine, Virginia Commonwealth University Massey Cancer Center, Richmond, VA 23298, USA
Blood 109:4415-23. 2007....
Mcl-1 down-regulation potentiates ABT-737 lethality by cooperatively inducing Bak activation and Bax translocationShuang Chen
Department of Medicine, Virginia Commonwealth University and Massey Cancer Center, Richmond, Virginia 23298, USA
Cancer Res 67:782-91. 2007..These findings provide a mechanistic basis for simultaneously targeting Mcl-1 and Bcl-2/Bcl-xL in leukemia...
Dissecting the roles of checkpoint kinase 1/CDC2 and mitogen-activated protein kinase kinase 1/2/extracellular signal-regulated kinase 1/2 in relation to 7-hydroxystaurosporine-induced apoptosis in human multiple myeloma cellsXin-Yan Pei
Division of Hematology/Oncology, Virginia Commonwealth University/Medical College of Virginia, MCV Station Box 230, Richmond VA 23298, USA
Mol Pharmacol 70:1965-73. 2006..They also suggest a role for Chk1 in UCN-01-induced ERK1/2 activation, implying the existence of a heretofore unrecognized link between Chk1 and ERK1/2 signaling...
CDK inhibitor targets: a hit or miss proposition?: cyclin-dependent kinase inhibitors kill tumor cells by downregulation of anti-apoptotic proteinsYun Dai
Division of Hematology Oncology and Department of Medicine, Virginia Commonwealth University Massey Cancer Center, Richmond, Virginia, USA
Cancer Biol Ther 5:171-3. 2006
Cyclin D1 overexpression increases the susceptibility of human U266 myeloma cells to CDK inhibitors through a process involving p130-, p107- and E2F-dependent S phase entryYun Dai
Division of Hematology/Oncology and Department of Medicine, Virginia Commonwealth University/Massey Cancer Center, Richmond, Virginia, USA
Cell Cycle 5:437-46. 2006....
Transient exposure of mammary tumors to PD184352 and UCN-01 causes tumor cell death in vivo and prolonged suppression of tumor regrowthWilliam Hawkins
Department of Biochemistry, Virginia Commonwealth University, Richmond, Virginia 23298-0058, USA
Cancer Biol Ther 4:1275-84. 2005..Collectively, these findings argue that UCN-01 and MEK1/2 inhibitors have the potential to suppress mammary tumor growth in vivo which is independent of p53 status, estrogen dependency, caspase 3 levels or oncogenic K-RAS expression...
Blockade of histone deacetylase inhibitor-induced RelA/p65 acetylation and NF-kappaB activation potentiates apoptosis in leukemia cells through a process mediated by oxidative damage, XIAP downregulation, and c-Jun N-terminal kinase 1 activationYun Dai
Department of Medicine, Virginia Commonwealth University Massey Cancer Center, Richmond, Virginia 23298, USA
Mol Cell Biol 25:5429-44. 2005....
The farnesyltransferase inhibitor L744832 potentiates UCN-01-induced apoptosis in human multiple myeloma cellsXin-Yan Pei
Department of Medicine, Virginia Commonwealth University/Medical College of Virginia, Richmond, Virginia 23298, USA
Clin Cancer Res 11:4589-600. 2005..They also raise the possibility that combined treatment with farnesyltransferase inhibitors and UCN-01 could represent a novel therapeutic strategy in multiple myeloma...
Coadministration of histone deacetylase inhibitors and perifosine synergistically induces apoptosis in human leukemia cells through Akt and ERK1/2 inactivation and the generation of ceramide and reactive oxygen speciesMohamed Rahmani
Department of Medicine, Virginia Commonwealth University, School of Medicine, Richmond, VA 23298, USA
Cancer Res 65:2422-32. 2005..They also raise the possibility that combining these agents may represent a novel antileukemic strategy...
The small-molecule Bcl-2 inhibitor HA14-1 interacts synergistically with flavopiridol to induce mitochondrial injury and apoptosis in human myeloma cells through a free radical-dependent and Jun NH2-terminal kinase-dependent mechanismXin-Yan Pei
Department of Medicine, Virginia Commonwealth University/Medical College of Virginia, Richmond, Virginia 23298, USA
Mol Cancer Ther 3:1513-24. 2004....
Interactions between bortezomib and romidepsin and belinostat in chronic lymphocytic leukemia cellsYun Dai
Department of Medicine, Virginia Commonwealth University Massey Cancer Center, Richmond, VA 23298, USA
Clin Cancer Res 14:549-58. 2008..The goal of this study was to characterize interactions between the proteasome inhibitor bortezomib and the histone deacetylase (HDAC) inhibitors (HDACI) romidepsin or belinostat in chronic lymphocytic leukemia (CLL) cells...
Transient exposure of carcinoma cells to RAS/MEK inhibitors and UCN-01 causes cell death in vitro and in vivoHossein Hamed
Department of Biochemistry, Virginia Commonwealth University, Richmond VA 23298 0035, USA
Mol Cancer Ther 7:616-29. 2008..These findings argue that UCN-01 and multiple inhibitors of the RAS-MEK pathway have the potential to suppress mammary tumor growth, and to interact with radiation, in vitro and in vivo...
Vorinostat synergistically potentiates MK-0457 lethality in chronic myelogenous leukemia cells sensitive and resistant to imatinib mesylateYun Dai
Department of Medicine, Virginia Commonwealth University Massey Cancer Center, Richmond, VA 23298, USA
Blood 112:793-804. 2008..Together, these findings indicate that vorinostat strikingly increases MK-0457 activity against IM-sensitive and -resistant CML cells through inactivation of Bcr/Abl and aurora kinases, as well as by induction of Bim...
Cytokinetically quiescent (G0/G1) human multiple myeloma cells are susceptible to simultaneous inhibition of Chk1 and MEK1/2Xin Yan Pei
Division of Hematology Oncology, Department of Medicine, Virginia Commonwealth University, Richmond, 23298, USA
Blood 118:5189-200. 2011..These findings provide evidence that cytokinetically quiescent MM cells are highly susceptible to simultaneous Chk1 and MEK1/2 inhibition...
Methods to study cancer therapeutic drugs that target cell cycle checkpointsYun Dai
Hematology Oncology, Virginia Commonwealth University, 23298, Richmond, VA, USA
Methods Mol Biol 782:257-304. 2011....
The role of Tyk2 in regulation of breast cancer growthQifang Zhang
Department of Biochemistry and Molecular Biology, Virginia Commonwealth University, Richmond, Virginia 23298, USA
J Interferon Cytokine Res 31:671-7. 2011..Our results provide the first evidence for a role of Tyk2 in suppressing the growth and metastasis of breast cancer...
Disruption of IkappaB kinase (IKK)-mediated RelA serine 536 phosphorylation sensitizes human multiple myeloma cells to histone deacetylase (HDAC) inhibitorsYun Dai
Department of Medicine, Virginia Commonwealth University Massey CancerCenter, Richmond, Virginia 23298, USA
J Biol Chem 286:34036-50. 2011....
Simultaneous exposure of transformed cells to SRC family inhibitors and CHK1 inhibitors causes cell deathClint Mitchell
Department of Neurosurgery, Virginia Commonwealth University, School of Medicine, Richmond, VA, USA
Cancer Biol Ther 12:215-28. 2011..Treatment of cells with [SRC + CHK1] inhibitors radio-sensitized tumor cells. These findings argue that multiple inhibitors of the SRC-RAS-MEK pathway interact with multiple CHK1 inhibitors to kill transformed cells...
CHK1 inhibitors in combination chemotherapy: thinking beyond the cell cyclePaul Dent
Department of Neurosurgery, Virginia Commonwealth University, Massey Cancer Center, 401 College Street, Richmond, VA 23298 0035, USA
Mol Interv 11:133-40. 2011..An understanding of Chk1 inhibition in multiple signaling contexts will be essential to the therapeutic development of Chk1 inhibitors...
HDAC inhibitors potentiate the activity of the BCR/ABL kinase inhibitor KW-2449 in imatinib-sensitive or -resistant BCR/ABL+ leukemia cells in vitro and in vivoTri Nguyen
Division of Hematology Oncology, Department of Biochemistry, and Massey Cancer Center, Virginia Commonwealth University Health Sciences Center, Richmond, Virginia 23298, USA
Clin Cancer Res 17:3219-32. 2011....
Bortezomib interacts synergistically with belinostat in human acute myeloid leukaemia and acute lymphoblastic leukaemia cells in association with perturbations in NF-κB and BimYun Dai
Division of Hematology Oncology, Department of Medicine, Virginia Commonwealth University and the Massey Cancer Center, VCU Health Sciences Center, 401 College Street, Richmond, VA 23298, USA
Br J Haematol 153:222-35. 2011..They also suggest that combined belinostat/bortezomib regimens warrant further attention in acute leukaemias...
Disruption of Src function potentiates Chk1-inhibitor-induced apoptosis in human multiple myeloma cells in vitro and in vivoYun Dai
Division of Hematology Oncology, Department of Medicine, Virginia Commonwealth University, and the Massey Cancer Center, Richmond, VA 23298, USA
Blood 117:1947-57. 2011..These findings suggest that Src kinase is required for Chk1-inhibitor-mediated Ras → ERK1/2 signaling activation, and that disruption of this event sharply potentiates the anti-MM activity of Chk1 inhi-bitors in vitro and in vivo...
The NF (Nuclear factor)-κB inhibitor parthenolide interacts with histone deacetylase inhibitors to induce MKK7/JNK1-dependent apoptosis in human acute myeloid leukaemia cellsYun Dai
Division of Hematology Oncology, Department of Medicine, Virginia Commonwealth University, 401 College Street, Richmond, VA 23298, USA
Br J Haematol 151:70-83. 2010..They also raise the possibility that this strategy may target leukaemic progenitor cells...
Targeting Chk1 in the replicative stress responseYun Dai
Virginia Commonwealth University Richmond, VA
Cell Cycle 9:1025-30. 2010..Comment on: McNeely et al. Cell Cycle 2010; 9:995-1004...
New insights into checkpoint kinase 1 in the DNA damage response signaling networkYun Dai
Department of Medicine, Institute for Molecular Medicine, and Division of Hematology Oncology, Department of Medicine, Virginia Commonwealth University Massey Cancer Center, Richmond, Virginia 23298, USA
Clin Cancer Res 16:376-83. 2010..Together, these new insights into the role of Chk1 in the DDR machinery could provide an opportunity for novel approaches to the development of Chk1 inhibitor strategies...
Interruption of the Ras/MEK/ERK signaling cascade enhances Chk1 inhibitor-induced DNA damage in vitro and in vivo in human multiple myeloma cellsYun Dai
Department of Medicine, Virginia Commonwealth University Massey Cancer Center, Richmond, VA 23298, USA
Blood 112:2439-49. 2008..Together, these findings identify a novel mechanism by which agents targeting the Ras/MEK/ERK pathway potentiate Chk1 inhibitor lethality in MM...
Cotreatment with suberanoylanilide hydroxamic acid and 17-allylamino 17-demethoxygeldanamycin synergistically induces apoptosis in Bcr-Abl+ Cells sensitive and resistant to STI571 (imatinib mesylate) in association with down-regulation of Bcr-Abl, abrogatMohamed Rahmani
Division of Hematology/Oncology, Virginia Commonwealth University, Medical College of Virginia, MCV Station Box 230, Richmond, VA 23298, USA
Mol Pharmacol 67:1166-76. 2005..Together, these findings raise the possibility that combining HDAC inhibitors with the Hsp90 antagonist 17-AAG may represent a novel strategy against Bcr-Abl(+) leukemias, including those resistant to STI571...
Farnesyltransferase inhibitors interact synergistically with the Chk1 inhibitor UCN-01 to induce apoptosis in human leukemia cells through interruption of both Akt and MEK/ERK pathways and activation of SEK1/JNKYun Dai
Department of Medicine, Virginia Commonwealth University/Medical College of Virginia, Richmond VA, 23298, USA
Blood 105:1706-16. 2005....
The lethal effects of pharmacological cyclin-dependent kinase inhibitors in human leukemia cells proceed through a phosphatidylinositol 3-kinase/Akt-dependent processChunrong Yu
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, USA
Cancer Res 63:1822-33. 2003....
Coadministration of UCN-01 with MEK1/2 inhibitors potently induces apoptosis in BCR/ABL+ leukemia cells sensitive and resistant to ST1571Chunrong Yu
Division of Hematology Oncology, Department of Medicine, Virginia Commonwealth University Medical College of Virginia, Richmond, Virginia 23298, USA
Cancer Biol Ther 1:674-82. 2002..These findings indicate that BcrAbl(+) leukemia cells are sensitive to a strategy combining UCN-01 with MEK/ERK inhibitors that simultaneously disrupts two signaling pathways...
Inhibitors of MEK1/2 interact with UCN-01 to induce apoptosis and reduce colony formation in mammary and prostate carcinoma cellsRobert McKinstry
Department of Radiation Oncology, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, USA
Cancer Biol Ther 1:243-53. 2002..Collectively, these data demonstrate that combined exposure of carcinoma cells to UCN-01 and MEK1/2 inhibitors induces apoptosis and interacts with radiation to further reduce clonogenic survival...
Induction of apoptosis in human leukemia cells by the CDK1 inhibitor CGP74514AYun Dai
Departments of Medicine, Medical College of Virginia; Virginia Commonwealth University; Richmond, Virginia 23298, USA
Cell Cycle 1:143-52. 2002..These findings indicate that the selective CDK1 inhibitor, CGP74514A, induces complex changes in cell cycle-related proteins in human leukemia cells accompanied by extensive mitochondrial damage, caspase activation, and apoptosis...
Combined treatment with the checkpoint abrogator UCN-01 and MEK1/2 inhibitors potently induces apoptosis in drug-sensitive and -resistant myeloma cells through an IL-6-independent mechanismYun Dai
Division of Hematology/Oncology, Department of Radiation Oncology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298, USA
Blood 100:3333-43. 2002....
Loss of the Bcl-2 phosphorylation loop domain is required to protect human myeloid leukemia cells from flavopiridol-mediated mitochondrial damage and apoptosisRoy H Decker
Department of Medicine, Biochemistry, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, USA
Cancer Biol Ther 1:136-44. 2002....
The histone deacetylase inhibitor sodium butyrate interacts synergistically with phorbol myristate acetate (PMA) to induce mitochondrial damage and apoptosis in human myeloid leukemia cells through a tumor necrosis factor-alpha-mediated processMohamed Rahmani
Department of Medicine, Virginia Commonwealth University, Richmond 23298, USA
Exp Cell Res 277:31-47. 2002....
Synergistic induction of apoptosis in human myeloid leukemia cells by phorbol 12-myristate 13-acetate and flavopiridol proceeds via activation of both the intrinsic and tumor necrosis factor-mediated extrinsic cell death pathwaysL Cartee
Department of Medicine, Virginia Commonwealth University, Medical College of Virginia, Richmond, Virginia 23298-0230, USA
Mol Pharmacol 61:1313-21. 2002....
Bryostatin 1 increases 1-beta-D-arabinofuranosylcytosine-induced cytochrome c release and apoptosis in human leukemia cells ectopically expressing Bcl-x(L)Zhiliang Wang
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia 23298, USA
J Pharmacol Exp Ther 301:568-77. 2002..In addition, they raise the possibility that activation of caspase cascades operating independently of Bcl-x(L)-associated mitochondrial actions may also contribute to enhanced lethality...
Aldosterone biosynthesis in extraadrenal tissuesP Wu
Department of Cardiology, Nanfang Hospital, First Military Medical University, Guangzhou 510515, China
Chin Med J (Engl) 112:414-8. 1999..To determine whether extraadrenal tissues synthesize aldosterone in addition to vascular tissue and brain...
The cyclin-dependent kinase inhibitor flavopiridol induces apoptosis in human leukemia cells (U937) through the mitochondrial rather than the receptor-mediated pathwayR H Decker
Department of Medicine, Medical College of Virginia, Richmond, VA 23298, USA
Cell Death Differ 8:715-24. 2001..Collectively, these findings indicate that FP induces apoptosis in U937 cells via the release of cytochrome c from the mitochondria and independently of activation of procaspase-8...
Pharmacological inhibitors of the mitogen-activated protein kinase (MAPK) kinase/MAPK cascade interact synergistically with UCN-01 to induce mitochondrial dysfunction and apoptosis in human leukemia cellsY Dai
Division of Hematology/Oncology, Medical College of Virginia, Richmond, Virginia 23298, USA
Cancer Res 61:5106-15. 2001..They also raise the possibility that disrupting multiple signaling pathways, e.g., by combining UCN-01 with MEK inhibitors, may represent a novel antileukemic strategy...
Interactions between 2-fluoroadenine 9-beta-D-arabinofuranoside and the kinase inhibitor UCN-01 in human leukemia and lymphoma cellsS Harvey
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298, USA
Clin Cancer Res 7:320-30. 2001..These findings indicate that UCN-01 increases F-ara-A-induced mitochondrial damage and apoptosis in human leukemia cells in a sequence-dependent manner, and that these events occur in at least some primary human lymphoma cells...
Enforced expression of the tumor suppressor p53 renders human leukemia cells (U937) more sensitive to 1-[beta-D-arabinofuranosyl]cytosine (ara-C)-induced apoptosisRoy H Decker
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298, USA
Biochem Pharmacol 65:1997-2008. 2003..Such findings raise the possibility that loss of functional p53 activity allows leukemia cells to circumvent ara-C lethality...
Cyclin-dependent kinase inhibitorsYun Dai
Division of Hematology/Oncology, Medical College of Virginia, Virginia Commonwealth University, MCV Station Box 230, Richmond, VA 23298, USA
Curr Opin Pharmacol 3:362-70. 2003..For all of these reasons, it is likely that interest in CDK inhibitors as antineoplastic agents will continue for the foreseeable future...
An intact NF-kappaB pathway is required for histone deacetylase inhibitor-induced G1 arrest and maturation in U937 human myeloid leukemia cellsYun Dai
Division of Hematology Oncology, Department of Medicine, Virginia Commonwealth University, Medical College of Virginia, Richmond, Virginia 23298, USA
Cell Cycle 2:467-72. 2003....
Potent antileukemic interactions between flavopiridol and TRAIL/Apo2L involve flavopiridol-mediated XIAP downregulationR R Rosato
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298, USA
Leukemia 18:1780-8. 2004....
Contribution of disruption of the nuclear factor-kappaB pathway to induction of apoptosis in human leukemia cells by histone deacetylase inhibitors and flavopiridolNing Gao
Department of Medicine, Virginia Commonwealth University/Medical College of Virginia, Richmond 23298, USA
Mol Pharmacol 66:956-63. 2004..g., down-regulation of Mcl-1, XIAP, and p21CIP1/WAF1) play particularly critical roles in this phenomenon...
A Bcr/Abl-independent, Lyn-dependent form of imatinib mesylate (STI-571) resistance is associated with altered expression of Bcl-2Yun Dai
Department of Medicine, Virginia Commonwealth University/Medical College of Virginia, Richmond, VA 23298, USA
J Biol Chem 279:34227-39. 2004....
Synergistic induction of oxidative injury and apoptosis in human multiple myeloma cells by the proteasome inhibitor bortezomib and histone deacetylase inhibitorsXin-Yan Pei
Department of Medicine, Virginia Commonwealth University, Medical College of Virginia, Richmond, Virginia 23298, USA
Clin Cancer Res 10:3839-52. 2004....
The histone deacetylase inhibitor MS-275 interacts synergistically with fludarabine to induce apoptosis in human leukemia cellsSonia C Maggio
Department of Medicine, Virginia Commonwealth University/Medical College of Virginia, Richmond, Virginia 23298, USA
Cancer Res 64:2590-600. 2004..They also provide insights into possible mechanisms by which novel, clinically relevant HDAC inhibitors might be used to enhance the antileukemic activity of established nucleoside analogues such as fludarabine...
Bortezomib and flavopiridol interact synergistically to induce apoptosis in chronic myeloid leukemia cells resistant to imatinib mesylate through both Bcr/Abl-dependent and -independent mechanismsYun Dai
Division of Hematology/Oncology, Virginia Commonwealth University/Medical College of Virginia, MCV Station Box 230, Richmond, VA 23298, USA
Blood 104:509-18. 2004..Collectively, these findings suggest that a strategy combining flavopiridol and bortezomib warrants further examination in chronic myelogenous leukemia and related hematologic malignancies...
Small molecule inhibitors targeting cyclin-dependent kinases as anticancer agentsYun Dai
Division of Hematology/Oncology, Virginia Commonwealth University/Medical College of Virginia, MCV Station Box 230, Richmond, VA 23298, USA
Curr Oncol Rep 6:123-30. 2004..Such findings may serve as a basis for the introduction of novel combination regimens into clinical trials...
Simultaneous activation of the intrinsic and extrinsic pathways by histone deacetylase (HDAC) inhibitors and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) synergistically induces mitochondrial damage and apoptosis in human leukemia cellsRoberto R Rosato
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298, USA
Mol Cancer Ther 2:1273-84. 2003....
Coadministration of the heat shock protein 90 antagonist 17-allylamino- 17-demethoxygeldanamycin with suberoylanilide hydroxamic acid or sodium butyrate synergistically induces apoptosis in human leukemia cellsMohamed Rahmani
Department of Medicine, Virginia Commonwealth University, Medical College of Virginia, Richmond, Virginia 23298, USA
Cancer Res 63:8420-7. 2003..They also raise the possibility that combining such agents with Hsp90 antagonists may represent a novel antileukemic strategy...
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) promotes mitochondrial dysfunction and apoptosis induced by 7-hydroxystaurosporine and mitogen-activated protein kinase kinase inhibitors in human leukemia cells that ectopically express Bcl-Yun Dai
Division of Hematology Oncology, Medical College of Virginia Virginia Commonwealth University, MCV Station Box 230, Richmond, VA 23298, USA
Mol Pharmacol 64:1402-9. 2003....
Interruption of the NF-kappaB pathway by Bay 11-7082 promotes UCN-01-mediated mitochondrial dysfunction and apoptosis in human multiple myeloma cellsYun Dai
Department of Medicine, Virginia Commonwealth University, Medical College of Virginia, Richmond 23298, USA
Blood 103:2761-70. 2004..Together, these findings suggest that a strategy combining UCN-01 with disruption of the IkappaB kinase (IKK)/IkappaB/NF-kappaB pathway warrants attention in MM...
Proteasome inhibitors potentiate leukemic cell apoptosis induced by the cyclin-dependent kinase inhibitor flavopiridol through a SAPK/JNK- and NF-kappaB-dependent processYun Dai
Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298, USA
Oncogene 22:7108-22. 2003..They also raise the possibility that combining proteasome and CDK inhibitors could represent a novel antileukemic strategy...
The proteasome inhibitor bortezomib promotes mitochondrial injury and apoptosis induced by the small molecule Bcl-2 inhibitor HA14-1 in multiple myeloma cellsX-Y Pei
Department of Medicine, Virginia Commonwealth University/Medical College of Virginia, Richmond, VA 23298, USA
Leukemia 17:2036-45. 2003..Together, these findings indicate that sequential exposure of myeloma cells to proteasome and small molecule Bcl-2 inhibitors such as HA14-1 may represent a novel therapeutic strategy in myeloma...
Evidence for thrombin-induced human platelet secretion regulated by the cytoskeletonY Dai
Department of Histology and Embryology, First Military Medical College, Guangzhou
Shi Yan Sheng Wu Xue Bao 28:236-40. 1995....
Bim upregulation by histone deacetylase inhibitors mediates interactions with the Bcl-2 antagonist ABT-737: evidence for distinct roles for Bcl-2, Bcl-xL, and Mcl-1Shuang Chen
Department of Medicine, Virginia Commonwealth University, Richmond, VA 23298, USA
Mol Cell Biol 29:6149-69. 2009....
