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Kang, Yubin

Positions:

Associate Professor of Medicine

Medicine, Cellular Therapy
School of Medicine

Member of the Duke Cancer Institute

Duke Cancer Institute
School of Medicine

Education:

M.D. 1991

M.D. — Shanghai Second Medical University (China)

Grants:

PHASE 2 STUDY OF POMALIDOMIDE WITH LOW-DOSE DEXAMETHASONE

Administered By
Duke Cancer Institute
AwardedBy
Celgene Corporation
Role
Principal Investigator
Start Date
March 13, 2017
End Date
May 31, 2022

Develop and Support of the RedCap database, bio-statistic analysis, and med writing for Dr Kang NIH SBIR award Clin Trial

Administered By
Duke Cancer Institute
AwardedBy
RedHill Biopharma Ltd.
Role
Principal Investigator
Start Date
May 01, 2016
End Date
December 31, 2021

Targeting sphingosine kinase 2 for the treatment of multiple myeloma

Administered By
Medicine, Hematological Malignancies
AwardedBy
National Institutes of Health
Role
Principal Investigator
Start Date
August 03, 2015
End Date
July 31, 2020

Ph III study to evaluate the safety of ALN-TTR02 in TTR-Medicated Polyneuropathy

Administered By
Duke Cancer Institute
AwardedBy
Alnylam Pharmaceuticals
Role
Principal Investigator
Start Date
November 01, 2014
End Date
October 31, 2019

Clinical Trial of ABC294640 in Patients with Refractory Multiple Myeloma

Administered By
Medicine, Hematological Malignancies
AwardedBy
Apogee Biotechnology Corporation
Role
Principal Investigator
Start Date
September 01, 2015
End Date
August 31, 2018

Thioredoxin for radioprotection

Administered By
Medicine, Hematological Malignancies
AwardedBy
Columbia University
Role
Principal Investigator
Start Date
August 01, 2016
End Date
July 31, 2017

Plerixafor for allogeneic hematopoietic stem cell transplantation

Administered By
Medicine, Hematological Malignancies
AwardedBy
National Institutes of Health
Role
Principal Investigator
Start Date
August 01, 2014
End Date
June 30, 2016

Transfusion Medicine and Hematology

Administered By
Medicine, Hematology
AwardedBy
National Institutes of Health
Role
Participating Faculty Member
Start Date
July 01, 1975
End Date
June 30, 2016
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Publications:

Outcomes of Maintenance Therapy with Bortezomib after Autologous Stem Cell Transplantation for Patients with Multiple Myeloma.

Comprehensive recommendations for maintenance therapy after autologous stem cell transplantation (ASCT) for patients with multiple myeloma (MM) have yet to be defined. Bortezomib has been utilized as maintenance therapy after ASCT, but data attesting to the safety and efficacy of this agent compared with lenalidomide in the post-ASCT setting are limited. Therefore, we retrospectively analyzed the outcomes of 102 patients with MM who received maintenance therapy with bortezomib after ASCT at Duke University's adult bone marrow transplant clinic between 2005 and 2015. Maintenance with bortezomib was initiated between 60 and 90 days after ASCT as a single agent 1.3 mg/m2 once every 2 weeks (n = 92) or in combination with lenalidomide (10 mg/day) (n = 10). The median age at ASCT was 64 (range, 31 to 78). Of the 99 patients with molecular data available, 42% had high-risk cytogenetics (including d17p, t(4;14), +1q, and t(14;16) by fluorescein in situ hybridization). Overall, 46% of patients experienced side effects from maintenance therapy, with 31% of all patients experiencing peripheral neuropathy. In total, 2% of patients required discontinuation of bortezomib maintenance because of adverse events. No secondary malignancies were reported from the therapy. The median progression-free survival (PFS) for patients receiving maintenance therapy with bortezomib after ASCT was 36.5 months (95% confidence interval [CI], 21.3 to not available) and median overall survival was 72.7 months (95% CI, 63.9 to not available). The PFS of patients with high-risk cytogenetics was not statistically significantly different from those with standard-risk cytogenetics, suggesting that maintenance with bortezomib may help overcome the impact of high-risk cytogenetics on early progression. These results indicate that maintenance therapy with bortezomib represents a safe, well-tolerated, and efficacious option for patients with high-risk cytogenetics, renal insufficiency, an inability to tolerate lenalidomide, or a previous history of another cancer.

Authors
Sivaraj, D; Green, MM; Li, Z; Sung, AD; Sarantopoulos, S; Kang, Y; Long, GD; Horwitz, ME; Lopez, RD; Sullivan, KM; Rizzieri, DA; Chao, NJ; Gasparetto, C
MLA Citation
Sivaraj, D, Green, MM, Li, Z, Sung, AD, Sarantopoulos, S, Kang, Y, Long, GD, Horwitz, ME, Lopez, RD, Sullivan, KM, Rizzieri, DA, Chao, NJ, and Gasparetto, C. "Outcomes of Maintenance Therapy with Bortezomib after Autologous Stem Cell Transplantation for Patients with Multiple Myeloma." Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation 23.2 (February 2017): 262-268.
PMID
27856369
Source
epmc
Published In
Biology of Blood and Marrow Transplantation
Volume
23
Issue
2
Publish Date
2017
Start Page
262
End Page
268
DOI
10.1016/j.bbmt.2016.11.010

Plerixafor (a CXCR4 antagonist) following myeloablative allogeneic hematopoietic stem cell transplantation enhances hematopoietic recovery.

The binding of CXCR4 with its ligand (stromal-derived factor-1) maintains hematopoietic stem/progenitor cells (HSPCs) in a quiescent state. We hypothesized that blocking CXCR4/SDF-1 interaction after hematopoietic stem cell transplantation (HSCT) promotes hematopoiesis by inducing HSC proliferation.We conducted a phase I/II trial of plerixafor on hematopoietic cell recovery following myeloablative allogeneic HSCT. Patients with hematologic malignancies receiving myeloablative conditioning were enrolled. Plerixafor 240 μg/kg was administered subcutaneously every other day beginning day +2 until day +21 or until neutrophil recovery. The primary efficacy endpoints of the study were time to absolute neutrophil count >500/μl and platelet count >20,000/μl. The cumulative incidence of neutrophil and platelet engraftment of the study cohort was compared to that of a cohort of 95 allogeneic peripheral blood stem cell transplant recipients treated during the same period of time and who received similar conditioning and graft-versus-host disease prophylaxis.Thirty patients received plerixafor following peripheral blood stem cell (n = 28) (PBSC) or bone marrow (n = 2) transplantation. Adverse events attributable to plerixafor were mild and indistinguishable from effects of conditioning. The kinetics of neutrophil and platelet engraftment, as demonstrated by cumulative incidence, from the 28 study subjects receiving PBSC showed faster neutrophil (p = 0.04) and platelet recovery >20 K (p = 0.04) compared to the controls.Our study demonstrated that plerixafor can be given safely following myeloablative HSCT. It provides proof of principle that blocking CXCR4 after HSCT enhances hematopoietic recovery. Larger, confirmatory studies in other settings are warranted.ClinicalTrials.gov NCT01280955.

Authors
Green, MMB; Chao, N; Chhabra, S; Corbet, K; Gasparetto, C; Horwitz, A; Li, Z; Venkata, JK; Long, G; Mims, A; Rizzieri, D; Sarantopoulos, S; Stuart, R; Sung, AD; Sullivan, KM; Costa, L; Horwitz, M; Kang, Y
MLA Citation
Green, MMB, Chao, N, Chhabra, S, Corbet, K, Gasparetto, C, Horwitz, A, Li, Z, Venkata, JK, Long, G, Mims, A, Rizzieri, D, Sarantopoulos, S, Stuart, R, Sung, AD, Sullivan, KM, Costa, L, Horwitz, M, and Kang, Y. "Plerixafor (a CXCR4 antagonist) following myeloablative allogeneic hematopoietic stem cell transplantation enhances hematopoietic recovery." Journal of hematology & oncology 9.1 (August 17, 2016): 71-.
PMID
27535663
Source
epmc
Published In
Journal of Hematology and Oncology
Volume
9
Issue
1
Publish Date
2016
Start Page
71
DOI
10.1186/s13045-016-0301-2

Pim1 kinase regulates c-Kit gene translation.

Receptor tyrosine kinase, c-Kit (CD117) plays a pivotal role in the maintenance and expansion of hematopoietic stem/progenitor cells (HSPCs). Additionally, over-expression and/or mutational activation of c-Kit have been implicated in numerous malignant diseases including acute myeloid leukemia. However, the translational regulation of c-Kit expression remains largely unknown.We demonstrated that loss of Pim1 led to specific down-regulation of c-Kit expression in HSPCs of Pim1-/- mice and Pim1-/-2-/-3-/- triple knockout (TKO) mice, and resulted in attenuated ERK and STAT3 signaling in response to stimulation with stem cell factor. Transduction of c-Kit restored the defects in colony forming capacity seen in HSPCs from Pim1-/- and TKO mice. Pharmacologic inhibition and genetic modification studies using human megakaryoblastic leukemia cells confirmed the regulation of c-Kit expression by Pim1 kinase: i.e., Pim1-specific shRNA knockdown down-regulated the expression of c-Kit whereas overexpression of Pim1 up-regulated the expression of c-Kit. Mechanistically, inhibition or knockout of Pim1 kinase did not affect the transcription of c-Kit gene. Pim1 kinase enhanced c-Kit 35S methionine labeling and increased the incorporation of c-Kit mRNAs into the polysomes and monosomes, demonstrating that Pim1 kinase regulates c-Kit expression at the translational level.Our study provides the first evidence that Pim1 regulates c-Kit gene translation and has important implications in hematopoietic stem cell transplantation and cancer treatment.

Authors
An, N; Cen, B; Cai, H; Song, JH; Kraft, A; Kang, Y
MLA Citation
An, N, Cen, B, Cai, H, Song, JH, Kraft, A, and Kang, Y. "Pim1 kinase regulates c-Kit gene translation." Experimental hematology & oncology 5 (January 2016): 31-.
PMID
28042518
Source
epmc
Published In
Experimental Hematology and Oncology
Volume
5
Publish Date
2016
Start Page
31
DOI
10.1186/s40164-016-0060-3

Similar dynamics of intraapheresis autologous CD34+ recruitment and collection efficiency in patients undergoing mobilization with or without plerixafor

Authors
Schade, H; Chhabra, S; Kang, Y; Stuart, RK; Edwards, KH; Kramer, C; Butcher, C; Littleton, A; Schneider, M; Budisavljevic, MN; Costa, LJ
MLA Citation
Schade, H, Chhabra, S, Kang, Y, Stuart, RK, Edwards, KH, Kramer, C, Butcher, C, Littleton, A, Schneider, M, Budisavljevic, MN, and Costa, LJ. "Similar dynamics of intraapheresis autologous CD34+ recruitment and collection efficiency in patients undergoing mobilization with or without plerixafor." Transfusion 54.12 (December 2014): 3131-3137.
Source
crossref
Published In
Transfusion
Volume
54
Issue
12
Publish Date
2014
Start Page
3131
End Page
3137
DOI
10.1111/trf.12761

Inhibition of sphingosine kinase 2 downregulates the expression of c-Myc and Mcl-1 and induces apoptosis in multiple myeloma.

Sphingolipid metabolism is being increasingly recognized as a key pathway in regulating cancer cell survival and proliferation. However, very little is known about its role in multiple myeloma (MM). We investigated the potential of targeting sphingosine kinase 2 (SK2) for the treatment of MM. We found that SK2 was overexpressed in MM cell lines and in primary human bone marrow (BM) CD1381 myeloma cells. Inhibition of SK2 by SK2- specific short hairpin RNA or ABC294640 (a SK2 specific inhibitor) effectively inhibited myeloma cell proliferation and induced caspase 3–mediated apoptosis. ABC294640 inhibited primary human CD1381 myeloma cells with the same efficacy as with MM cell lines. ABC294640 effectively induced apoptosis of myeloma cells, even in the presence of BM stromal cells. Furthermore, we found that ABC294640 downregulated the expression of pS6 and directed c-Myc and myeloid cell leukemia 1 (Mcl-1) for proteasome degradation. In addition, ABC294640 increased Noxa gene transcription and protein expression. ABC294640, per se, did not affect the expression of B-cell lymphoma 2 (Bcl-2), but acted synergistically with ABT-737 (a Bcl-2 inhibitor) in inducing myeloma cell death. ABC294640 suppressed myeloma tumor growth in vivo in mouse myeloma xenograft models. Our data demonstrated that SK2 provides a novel therapeutic target for the treatment of MM.This trial was registered at www.clinicaltrials.gov as #NCT01410981.

Authors
Venkata, JK; An, N; Stuart, R; Costa, LJ; Cai, H; Coker, W; Song, JH; Gibbs, K; Matson, T; Garrett-Mayer, E; Wan, Z; Ogretmen, B; Smith, C; Kang, Y
MLA Citation
Venkata, JK, An, N, Stuart, R, Costa, LJ, Cai, H, Coker, W, Song, JH, Gibbs, K, Matson, T, Garrett-Mayer, E, Wan, Z, Ogretmen, B, Smith, C, and Kang, Y. "Inhibition of sphingosine kinase 2 downregulates the expression of c-Myc and Mcl-1 and induces apoptosis in multiple myeloma." Blood 124.12 (September 2014): 1915-1925.
PMID
25122609
Source
epmc
Published In
Blood
Volume
124
Issue
12
Publish Date
2014
Start Page
1915
End Page
1925
DOI
10.1182/blood-2014-03-559385

Prediction of Poor Mobilization of Autologous CD34+ Cells with Growth Factor in Multiple Myeloma Patients: Implications for Risk-Stratification

Authors
Costa, LJ; Nista, EJ; Buadi, FK; Lacy, MQ; Dispenzieri, A; Kramer, CP; Edwards, KH; Kang, Y; Gertz, MA; Stuart, RK; Kumar, S
MLA Citation
Costa, LJ, Nista, EJ, Buadi, FK, Lacy, MQ, Dispenzieri, A, Kramer, CP, Edwards, KH, Kang, Y, Gertz, MA, Stuart, RK, and Kumar, S. "Prediction of Poor Mobilization of Autologous CD34+ Cells with Growth Factor in Multiple Myeloma Patients: Implications for Risk-Stratification." Biology of Blood and Marrow Transplantation 20.2 (February 2014): 222-228.
Source
crossref
Published In
Biology of Blood and Marrow Transplantation
Volume
20
Issue
2
Publish Date
2014
Start Page
222
End Page
228
DOI
10.1016/j.bbmt.2013.11.003

Thioredoxin and hematologic malignancies.

Thioredoxin (Trx) is an inflammation-inducible small oxidoreductase protein ubiquitously expressed in all organisms. Trx acts both intracellularly and extracellularly and is involved in a wide range of physiological cellular responses. Inside the cell, Trx alleviates oxidative stress by scavenging reactive oxygen species (ROS), regulates a variety of redox-sensitive signaling pathways as well as ROS-independent genes, and exerts cytoprotective effects. Outside the cell, Trx acts as growth factors or cytokines and promotes cell growth and many other cellular responses. Trx is also implicated in tumorigenesis. Trx is a proto-oncogene and is overexpressed in many cancers and correlates with poor prognosis. Trx stimulates cancer cell survival, promotes tumor angiogenesis, and inhibits both spontaneous apoptosis and drug-induced apoptosis. Inhibitors targeting Trx pathway provide a promising therapeutic strategy for cancer prevention and intervention. More recently, data from our laboratory demonstrate an important role of Trx in expanding long-term repopulating hematopoietic stem cells. In this chapter, we first provide an overview of Trx including its isoforms, compartmentation, and functions. We then discuss the roles of Trx in hematologic malignancies. Finally, we summarize the most recent findings from our lab on the use of Trx to enhance hematopoietic reconstitution following hematopoietic stem cell transplantation.

Authors
An, N; Kang, Y
MLA Citation
An, N, and Kang, Y. "Thioredoxin and hematologic malignancies." Advances in cancer research 122 (January 2014): 245-279.
PMID
24974184
Source
epmc
Published In
Advances in cancer research
Volume
122
Publish Date
2014
Start Page
245
End Page
279
DOI
10.1016/b978-0-12-420117-0.00007-4

Senile transthyretin cardiac amyloidosis in patients with plasma cell dyscrasias: importance of cardiac biopsy for making the correct diagnosis.

Amyloidosis refers to a group of widely diverse conditions characterized by the deposition of insoluble protein within the extracellular space, leading to disruption of normal organ function. AL primary amyloidosis is associated with plasma cell dyscrasias and is caused by the deposition of insoluble kappa or lambda light chains. Cardiac involvement by AL primary amyloidosis has a very poor prognosis, and patients are treated with systemic chemotherapy. Clinically, the presence of cardiac amyloidosis in patients with plasma cell disorders is usually presumed to represent AL primary amyloidosis, and they are often managed as such. We reported four cases of elderly patients with plasma cell disorders who were found to have biopsy-proven cardiac senile transthyretin amyloidosis. Our cases demonstrated that cardiac amyloidosis in patients with plasma cell disorders does not necessarily represent AL primary amyloidosis. Cardiac biopsy is important in making the correct diagnosis. Accurate subtyping of the amyloid has significant implications in the management of patients and discussion of prognosis.

Authors
Roof, L; Coker, WJ; Lazarchick, J; Kang, Y
MLA Citation
Roof, L, Coker, WJ, Lazarchick, J, and Kang, Y. "Senile transthyretin cardiac amyloidosis in patients with plasma cell dyscrasias: importance of cardiac biopsy for making the correct diagnosis." Aperito journal of cellular and molecular biology 1.1 (January 2014).
PMID
26618200
Source
epmc
Published In
Aperito journal of cellular and molecular biology
Volume
1
Issue
1
Publish Date
2014

Proteomic analysis of murine bone marrow niche microenvironment identifies thioredoxin as a novel agent for radioprotection and for enhancing donor cell reconstitution

Authors
An, N; Janech, MG; Bland, AM; Lazarchick, J; Arthur, JM; Kang, Y
MLA Citation
An, N, Janech, MG, Bland, AM, Lazarchick, J, Arthur, JM, and Kang, Y. "Proteomic analysis of murine bone marrow niche microenvironment identifies thioredoxin as a novel agent for radioprotection and for enhancing donor cell reconstitution." Experimental Hematology 41.11 (November 2013): 944-956.
Source
crossref
Published In
Experimental Hematology
Volume
41
Issue
11
Publish Date
2013
Start Page
944
End Page
956
DOI
10.1016/j.exphem.2013.08.004

Pim1 Serine/Threonine Kinase Regulates the Number and Functions of Murine Hematopoietic Stem Cells

Authors
An, N; Lin, Y-W; Mahajan, S; Kellner, JN; Wang, Y; Li, Z; Kraft, AS; Kang, Y
MLA Citation
An, N, Lin, Y-W, Mahajan, S, Kellner, JN, Wang, Y, Li, Z, Kraft, AS, and Kang, Y. "Pim1 Serine/Threonine Kinase Regulates the Number and Functions of Murine Hematopoietic Stem Cells." STEM CELLS 31.6 (June 2013): 1202-1212.
Source
crossref
Published In
Stem Cells
Volume
31
Issue
6
Publish Date
2013
Start Page
1202
End Page
1212
DOI
10.1002/stem.1369

Insulin-like growth factor 1 mitigates hematopoietic toxicity after lethal total body irradiation.

To investigate whether and how insulin-like growth factor 1 (IGF-1) mitigates hematopoietic toxicity after total body irradiation.BALB/c mice were irradiated with a lethal dose of radiation (7.5 Gy) and treated with IGF-1 at a dose of 100 μg/dose intravenously once a day for 5 consecutive days starting within 1 hour after exposure. Survival and hematopoietic recovery were monitored. The mechanisms by which IGF-1 promotes hematopoietic recovery were also studied by use of an in vitro culture system.IGF-1 protected 8 of 20 mice (40%) from lethal irradiation, whereas only 2 of 20 mice (10%) in the saline control group survived for more than 100 days after irradiation. A single dose of IGF-1 (500 μg) was as effective as daily dosing for 5 days. Positive effects were noted even when the initiation of treatment was delayed as long as 6 hours after irradiation. In comparison with the saline control group, treatment with IGF-1 significantly accelerated the recovery of both platelets and red blood cells in peripheral blood, total cell numbers, hematopoietic stem cells, and progenitor cells in the bone marrow when measured at day 14 after irradiation. IGF-1 protected both hematopoietic stem cells and progenitor cells from radiation-induced apoptosis and cell death. In addition, IGF-1 was able to facilitate the proliferation and differentiation of nonirradiated and irradiated hematopoietic progenitor cells.IGF-1 mitigates radiation-induced hematopoietic toxicity through protecting hematopoietic stem cells and progenitor cells from apoptosis and enhancing proliferation and differentiation of the surviving hematopoietic progenitor cells.

Authors
Zhou, D; Deoliveira, D; Kang, Y; Choi, SS; Li, Z; Chao, NJ; Chen, BJ
MLA Citation
Zhou, D, Deoliveira, D, Kang, Y, Choi, SS, Li, Z, Chao, NJ, and Chen, BJ. "Insulin-like growth factor 1 mitigates hematopoietic toxicity after lethal total body irradiation." International journal of radiation oncology, biology, physics 85.4 (March 2013): 1141-1148.
PMID
23021438
Source
epmc
Published In
International Journal of Radiation Oncology, Biology, Physics
Volume
85
Issue
4
Publish Date
2013
Start Page
1141
End Page
1148
DOI
10.1016/j.ijrobp.2012.08.014

Abnormal hematopoietic phenotypes in Pim kinase triple knockout mice

Authors
An, N; Kraft, AS; Kang, Y
MLA Citation
An, N, Kraft, AS, and Kang, Y. "Abnormal hematopoietic phenotypes in Pim kinase triple knockout mice." Journal of Hematology & Oncology 6.1 (2013): 12-12.
Source
crossref
Published In
Journal of Hematology and Oncology
Volume
6
Issue
1
Publish Date
2013
Start Page
12
End Page
12
DOI
10.1186/1756-8722-6-12

Using Quantitative Real-time PCR to Determine Donor Cell Engraftment in a Competitive Murine Bone Marrow Transplantation Model

Authors
An, N; Kang, Y
MLA Citation
An, N, and Kang, Y. "Using Quantitative Real-time PCR to Determine Donor Cell Engraftment in a Competitive Murine Bone Marrow Transplantation Model." Journal of Visualized Experiments 73 (2013).
Source
crossref
Published In
Journal of Visualized Experiments
Issue
73
Publish Date
2013
DOI
10.3791/50193

Fact or fiction - identifying the elusive multiple myeloma stem cell

Authors
Kellner, J; Liu, B; Kang, Y; Li, Z
MLA Citation
Kellner, J, Liu, B, Kang, Y, and Li, Z. "Fact or fiction - identifying the elusive multiple myeloma stem cell." Journal of Hematology & Oncology 6.1 (2013): 91-91.
Source
crossref
Published In
Journal of Hematology and Oncology
Volume
6
Issue
1
Publish Date
2013
Start Page
91
End Page
91
DOI
10.1186/1756-8722-6-91

Plasma cell disorders in HIV-infected patients: epidemiology and molecular mechanisms

Authors
Coker, WJ; Jeter, A; Schade, H; Kang, Y
MLA Citation
Coker, WJ, Jeter, A, Schade, H, and Kang, Y. "Plasma cell disorders in HIV-infected patients: epidemiology and molecular mechanisms." Biomarker Research 1.1 (2013): 8-8.
Source
crossref
Published In
Biomarker Research
Volume
1
Issue
1
Publish Date
2013
Start Page
8
End Page
8
DOI
10.1186/2050-7771-1-8

In vivo BrdU Incorporation Assay for Murine Hematopioetic Stem Cells

Authors
An, N; Kang, Y
MLA Citation
An, N, and Kang, Y. "In vivo BrdU Incorporation Assay for Murine Hematopioetic Stem Cells." (2013).
Source
manual
Publish Date
2013

Association of age with fluorescence in situ hybridization abnormalities in multiple myeloma reveals higher rate of IGH translocations among older patients

Authors
Butler, C; Wolff, DJ; Kang, Y; Stuart, RK; Costa, LJ
MLA Citation
Butler, C, Wolff, DJ, Kang, Y, Stuart, RK, and Costa, LJ. "Association of age with fluorescence in situ hybridization abnormalities in multiple myeloma reveals higher rate of IGH translocations among older patients." Leukemia & Lymphoma 53.12 (December 2012): 2444-2448.
Source
crossref
Published In
Leukemia & Lymphoma (Informa)
Volume
53
Issue
12
Publish Date
2012
Start Page
2444
End Page
2448
DOI
10.3109/10428194.2012.691483

Outcomes of patients with multiple myeloma and renal impairment treated with bortezomib, cyclophosphamide, and dexamethasone without plasma exchange

Authors
Costa, LJ; Abbas, J; Ortiz-Cruz, KL; Kang, Y; Stuart, RK
MLA Citation
Costa, LJ, Abbas, J, Ortiz-Cruz, KL, Kang, Y, and Stuart, RK. "Outcomes of patients with multiple myeloma and renal impairment treated with bortezomib, cyclophosphamide, and dexamethasone without plasma exchange." European Journal of Haematology 89.5 (November 2012): 432-434.
Source
crossref
Published In
European Journal of Haematology
Volume
89
Issue
5
Publish Date
2012
Start Page
432
End Page
434
DOI
10.1111/ejh.12008

Growth factor plus preemptive (‘just-in-time’) plerixafor successfully mobilizes hematopoietic stem cells in multiple myeloma patients despite prior lenalidomide exposure

Authors
Costa, LJ; Abbas, J; Hogan, KR; Kramer, C; McDonald, K; Butcher, CD; Littleton, A; Shoptaw, K; Kang, Y; Stuart, RK
MLA Citation
Costa, LJ, Abbas, J, Hogan, KR, Kramer, C, McDonald, K, Butcher, CD, Littleton, A, Shoptaw, K, Kang, Y, and Stuart, RK. "Growth factor plus preemptive (‘just-in-time’) plerixafor successfully mobilizes hematopoietic stem cells in multiple myeloma patients despite prior lenalidomide exposure." Bone Marrow Transplantation 47.11 (November 2012): 1403-1408.
Source
crossref
Published In
Bone Marrow Transplantation
Volume
47
Issue
11
Publish Date
2012
Start Page
1403
End Page
1408
DOI
10.1038/bmt.2012.60

Pegfilgrastim- versus filgrastim-based autologous hematopoietic stem cell mobilization in the setting of preemptive use of plerixafor: efficacy and cost analysis

Authors
Costa, LJ; Kramer, C; Hogan, KR; Butcher, CD; Littleton, AL; Shoptaw, KB; Kang, Y; Stuart, RK
MLA Citation
Costa, LJ, Kramer, C, Hogan, KR, Butcher, CD, Littleton, AL, Shoptaw, KB, Kang, Y, and Stuart, RK. "Pegfilgrastim- versus filgrastim-based autologous hematopoietic stem cell mobilization in the setting of preemptive use of plerixafor: efficacy and cost analysis." Transfusion 52.11 (November 2012): 2375-2381.
Source
crossref
Published In
Transfusion
Volume
52
Issue
11
Publish Date
2012
Start Page
2375
End Page
2381
DOI
10.1111/j.1537-2995.2012.03579.x

Strategies to enhance hematopoietic stem cell engraftment following transplantation

© Springer Science+Business Media, LLC 2012.Following intravenous infusion of hematopoietic stem/progenitor cells (HSPCs) during hematopoietic cell transplantation (HCT), HSPCs home to and engraft in marrow niche microenvironment, which ultimately leads to reconstitution of whole immunological and hematological repertoire of the recipient. The homing and engraftment of HSPCs occur relatively early (during the initial stage of HCT), but have major impacts on the success and outcomes of transplantation. HSPC homing and engraftment require well-coordinated interplay involving various cells (endothelial cells, osteoblasts, osteoclasts, and other mesenchymal stem cells), cytokines and chemokines, soluble and membrane-bound factors, as well as extracellular matrix. Many aspects and the detailed mechanisms regulating HSPC homing and engraftment still remain to be elucidated. In this chapter, we first provide a brief overview of HSPC homing and engraftment processes and the interactions between HSPCs and various cell types and different molecules in the niche microenvironment. We then summarize several strategies to enhance HSPC homing and engraftment during HCT. In particular, we present ongoing studies in our laboratories using CXCR4 antagonists to enhance donor cell engraftment following HCT.

Authors
Kang, Y; Chao, NJ
MLA Citation
Kang, Y, and Chao, NJ. "Strategies to enhance hematopoietic stem cell engraftment following transplantation." Novel Developments in Stem Cell Mobilization: Focus on CXCR4. January 1, 2012. 439-456.
Source
scopus
Publish Date
2012
Start Page
439
End Page
456
DOI
10.1007/978-1-4614-1960-0_23

Immune modulation therapy in the management of bortezomib-induced peripheral neuropathy

Authors
Jeter, A; Kang, Y
MLA Citation
Jeter, A, and Kang, Y. "Immune modulation therapy in the management of bortezomib-induced peripheral neuropathy." Experimental Hematology & Oncology 1.1 (2012): 20-20.
Source
crossref
Published In
Experimental Hematology and Oncology
Volume
1
Issue
1
Publish Date
2012
Start Page
20
End Page
20
DOI
10.1186/2162-3619-1-20

Selective enhancement of donor hematopoietic cell engraftment by the CXCR4 antagonist AMD3100 in a mouse transplantation model.

The interaction between stromal cell-derived factor-1 (SDF-1) with CXCR4 chemokine receptors plays an important role in hematopoiesis following hematopoietic stem cell transplantation. We examined the efficacy of post transplant administration of a specific CXCR4 antagonist (AMD3100) in improving animal survival and in enhancing donor hematopoietic cell engraftment using a congeneic mouse transplantation model. AMD3100 was administered subcutaneously at 5 mg/kg body weight 3 times a week beginning at day +2 post-transplant. Post-transplant administration of AMD3100 significantly improves animal survival. AMD3100 reduces pro-inflammatory cytokine/chemokine production. Furthermore, post transplant administration of AMD3100 selectively enhances donor cell engraftment and promotes recovery of all donor cell lineages (myeloid cells, T and B lymphocytes, erythrocytes and platelets). This enhancement results from a combined effect of increased marrow niche availability and greater cell division induced by AMD3100. Our studies shed new lights into the biological roles of SDF-1/CXCR4 interaction in hematopoietic stem cell engraftment following transplantation and in transplant-related mortality. Our results indicate that AMD3100 provides a novel approach for enhancing hematological recovery following transplantation, and will likely benefit patients undergoing transplantation.

Authors
Kang, Y; Chen, BJ; Deoliveira, D; Mito, J; Chao, NJ
MLA Citation
Kang, Y, Chen, BJ, Deoliveira, D, Mito, J, and Chao, NJ. "Selective enhancement of donor hematopoietic cell engraftment by the CXCR4 antagonist AMD3100 in a mouse transplantation model." PloS one 5.6 (June 28, 2010): e11316-.
Website
http://hdl.handle.net/10161/5087
PMID
20596257
Source
epmc
Published In
PloS one
Volume
5
Issue
6
Publish Date
2010
Start Page
e11316
DOI
10.1371/journal.pone.0011316

Immune reconstitution

Authors
Kang, Y; Chao, N
MLA Citation
Kang, Y, and Chao, N. "Immune reconstitution." Hematopoietic Stem Cell Transplantation A Handbook for Clinicians. Ed. JR Wingard, D Gastineau, H Leather, EC Snyder, and ZM Szczepiokowski. Bethesda, MD: AABB Press, 2010. 181-196. (Chapter)
Source
manual
Publish Date
2010
Start Page
181
End Page
196

Unmanipulated or CD34 selected haplotype mismatched transplants.

Unmanipulated or CD34 selected haplotype mismatched transplantation provides the benefits of hematopoietic stem cell transplant for nearly all patients who do not have a human leukocyte antigen fully matched sibling or who urgently need transplantation. Haplotype mismatched transplant is, however, complicated by delayed immune reconstitution, leading to increased risks of fatal posttransplant opportunistic infections. This review summarizes recent investigations aimed at optimizing outcomes.The graft is a megadose of positively/negatively T-cell-depleted or unmanipulated progenitor cells. Although haploidentical transplant modalities are based mainly on high-intensity conditioning regimens, recently introduced reduced-intensity regimens showed promise in decreasing early transplant-related mortality and in extending the opportunity of hematopoietic stem cell transplantation to an elderly population with more comorbidities. Natural killer cell alloreactivity reduces graft-versus-host disease while augmenting graft-versus-malignancy. Immune reconstitution was highly predictive of outcome following T-cell-depleted transplantation.Mismatched/haploidentical transplant provides an alternative approach for patients with high-risk hematological malignancies or marrow failure syndromes. Overall survival and clinical outcome continue to improve. Future challenges lie in determining the safest preparative conditioning regimen, minimizing graft-versus-host disease while preserving effective graft-versus-malignancy and promoting rapid immune reconstitution.

Authors
Kang, Y; Chao, NJ; Aversa, F
MLA Citation
Kang, Y, Chao, NJ, and Aversa, F. "Unmanipulated or CD34 selected haplotype mismatched transplants." Current opinion in hematology 15.6 (November 2008): 561-567.
PMID
18832926
Source
epmc
Published In
Current Opinion in Hematology
Volume
15
Issue
6
Publish Date
2008
Start Page
561
End Page
567
DOI
10.1097/moh.0b013e32831366eb

Integration Site Choice of a Feline Immunodeficiency Virus Vector

Authors
Kang, Y; Moressi, CJ; Scheetz, TE; Xie, L; Tran, DT; Casavant, TL; Ak, P; Benham, CJ; Davidson, BL; McCray, PB
MLA Citation
Kang, Y, Moressi, CJ, Scheetz, TE, Xie, L, Tran, DT, Casavant, TL, Ak, P, Benham, CJ, Davidson, BL, and McCray, PB. "Integration Site Choice of a Feline Immunodeficiency Virus Vector." Journal of Virology 80.17 (September 1, 2006): 8820-8823.
Source
crossref
Published In
Journal of virology
Volume
80
Issue
17
Publish Date
2006
Start Page
8820
End Page
8823
DOI
10.1128/JVI.00719-06

Persistent expression of factor VIII in vivo following nonprimate lentiviral gene transfer

Authors
Kang, Y
MLA Citation
Kang, Y. "Persistent expression of factor VIII in vivo following nonprimate lentiviral gene transfer." Blood 106.5 (September 1, 2005): 1552-1558.
Source
crossref
Published In
Blood
Volume
106
Issue
5
Publish Date
2005
Start Page
1552
End Page
1558
DOI
10.1182/blood-2004-11-4358

Retroviral delivery of GAD-IgG fusion construct induces tolerance and modulates diabetes: a role for CD4+ regulatory T cells and TGF-β?

Authors
Song, L; Wang, J; Wang, R; Yu, M; Sun, Y; Han, G; Li, Y; Qian, J; Scott, DW; Kang, Y; Soukhareva, N; Shen, B
MLA Citation
Song, L, Wang, J, Wang, R, Yu, M, Sun, Y, Han, G, Li, Y, Qian, J, Scott, DW, Kang, Y, Soukhareva, N, and Shen, B. "Retroviral delivery of GAD-IgG fusion construct induces tolerance and modulates diabetes: a role for CD4+ regulatory T cells and TGF-β?." Gene Therapy 11.20 (October 2004): 1487-1496.
Source
crossref
Published In
Gene Therapy
Volume
11
Issue
20
Publish Date
2004
Start Page
1487
End Page
1496
DOI
10.1038/sj.gt.3302327

CCL20 Is an Inducible Product of Human Airway Epithelia with Innate Immune Properties

Authors
Starner, TD; Barker, CK; Jia, HP; Kang, Y; McCray, PB
MLA Citation
Starner, TD, Barker, CK, Jia, HP, Kang, Y, and McCray, PB. "CCL20 Is an Inducible Product of Human Airway Epithelia with Innate Immune Properties." American Journal of Respiratory Cell and Molecular Biology 29.5 (November 2003): 627-633.
Source
crossref
Published In
American journal of respiratory cell and molecular biology
Volume
29
Issue
5
Publish Date
2003
Start Page
627
End Page
633
DOI
10.1165/rcmb.2002-0272OC

In Vivo Gene Transfer Using a Nonprimate Lentiviral Vector Pseudotyped with Ross River Virus Glycoproteins

Authors
Kang, Y; Stein, CS; Heth, JA; Sinn, PL; Penisten, AK; Staber, PD; Ratliff, KL; Shen, H; Barker, CK; Martins, I; Sharkey, CM; Sanders, DA; McCray, PB; Davidson, BL
MLA Citation
Kang, Y, Stein, CS, Heth, JA, Sinn, PL, Penisten, AK, Staber, PD, Ratliff, KL, Shen, H, Barker, CK, Martins, I, Sharkey, CM, Sanders, DA, McCray, PB, and Davidson, BL. "In Vivo Gene Transfer Using a Nonprimate Lentiviral Vector Pseudotyped with Ross River Virus Glycoproteins." Journal of Virology 76.18 (September 15, 2002): 9378-9388.
Source
crossref
Published In
Journal of virology
Volume
76
Issue
18
Publish Date
2002
Start Page
9378
End Page
9388
DOI
10.1128/JVI.76.18.9378-9388.2002

Gene transfer of immunoglobulin-fusion proteins prevents and treats autoimmune diseases

Authors
Melo, MEF; Qian, J; El-Amine, M; Soukhareva, N; Kang, Y; Scott, DW
MLA Citation
Melo, MEF, Qian, J, El-Amine, M, Soukhareva, N, Kang, Y, and Scott, DW. "Gene transfer of immunoglobulin-fusion proteins prevents and treats autoimmune diseases." J. Immunol 168.9 (2002): 4788-4795.
Source
manual
Published In
J. Immunol
Volume
168
Issue
9
Publish Date
2002
Start Page
4788
End Page
4795

In vivo treatment of hemophilia A and mucopolysaccharidosis type VII using non-primate lentiviral vectors

Authors
Stein, CS; Kang, Y; Sauter, SL; Townsend, K; Staber, P; Derken, TA; Martins, I; Qian, J; Davidson, BL; McCray, PB
MLA Citation
Stein, CS, Kang, Y, Sauter, SL, Townsend, K, Staber, P, Derken, TA, Martins, I, Qian, J, Davidson, BL, and McCray, PB. "In vivo treatment of hemophilia A and mucopolysaccharidosis type VII using non-primate lentiviral vectors." Molecular Therapy 3 (2001): 850-856.
Source
manual
Published In
Molecular Therapy
Volume
3
Publish Date
2001
Start Page
850
End Page
856

Retroviral gene therapy with an immunoglobulin-antigen fusion construct protects from experimental autoimmune uveitis

Authors
Agarwal, RK; Kang, Y; Zambidis, E; Scott, DW; Chan, C-C; Caspi, RR
MLA Citation
Agarwal, RK, Kang, Y, Zambidis, E, Scott, DW, Chan, C-C, and Caspi, RR. "Retroviral gene therapy with an immunoglobulin-antigen fusion construct protects from experimental autoimmune uveitis." Journal of Clinical Investigation 106.2 (July 15, 2000): 245-252.
Source
crossref
Published In
Journal of Clinical Investigation
Volume
106
Issue
2
Publish Date
2000
Start Page
245
End Page
252
DOI
10.1172/JCI9168

Mechanisms of tolerance induction by an Ig-peptide molecule expressed and secreted by B cells

Authors
El-Amine, M; Melo, MEF; Kang, Y; Qian, J; Scott, DW
MLA Citation
El-Amine, M, Melo, MEF, Kang, Y, Qian, J, and Scott, DW. "Mechanisms of tolerance induction by an Ig-peptide molecule expressed and secreted by B cells." Journal of immunology (Baltimore, Md. : 1950) 165 (2000): 5631-5636.
Source
manual
Published In
Journal of immunology (Baltimore, Md. : 1950)
Volume
165
Publish Date
2000
Start Page
5631
End Page
5636

Induction of hyporesponsiveness to intact foreign protein via retroviral-mediated gene expression: The IgG scaffold is important for induction and maintenance of immune hyporesponsiveness

Authors
Kang, Y; Melo, M; Deng, E; Tisch, R; El-Amine, M; Scott, DW
MLA Citation
Kang, Y, Melo, M, Deng, E, Tisch, R, El-Amine, M, and Scott, DW. "Induction of hyporesponsiveness to intact foreign protein via retroviral-mediated gene expression: The IgG scaffold is important for induction and maintenance of immune hyporesponsiveness." Proceedings of the National Academy of Sciences 96.15 (July 20, 1999): 8609-8614.
Source
crossref
Published In
Proceedings of the National Academy of Sciences of USA
Volume
96
Issue
15
Publish Date
1999
Start Page
8609
End Page
8614
DOI
10.1073/pnas.96.15.8609

An Ongoing Immune Response to HIV Envelope gp120 in Human CD4 Transgenic Mice Contributes to T Cell Decline upon Intravenous Administration of gp120

Authors
Kang, Y; Melo, MEF; Scott, DW
MLA Citation
Kang, Y, Melo, MEF, and Scott, DW. "An Ongoing Immune Response to HIV Envelope gp120 in Human CD4 Transgenic Mice Contributes to T Cell Decline upon Intravenous Administration of gp120." European Journal of Immunology 28 (1998): 2253-2264.
Source
manual
Published In
European Journal of Immunology
Volume
28
Publish Date
1998
Start Page
2253
End Page
2264

Effect of methylglyoxal on human leukaemia 60 cell growth: Modification of DNA, G1 growth arrest and induction of apoptosis

Authors
Kang, Y; Edwards, LG; Thornalley, PJ
MLA Citation
Kang, Y, Edwards, LG, and Thornalley, PJ. "Effect of methylglyoxal on human leukaemia 60 cell growth: Modification of DNA, G1 growth arrest and induction of apoptosis." Leukemia Research 20.5 (May 1996): 397-405.
Source
crossref
Published In
Leukemia Research
Volume
20
Issue
5
Publish Date
1996
Start Page
397
End Page
405
DOI
10.1016/0145-2126(95)00162-X

Anti-tumor Activity of S-(p-bromobenzyl)glutathione Diesters in vitro: a Structure-Activity Study

Authors
Thornalley, PJ; Ladan, M; Ridgeway, S; Kang, Y
MLA Citation
Thornalley, PJ, Ladan, M, Ridgeway, S, and Kang, Y. "Anti-tumor Activity of S-(p-bromobenzyl)glutathione Diesters in vitro: a Structure-Activity Study." Journal of Medicinal Chemistry 39.17 (1996): 3409-3411.
Source
manual
Published In
Journal of Medicinal Chemistry
Volume
39
Issue
17
Publish Date
1996
Start Page
3409
End Page
3411

Anti-tumor Activity of S- (p-bromobenzyl)glutathione Cyclopentyl Diesters In Vitro and In Vivo: Inhibition of Glyoxalase I and Induction of Apoptosis

Authors
Thornalley, PJ; Edwards, L; Kang, Y; Wyatt, C; Davies, N; Ladan, MJ; Double, J
MLA Citation
Thornalley, PJ, Edwards, L, Kang, Y, Wyatt, C, Davies, N, Ladan, MJ, and Double, J. "Anti-tumor Activity of S- (p-bromobenzyl)glutathione Cyclopentyl Diesters In Vitro and In Vivo: Inhibition of Glyoxalase I and Induction of Apoptosis." Biochemical Pharmacology 51.10 (1996): 1365-1372.
Source
manual
Published In
Biochemical Pharmacology
Volume
51
Issue
10
Publish Date
1996
Start Page
1365
End Page
1372

A Handbook of Human Cytokines

Authors
Kang, Y; Cheng, YB
MLA Citation
Kang, Y, and Cheng, YB. "A Handbook of Human Cytokines." Interleukin-3. Ed. J He and DX Wang. China: Tong Zi University Press, 1996. 79-96. (Chapter)
Source
manual
Publish Date
1996
Start Page
79
End Page
96

Interleukin-4

Authors
Kang, Y; He, J
MLA Citation
Kang, Y, and He, J. "Interleukin-4." A Handbook of Human Cytokines. Ed. J He and DX Wang. China: Tong Zi University Press, 1996. 97-112. (Chapter)
Source
manual
Publish Date
1996
Start Page
97
End Page
112

Monitoring of Blood Cyclosporine A Concentration and Clinical Observation in Patients with HLA-semimatched Bone Marrow Transplantation

Authors
Kang, Y; Gu, CN; Meng, PL; Cao, LX; Huang, LA
MLA Citation
Kang, Y, Gu, CN, Meng, PL, Cao, LX, and Huang, LA. "Monitoring of Blood Cyclosporine A Concentration and Clinical Observation in Patients with HLA-semimatched Bone Marrow Transplantation." Ed. BT Liu and GY Ye. (1994): 402-409.
Source
manual
Publish Date
1994
Start Page
402
End Page
409

Capillary Leakage Syndrome Associated with Acute Radiation Disease

Authors
Kang, Y; Zing, SW; Meng, PL; Cao, LX; Huang, LA
MLA Citation
Kang, Y, Zing, SW, Meng, PL, Cao, LX, and Huang, LA. "Capillary Leakage Syndrome Associated with Acute Radiation Disease." Ed. BT Liu and GY Ye. (1994): 311-314.
Source
manual
Publish Date
1994
Start Page
311
End Page
314

Clinical Observation and Prevention of Coagulation Abnormality in 7 Cases of Patients with Acute Radiation Sickness

Authors
Huang, LA; Meng, PL; Kang, Y; Cheng, QS; Liu, BT
MLA Citation
Huang, LA, Meng, PL, Kang, Y, Cheng, QS, and Liu, BT. "Clinical Observation and Prevention of Coagulation Abnormality in 7 Cases of Patients with Acute Radiation Sickness." Ed. BT Liu and GY Ye. (1994): 348-356.
Source
manual
Publish Date
1994
Start Page
348
End Page
356

Cytomegalovirus Infection in Bone Marrow Transplant Patients with Acute Radiation Sickness

Authors
Huang, LA; Cheng, QS; Kang, Y; Li, YH
MLA Citation
Huang, LA, Cheng, QS, Kang, Y, and Li, YH. "Cytomegalovirus Infection in Bone Marrow Transplant Patients with Acute Radiation Sickness." Ed. BT Liu and GY Ye. (1994): 315-319.
Source
manual
Publish Date
1994
Start Page
315
End Page
319

Tumor Cell Surface Markers and Differentiation on Multiple Myeloma

Authors
Kang, Y; Yu, RQ; Kong, XT
MLA Citation
Kang, Y, Yu, RQ, and Kong, XT. "Tumor Cell Surface Markers and Differentiation on Multiple Myeloma." Chinese Journal of Hematology 7 (1992): 384-387. (Review)
Source
manual
Published In
Chinese Journal of Hematology
Volume
7
Publish Date
1992
Start Page
384
End Page
387

Hypertension Associated with Cyclosporine A Treatment in Bone Marrow Transplantation

Authors
Kang, Y; Yu, RQ
MLA Citation
Kang, Y, and Yu, RQ. "Hypertension Associated with Cyclosporine A Treatment in Bone Marrow Transplantation." Foreign Medicine (Blood Transfusion & Hematology) 5 (1991): 288-291. (Review)
Source
manual
Published In
Foreign Medicine (Blood Transfusion & Hematology)
Volume
5
Publish Date
1991
Start Page
288
End Page
291

Therapeutic Progress in Multiple Myeloma

Authors
Kang, Y; Yu, RQ
MLA Citation
Kang, Y, and Yu, RQ. "Therapeutic Progress in Multiple Myeloma." Foreign Medicine (Blood Transfusion & Hematology) 3 (1990): 140-143. (Review)
Source
manual
Published In
Foreign Medicine (Blood Transfusion & Hematology)
Volume
3
Publish Date
1990
Start Page
140
End Page
143
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