• Ochsenbauer C 2014Rank:
    Assistant Professor 

    Division:

    Hematology & Oncology

    Campus Address:
    LHRB 611

    Phone:
    (205) 975-7872

    Email:
    christinaochsenbauer@uabmc.edu


    Departmental Affiliation(s):
    Primary: Medicine

    In her post-graduate work Dr. Ochsenbauer trained as a molecular retrovirologist with Dr. Eric Hunter at UAB. She studied intracellular trafficking pathways of retroviral Env glycoproteins (1, 2) and developed the first neutralizing monoclonal antibody directed against the avian Rous Sarcoma Virus Env glycoprotein (3) as well as its receptor. These reagents have proven valuable both for basic research as well as for animal models employing retroviral vector approaches (4).

    Returning to HIV-1 research, Dr. Ochsenbauer pursued her interest in the interaction of HIV-1 with cells of mucosal origins (5) and began developing novel robust tools to study HIV-1 infection and inhibition thereof (6). She joined the Division of Hematology/Oncology in mid-2006 as an Assistant Professor to establish a new research program within the Mucosal Immunity Discovery Team of the NIH-funded CHAVI (Center for HIV/AIDS Vaccine Immunology). Dr. Ochsenbauer's work in this area is providing fundamental underpinning to HIV/AIDS vaccine research as it has resulted in the generation and initial biological characterization of the first infectious HIV-1 molecular clones representing nucleotide-exact copies of bona fide mucosally transmitted viruses (Ochsenbauer-Jambor et al., in preparation). Using these transmitted/founder viruses, Dr. Ochsenbauer has established multidisciplinary research collaborations to investigate viral and cellular factors that affect mucosal HIV-1 transmission. With new funding from the Gates Foundation's CAVD (Collaboration for AIDS Vaccine Discovery), Dr. Ochsenbauer is working towards standardization of newly developed state-of-the-art assay methods (Edmonds et al., submitted) which will facilitate monitoring HIV/AIDS vaccine efficacy and the elicitation of broadly neutralizing antibodies.
  • Tabengwa Edlue - Copy smallRank:
    Assistant Professor

    Division:

    Hematology & Oncology

    Campus Address:
    SHEL 420

    Phone:
    (205) 975-0963

    Email:
    tabengwa@uab.edu

    Departmental Affiliation(s):
    Primary: Medicine

    Biosketch:

    Research Interests:
    Dr. Tabengwa joined Dr. Randall Davis’ laboratory July 1, 2010 as an Assistant Professor with a strong scientific background to help establish and lead the management of a new facility on campus termed the Multidisciplinary Molecular Interaction Core (MMIC). This facility supports an NIH-funded Biacore T200 instrument that enables the characterization of protein-protein and other biomolecular interactions by surface plasmon resonance (SPR) technology. She has led in the establishment of this facility and instrumentation which has quickly grown under her management. She currently manages and operates the instrument, trains and educates new and established users, and analyzes data generated from this valuable resource for a current user base of eight different laboratories including Dr. Davis’.

    Publications:

    1. Li X.N., Varma V.K., Parks J.M., Benza R.L., Koons J.C., Grammer J.R., Grenett H.E., Tabengwa E.M., Booyse F.M.: Thrombin decreases the urokinase receptor and surface-localized fibrinolysis in cultured endothelial cells. (1995) Arterioscler Thromb Vasc Biol.15: 410-419. PMID:7749851
    2. Li X.N., Koons J.C., Benza R.L., Parks J.M., Varma V.K., Bradley W.A., Gianturco S.H., Taylor K.B., Grammer J.R., Tabengwa E.M., Booyse F.M.: Hypertriglyceridemic VLDL decreases plasminogen binding to endothelial cells and surface-localized fibrinolysis. (1996) Biochemistry35: 6080-6088. PMID:8634250
    3. Aikens M.L., Grenett H.E., Benza R.L., Tabengwa E.M., Davis G.C., Demissie S., Booyse F.M.: Ethanol increases surface-localized fibrinolytic activity in cultured endothelial cells. (1997) Alcohol Clin Exp Res.21: 1471-1478. PMID:9394120
    4. Li X.N., Grenett H.E., Benza R.L., Demissie S., Brown S.L., Tabengwa E.M., Bradley W.A., Gianturco S.H., Fless G.M., Booyse F.M.: Genotype-specific transcriptional regulation of PAI-1 expression by hypertriglyceridemic (HTG)-VLDL and Lp(a) in cultured human endothelial cells. (1997) Arterioscler Thromb Vasc Biol. 17: 3215-3223. PMID:9409314
    5. Grenett H.E., Aikens M.L., Tabengwa E.M., Davis G.C., Booyse F.M.: Ethanol downregulates transcription of the PAI-1 gene in cultured human endothelial cells. (2000) Thromb Res. 97:247-255. PMID:10674412
    6. Tabengwa E.M., Abou-Agag L.H., Benza R.L., Torres J.A. Aikens M.L., Booyse F.M.: Ethanol-induced upregulation of candidate plasminogen receptor annexin II in cultured human endothelial cells. (2000) Alcohol Clin Exp Res. 24(6):754-761. PMID:10888061
    7. Tabengwa E.M., Benza R.L., Grenett H.E., Booyse F.M.: Hypertriglyceridemic VLDL downregulates tissue plasminogen activator gene transcription though cis-repressive region(s) in the tissue plasminogen activator promoter in cultured human endothelial cells. (2000) Arterioscler Thromb Vasc Biol. 20(6):1675-1681. PMID:10845888
    8. Tabengwa E.M., Grenett H.E., Benza, R.L., Abou-Agag L.H., Tresnak, J.A., Wheeler C.G., Booyse F.M.: Ethanol-induced upregulation of the urokinase receptor in cultured human endothelial cells. (2001) Alcohol Clin Exp Res. 25 (2):163-170. PMID:11236828.
    9. Abou-Agag L.H., Tabengwa E.M., Tresnak, J.A., Wheeler C.G., Taylor K.B., Booyse F.M.: Ethanol-Induced Increased Surface-Localized Fibrinolytic Activity in Cultured Human Endothelial Cells: Kinetic Analysis. (2001) Alcohol Clin Exp Res. 25 (3):351-361. PMID:11290845
    10. Tabengwa E.M., Wheeler C.G., Yancey D.A., Grenett H.E., Booyse F.M.: Alcohol-induced upregulation of fibrinolytic activity and plasminogen activators in cultured human monocytes. (2002) Alcohol Clin Exp Res. 26: (8) 1121-1127. PMID:12198385
    11. Schmidt E., Wehr B., Tabengwa E.M., Reimer S., Brocker E.B., Zillikens D.: Elevated expression and release of tissue-type, but not urokinase-type plasminogen activator, after binding of autoantibodies to bullous pemphigoid antigen 180 in cultured human keratinocytes. (2004) Clin Exp Immunol. 135: 497-504. PMID:15008985
    12. Booyse F.M., Pan W., Grenett H.E., Parks D.A., Darley-Usmar V.M., Bradley K.M., Tabengwa EM: Mechanism by which alcohol and wine polyphenols affect coronary heart disease risk. (2007) Annals of Epidemiol. 17(S5): S24-S31. PMID:17478321
    13. Pasten C., Olave N.C., Zhou L., Tabengwa E.M., Wolkowicz P.E., Grenett H.E.:   Polyphenols downregulate PAI-1 gene expression in cultured human coronary artery endothelial cells: Molecular contributor to cardiovascular protection. (2007) Thromb Res. 121 (1): 59-65. PMID:17379280
    14. Pan W., Chang M.J., Booyse F.M., Grenett H.M., Bradley K.M., Wolkowizc P.E., Chang Q., Tabengwa E.M.: Quercetin induced tissue plasminogen activator expression is mediated through Sp1 and p38 mitogen activated protein kinase in human endothelial cells. (2008) J Throb Haemost. (6): 976-985. PMID:18419748
    15. Wolkowicz P.E., Huang J., Umeda P.K., Sharifov O.F., Tabengwa E., Halloran B.A., Urthaler F., Grenett H.E.: Pharmacological evidence for Orai channel activation as a source of cardiac abnormal automaticity. (2011) Eur J Pharmacol.668(1-2):208-16. PMID:217454
  • Rank:                    
    Assistant Professor

    Division:
                   
    Hematology & Oncology

    Campus Address:
    WTI 520A

    Mailing Address:  
    1720 2nd Avenue South, WTI 520B
    Birmingham, AL 35294-3300

    Phone:                   
    (205) 996-9241


    Departmental Affiliation(s):
    Primary: Medicine, Hematology/Oncology


    EDUCATION             

    9/1981- 7/1986  M.D., Zhejiang University School of Medicine, China

    8/1986- 12/1991 Residency training, Department of Obstetrics and Gynecology, 3rd Hospital of Ningbo and Hangzhou, Zhejiang, China

    9/1993- 8/1994  Fellowship, Gynecologic Oncology, Women Hospital, Zhejiang University School of Medicine, Hangzhou, Zhejiang, China     


    Professional experience

    5/1998-6/2006 Research Associate (II and III), Laboratory Manager, Division of Surgical Oncology, Department of Surgery, David Geffen School of Medicine, University of California at Los Angeles (Dr. Helena Chang)  
              
    7/2006-7/2012   Assistant Research Scientist IV, Laboratory Manager, Gonda /UCLA Breast Cancer Research Laboratory, Division of Surgical Oncology, Department of Surgery, David Geffen School of Medicine, University of California at Los Angeles (Dr. Helena Chang)
                              
    8/2012- 1/2014 Research Associate, Department of Pathology -Molecular & Cellular Pathology, University of Alabama at Birmingham (Dr. Ralph Sanderson)

    3/2014- 3/2017   Researcher V, Laboratory Manager, Department of Medicine-Hematology & Oncology, University of Alabama at Birmingham (Dr. Ravi Bhatia)                          

    4/2017- current   Assistant Professor, Laboratory Manager, Department of Medicine-Hematology & Oncology, University of Alabama at Birmingham (Dr. Ravi Bhatia)                                                                           


    SELECTED PUBLICATIONS
    1. Ramani VCZhan F,  He JBarbieri PNoseda ATricot GSanderson RD. Targeting heparanase overcomes chemoresistance and diminishes relapse in myeloma. 2016 Jan 12;7(2):1598-607. PMID: 26624982
    2. Ping Z, Xia Y, Shen T, Parekh V, Siegal GP, Eltoum IE, He J, Chen D, Deng M, Xi R, Shen D. A microscopic landscape of the invasive breast cancer genome. Sci Rep. 2016; 6: 27545. PMID: 27283966
    3. Ping Z, Siegal GP, Harada S, Eltoum IE, Youssef M, Shen T, He J, Huang Y, Chen D, Li Y, Bland KI, Chang HR, Shen D. ERBB2 mutation is associated with a worse prognosis in patients with CDH1 altered invasive lobular cancer of the breast. Oncotarget. 2016 Dec 6; 7(49):80655-80663. PMID: 27811364
    4. Gibson CJ, Lindsley CR, Tchekmedyian V, Mar B, Shi J, Jaiswal S, Bosworth A, Francisco LF, He J, Morgan E, Lacasce A, Koreth J, Ho V, Soiffer R, Antin J, Ritz J, Nikiforow S, Forman SJ, Michor F, Neuberg D, Bhatia R, Bhatia S, Ebert B L. Clonal hematopoiesis associated with adverse outcomes following autologous stem cell transplantation for lymphoma. J Clin Oncol. 2017 May 10;35(14):1598-1605. PMID: 28068180


    Publications:See a listing of publications on PubMed, a service of the National Library of Medicine.

  • Rank:
    Associate Professor Kappes John 2016 for web 

    Division: Hematology & Oncology

    Campus Address: LHRB 613B

    Phone: (205) 934-0051

    Email: johnkappes@uabmc.edu

    Departmental Affiliation(s):
    Primary: Medicine
    Secondary: Microbiology

    Biosketch:
    John C. Kappes (b. 1957), Associate Professor of Medicine and Microbiology, completed his undergraduate studies in biology at Thomas More College (B.A. in Biology, 1981) and received his Ph.D. in Microbiology and Experimental Medicine from St. Thomas Institute in 1986. Dr. Kappes completed his postdoctoral fellowship studying the molecular pathogenesis of human immunodeficiency viruses and joined the UAB faculty in 1989.

    Research Description:
    Dr. Kappes' research is focused on studying the molecular biology of the human immunodeficiency virus type 1 (HIV-1), and the development of lentiviral-based vectors for gene delivery. These studies are helping to understand how infectious virions are formed and how the viral enzymes [reverse transcriptase (RT) and integrase (IN)], function during the early stages of the virus life cycle. By using virion associated HIV accessory proteins (Vpr and Vpx), Dr. Kappes has developed an approach for incorporating functional RT and IN into virions independently of the normal Gag-Pol packaging pathway. This has uncoupled the RT and IN function from Gag-Pol function and enabled, for the first time, a detailed molecular analysis of reverse transcription and integration in the context of replicating virus (in vivo). Based on the principles of incorporating RT and IN in trans, Dr. Kappes has developed a new generation of HIV/lentiviral-based vectors for gene therapy. Lentiviral vectors appear to be well suited for gene therapy since they can transduce nondividing (somatic) cells. By separating the expression of RT and IN from the other vector components it is possible to produce lentiviral vectors with minimal risk of recombination and the generation of replication competent virus.




  • Kenzik Kelly 2015 webRank:                  
    Assistant Professor

    Division:              
    Hematology & Oncology
    The Institute for Cancer Outcomes and Survivorship

    Campus Address:
    Lowder Building, Room 500

    Mailing Address:
       
    Institute for Cancer Outcomes and Survivorship
    1600 7th Avenue South, Lowder 500
    Birmingham, AL  35233

    Phone:                  (205) 638-2142


    EDUCATION

    Doctor of Philosophy in Epidemiology 2009 – 2013
    Department of Epidemiology
    College of Medicine and College of Public Health & Health Professions
    University of Florida
    Gainesville, Florida

    Master of Science in Health Behavior 2008 – 2008
    Department of Health Education and Behavior
    College of Health and Human Performance
    University of Florida
    Gainesville, Florida

    Bachelor of Science in Health Education, Summa cum laude 2004 – 2007
    Department of Health Education
    College of Health and Human Performance
    University of Florida
    Gainesville, Florida

    Post-Doctoral Fellowship
    Agency for Health Care Research National Research Service Award
    Center for Outcomes and Effectiveness Research and Education
    School of Medicine
    University of Alabama at Birmingham

     


    Awards:
    • American Society of Preventive Oncology Travel Award for Top-ranked Post-doctoral Fellow Abstract (2015)
    • American Society of Preventive Oncology New Investigator Workshop awardee (2015)
    • Top poster award: Head-to-Head Comparisons of Four Legacy Pediatric Health-Related Quality of Life Instruments: A Study on Parent Proxy-Report (ISOQOL, 2011)
    • Institute for Child Health Policy Pre-doctoral Research Fellowship
    • Summa cum laude, Bachelor of Science, Health Education and Behavior
    • 100% Florida Bright Future’s Scholarship recipient (Academic full scholarship, 2004-2007)




    Publications: See a listing of publications on PubMed , a service of the National Library of Medicine.

  • Rank:
        Timares L                
    Associate Professor

    Division:               
    Hematology & Oncology
    CFAR Center For AIDS Research


    Campus Address:

    LHRB 613A

    Mailing Address:
      
    1720 2nd Avenue South, LHRB 613A
    Birmingham, AL 35294-3300

    Phone:                   
    (205) 975-4157

    E-mail Address:
    timares@uab.edu


    Departmental Affiliation(s):
    Primary: Medicine, Hematology/Oncology

    Biography:

    Laura Timares is an Associate Professor in the Division of Hematology-Oncology in the School of Medicine who recently transferred (2017) from Department of Dermatology at the University of Alabama at Birmingham (UAB). She obtained both her undergraduate (BA Biology) and graduate degrees (Ph.D., Microbiology and Immunology School of Medicine) from the University of California at Los Angeles (UCLA). Her postdoctoral training at the California Institute of Technology (1991-1993) and Cedars Sinai Medical Center/UCLA (1993-1996) developed her interest in genetic engineering of transplantable cells and their translational application in treating liver diseases and diabetes.  After joining the University of Texas, Southwestern Medical Center at Dallas (UTSW) (1996), she became faculty in the Department of Medicine in the Center for Biomedical Inventions.  There she studied the role of transfected dendritic cells in skin generated by topical genetic immunization and characterized their role as inducers of vaccine immunity.  She was recruited to the University of Alabama in Birmingham (UAB) in the Department of Dermatology (1999) where she continued her research on cutaneous immunology with a focus on the development of prophylactic skin cancer vaccines. In the Division of Heme-Onc, she is currently applying her expertise toward understanding the role of human mucosal immunology in heterosexual HIV transmission.

    Research/Interest Description:

    To address the urgent need to halt the spread of heterosexual HIV transmission, we must understand how HIV infects immune cells that are normally present in the female reproductive tract.  Drs. John Kappes and Christina Oschenbauer and colleagues revealed that blood-derived monocyte/macrophages engulf not only dead and dying T cells, but also viable T cells that are infected with HIV (but not uninfected viable T cells). This was shown to be dependent on the surface expression of the HIV envelope on T cells.  Furthermore, a significant portion of engulfed infected T cells remained viable over days, during which HIV replicated in the T cell and spread to the macrophage cytoplasm.  We hypothesize that macrophages in the female reproductive tract are also capable of engulfing infected T cells during the earliest phases of HIV infection. Normally,  T cells and macrophages are present as resident cells in the stroma that underlies the transitional epithelium of the cervix, a site that may be a favored portal for heterosexual HIV transmission. Thus, we are interested in knowing whether engulfment of HIV-infected T cells is attributed to a certain subset of tissue resident macrophages, whether the HIV-infected T cell type impacts engulfment, whether this process represents an early form of HIV immune evasion, whether cell-to cell transmission efficiency of surrounding mucosal T cells is enhanced, and whether this process plays an important role in generating cellular reservoirs of hidden HIV.  Both molecular and cellular techniques / assays are employed to elucidate early events of HIV infection. Informative panels of HIV-reporter viruses, representing a variety of relevant infectious virus strains (generated in the Kappes-Oschenbaur lab) are used to investigate infection in ex-vivo culture systems and purified cell populations isolated from remnant tissues of human female reproductive tract surgeries.     

    Publications:See a listing of publications on PubMed, a service of the National Library of Medicine.
         

  • Rank:
    Professor RS17535 Larry Lamb webof Medicine
               Blood and Marrow Transplantation and Cell Therapy Program

    Website: https://www.uab.edu/medicine/bonemarrow/

    Division: Hematology & Oncology

    Campus Address: WTI 510F

    Phone: (205) 996-2335

    Email: lslamb@uabmc.edu

    Departmental Affiliation(s):
    Primary: Medicine
    Secondary: Pediatrics
    Secondary: Pathology

    Research Description:
    Dr. Lawrence Lamb is a Clinical Laboratory Immunologist and Professor of Medicine specializing in transplantation immunology. He also is cross-appointed as Professor of Pathology and Pediatrics and is boarded by the Oncology Nursing Certification Corporation for Advanced Practice in Oncology Nursing (AOCNS). Dr. Lamb directs the UAB Cell Therapy Laboratory and cGMP Cell Manufacturing Facility in the Section of Bone Marrow Transplant and Cellular Therapy. Dr. Lamb's group was the first to describe homeostatic reconstitution of gamma/delta T cells in patients who receive alpha/beta T cell depleted bone marrow grafts and an association between gamma/delta T cell recovery with disease-free survival in allogeneic bone marrow transplantation patients as well as gamma/delta T cell receptor CDR3 conservation in leukemia patients. He currently directs an independent research program for evaluation and translation of innate cell-based therapies for Glioblastoma Multiforme and has been funded by the NINDS (5R21NS57341), NCI (2 P50 CA097247), Elsa Pardee Foundation, Leukemia and Lymphoma Society. He also held the National Brain Tumor Society's Samuel Gershon Leadership Chair for Glioblastoma Research for 2008-2010. Dr. Lamb's laboratory anticipates the initial clinical trials for this therapy to initiate in late 2013.

    Selected Publications:
    Godder, K.T. et al. Long term disease-free survival in acute leukemia patients recovering with increased gamma/delta T cells after partially mismatched related donor bone marrow transplantation. Bone Marrow Transplant 39, 751-7 (2007).

    Lamb, L.S., Jr. et al. Increased frequency of TCR gamma delta + T cells in disease-free survivors following T cell-depleted, partially mismatched, related donor bone marrow transplantation for leukemia. Journal of Hematotherapy. 5, 503-9 (1996).

    Lamb LS, Gee AP, Musk P, O'Hanlon TP, Hazlett LJ, Geier SS, Folk RS, Harris WG, McPherson K, Lee C, Henslee-Downey PJ Influence of T cell depletion method on circulating gd T cell reconstitution and potential role in the graft versus leukemia effect. Cytotherapy 1: 7-19 (1999)

    Meeh, P.F. et al. Characterization of the gamma/delta T cell response to acute leukemia. Cancer Immunol Immunother 55, 1072-80 (2006).

    Godder K, Henslee-Downey PJ, Mehta J, Park B, Chiang KY, Abhyankar S, Lamb LS Long term disease-free survival in acute leukemia patients with increased gd T cells after partially mismatched related donor bone marrow transplantation. Bone Marrow Transplantation 39: 751 – 757 (2007).

    Bryant NL, Suarez-Cuervo C, Gillespie GY, Markert JM, Nabors LB. Meleth S, Lopez RD, Lamb LS Characterization and Immunotherapeutic Potential of γδ T Cells in Patients with Glioblastoma Neuro-Oncology (2009) in press

    Bryant, NL, Gillespie GY, Lopez, RD, Markert JM, Cloud GA, Langford CP, Arnouk H, Su Y, Hanes H, Suarez-Cuervo, Lamb LS Preclinical Evaluation of ex vivo Expanded/Activated γδ T Cells for Immunotherapy of Glioblastoma Multiforme J Neuro-Oncology 101: 179 – 188 (2011)

    Lamb LS, Bowersock J, Dasgupta A, Gillespie GY, Su Y, Johnson A, Spencer HT Engineered drug resistant γδ T cells kill glioblastoma cell lines during a chemotherapy challenge: A strategy for combining chemo- and immunotherapy PloS One December 2012
  • Rank: Professordatta_pran and Director of Research
     
    Division:
    Hematology & Oncology

    Campus Address:  WTI 520C

    Email: prandatta@uabmc.edu


    Departmental Affiliation(s):
    Primary: Medicine

    Biosketch:

    Dr. Datta earned his Bachelor of Science (BS), Honors in Chemistry; Physics and Mathematics, and his Master of Science (MS), Organic Chemistry from The University of Burdwan, India.  He erned his Ph.D. in Organic Chemistry, from the Bose Institute, Calcutta, India.  His thesis title was Studies on Natural Carbocyclic Compounds. 

    He worked as a research associate with Dr. Srilata Bagchi at the University of Illinois in Chicago and with Dr. Harold L. Moses at The Vanderbilt-Ingram Cancer Center in Nashville. He began work as assistant professor in Surgical Oncology Cancer Biology at Vanderbilt University in 2000.  Dr. Datta also served as a research scientist at the Veterans Affairs Medical Center in Nasvhille.

    In 2012, Dr. Datta joined the faculty at UAB, where he is Professor and Director of Research in the Division of Hematology/Oncology.  He is also leader of the Colon and Lung Cancer Basic Research Program.  He is senior scientist in the Cancer Cell Biology Program at the UAB Comprehensive Cancer Center.  In addition, Dr. Datta also serves as Research Scientist at the Veterans Affairs Medical Center in Birmingham.

    Recent Publications:

    1. Rachakonda, G., and Datta, P.K., Jun kinase pathway is important for TGF-ß-induced downregulation of Claudin-4 in non-small cell lung cancer. Communicated, 2012.
    2. Zhang, W., Zhang, B., Halder, S.K., Washington, K., and Datta, P.K., Functional role of Integrin ß4 in the metastasis of colorectal cancer. Communicated, 2012.
    3. Nagathihali, N.S., Massion, P., Gonjalez, A, and Datta, P.K., Smoking induces epithelial-to-mesenchymal transition in non-small cell lung cancer through HDAC-mediated downregulation of E-cadherin. Molecular Cancer Therapeutics, 11(11):2362-2372. Nov. 6, 2012.
    4. Samanta, D., Kauffmann, J., Carbone D.P., and Datta, P.K., Long-term smoking mediated downregulation of Smad3 induces resistance to carboplatin in non-small cell lung cancer. Neoplasia, 14(7): 644-655, 2012.
    5. Samanta, D., Gonjalez, A., Carbone, D.P., and Datta, P.K., Smoking attenuates TGF-β-mediated tumor suppression function through down-regulation of Smad3 in lung cancer. Cancer Prevention Research (AACR), 5(3): 453-463, 2012.
    6. Halder, S.K., Cho, Y-J, Datta, A., Anumanthan, G., Ham, A-J.L., Carbone, D.P., and Datta, P.K., Elucidating the mechanism of regulation of TGF-ß type II receptor expression in human lung cancer cell lines, Neoplasia, 13(10): 912-922, 2011.
    7. Kashikar, N., Zhang, W., Massion, P., Gonjalez, A and Datta, P.K., Role of STRAP in regulating GSK3ß function and Notch3 stabilization. Cell Cycle, 10(10): 1639-1654, 2011.
    8. Reiner, J., Ye, F., Kashikar, N., and Datta, P.K., STRAP Regulates Cellular Proliferation and Ubiquitin-mediated Proteolysis of the c-Jun Oncogene. BBRC, 407(2): 372-377, 2011.
    9. Girish Rachakonda, Konjeti R. Sekhar, Dawit Jowhar, Philip C. Samson, John P. Wikswo, R. Daniel Beauchamp, Pran K. Datta, and Michael L. Freeman, Increased Cell Migration and Plasticity in Nrf2 Deficient Cancer Cell Lines. Oncogene, 29(25): 3703–3714, 2010.
    10. Kashikar, N., Reiner, J., Datta, A., and Datta, P.K., STRAP plays a role in the maintenance of mesenchymal morphology. Cellular Signaling, 22: 138-149, 2010.
    11. Zhang, B., Halder, S.K., Kashikar, N., Cho, Y-J., Datta, A., Gorden, D.L., and Datta, P.K., Anti-metastatic role of Smad4 signaling in colorectal cancer. Gastroenterology, 138: 969-980, 2010.
    12. Zhang, B., Halder, S., Sanguo, Z., and Datta, P.K., Targeting Transforming Growth Factor-ß signaling in liver metastasis of colorectal cancer. Cancer Letters, 277: 114-120, 2009.
    13. Halder, S.K., Rachakonda, G., Deane, N.G., and Datta, P.K., Smad7 induces hepatic metastasis in colorectal cancer. British Journal of Cancer, 99: 957-965, 2008.
    14. Shiou, S-R, Singh, A.B., Moorthy, K., Datta, P.K., Washington M.K., Beauchamp, R.D., and Dhawan, P., Smad4 regulates claudin-1 expression in a TGF-ß-independent manner in colon cancer cells. Cancer Research, 67(4): 1571-9, 2007.
    15. Anumanthan, G., Halder, S.K., Friedman, D., and Datta, P.K., Oncogenic STRAP modulates the function of Ewing Sarcoma Protein through a novel mechanism. Cancer Research, 66(22):10824-32, 2006.
    16. Shiou, S-R, Datta, P.K., Dhawan, P., Law, B.K., Yingling, J., Dixon, D.A., and Beauchamp, R.D., Smad4-dependent regulation of uPA secretion and RNA stability associated with invasiveness by autocrine and paracrine TGF-ß. The Journal of Biological Chemistry, 281(45):33971-81, 2006.
    17. Halder, S.K., Anumanthan, G., Maddula R., Mann, J., Chytil, A., Gonzalez, A., Washington, M.K., Moses, H. L., Beauchamp, R. D., and Datta, P.K., Oncogenic function of a novel WD-domain protein STRAP in Human Carcinogenesis. Cancer Research, 66(12):6156-66, 2006.
    18. Grau, A.M.*, Datta, P.K.*, Zi, J., Halder, S.K., and Beauchamp, R.D., TGF-ß activates NF-kB through a novel Smad regulated mechanism in colon cancer cells. Cellular Signaling, 18, 2006.  *Contributed equally
    19. Halder, S.K., Beauchamp, R.D., and Datta, P.K., A specific inhibitor of TGF-ß receptor kinase, SB431542, as a potent antitumor agent for advanced human cancers. Neoplasia, 7(5), 509-521, 2005.
    20. Halder, S.K., Beauchamp, R.D., and Datta, P.K., Smad7 Induces tumorigenicity by blocking TGF-ß-induced growth inhibition and apoptosis. Exp Cell Res, 307, 231-246, 2005.
    21. Anumanthan, G., Halder, S.K., Osada, H., Takahashi, K., Massion, P., Carbone, D., and Datta, P.K., Restoration of TGF-ß-mediated tumor suppression function by stable expression of type II receptor in human lung cancer cells. British Journal of Cancer, 93, 1157-1167, 2005.
    22. Mithani, S.K., Balch G.C., Shiou, S., Whitehead, R.H., Datta, P.K., and Beauchamp, R.D. Smad3 has a critical role in TGF-ß mediated growth inhibition and apoptosis in colonic epithelial cells. J Surg Res., 117, 296-305, 2004.
    23. Yu, B., Datta, P. K., and Bagchi, S. Stability of the Sp3-DNA complex is promoter-specific: Sp3 efficiently competes with Sp1 for binding to promoters containing multiple Sp-sites. Nucleic Acids Res 31:5368-76, 2003.
    24. Monica A. Parker, Natasha G. Deane, E. Aubrey Thompson, Robert H. Whitehead, Suhail K. Mithani, M. Kay Washington, Pran K. Datta, Dan A. Dixon, R. Daniel Beauchamp, Overexpression of Cyclin D1 Regulates Cdk4 Protein Synthesis. Cell Prolif., 36(6), 347-360, 2003.
    25. Saha, D., Datta, P.K., and Beauchamp, R.D., Oncogenic Ras represses TGF-/SMAD signaling by degrading tumor suppressor Smad4. The Journal of Biological Chemistry, 276(31), 29531-29537, 2001.
    26. Datta, P. K., Blake, M.C., and Moses, H.L., Regulation of Plasminogen Activator Inhibitor-1 Expression by Transforming Growth Factor--induced Physical and Functional Interactions between Smads and Sp1. The Journal of Biological Chemistry, 275(51), 40014-40019, 2000.
    27. Datta, P. K., and Moses, H. L., STRAP and Smad7 synergize in the inhibition of Transforming Growth Factor-ß signaling. Molecular and Cellular Biology, 20(9), 3157-3167, 2000.
  • Welner RobRank:                    
    Assistant Professor

    Division:
                   
    Hematology & Oncology

    Campus Address:
    WTI 510D

    Mailing Address:  
    1720 2nd Avenue South, WTI 510D
    Birmingham, AL 35294-3300

    Phone:                   
    (205) 934-0439


    Departmental Affiliation(s):
    Primary: Medicine, Hematology/Oncology


    EDUCATION             

     
    Graduate School
    University of Oklahomas Health Sciences Center, PhD Immunology/Microbiology

    Fellowship
    Harvard Medical School, Postdoc Fellowship

    PROFESSIONAL SOCIETIES
    American Society of Hematology (ASH)
    American Association of Immunologists

    BIOGRAPHICAL SKETCH
    I received my PhD degree in Immunology and Microbiology from University of Oklahoma with Dr. Paul Kincade. I later moved to the Beth Israel Deaconess Medical Center/Harvard Medical School for my post-doctoral training with Dr. Daniel Tenen.

    RESEARCH/CLINICAL INTERESTS
    Altered hematopoietic environment in leukemia.
    My research has focused on stem cell biology, transcription factors, and gene regulation differences between normal adult cells and their diseased counterpart. Major advances have been made recently in describing the transcriptional networks dictating self-renewal of stem cells, and a number of important transcriptional regulators have been characterized during hematopoiesis; meanwhile, understanding how these processes become dysregulated in their function in hematopoietic stem cells has not been well established. My research projects investigate the role of steady-state and perturbed microenvironments on the stem cell self-renewal and differentiation, and more importantly the interplay between these contradictory forces within the stem cell niche.

    SELECTED PUBLICATIONS
    Treatment of chronic myelogenous leukemia by blocking cytokine alterations found in normal stem and progenitor cells.
    Welner RS, Amabile G, Bararia D, Czibere A, Yang H, Zhang H, Pontes LL, Ye M, Levantini E, Di Ruscio A, Martinelli G, Tenen DG. Cancer Cell. 2015 May 11;27(5):671-81.

    Publications:See a listing of publications on PubMed, a service of the National Library of Medicine.
  • Rank:                    
    Assistant Professor

    Division:
                   
    Hematology & Oncology

    Campus Address:
    WTI 520A

    Mailing Address:  
    1720 2nd Avenue South, WTI 520A
    Birmingham, AL 35294-3300

    Phone:                   
    (205) 975-5973


    Departmental Affiliation(s):
    Primary: Medicine, Hematology/Oncology


    EDUCATION             

     
    Certificate in Project Management, 2013
    California Institute of Technology, Pasadena, USA 

    PhD,Molecular Biology & Biotechnology, 2002G.B. Pant University, India 

    MS, Molecular Biology & Biotechnology, 1995G.B. Pant University, India


    PROFESSIONAL SOCIETIES
    2017 – present ASMBT
    2005-2013  American Society for Cell Biology
    2005-2013  American Association for the Advancement of Science                           
    2004-2010  American Society for Microbiology
    2010-2013  ISSCR

    Appointments

    2017- Present: Lead GMP Cell Prep Tech. (SANBIO Clinical Trial for Ischemic Stroke)
    2016-Present:Assistant Professor, Division of Hematology & Oncology), UAB, Birmingham, AL, USA
    2014-2016: Assistant Research Professor, Immuno-Oncology, City of Hope, Duarte, CA, USA
    2013-2014
    : Staff Scientist, Immuno-Oncology, City of Hope, Duarte, CA, USA
    2008-2013
    : Assistant Research Professor, BRI, City of Hope, Duarte, CA, USA
    2002-2008
    : Postdoctoral Fellow, City of Hope, Duarte, CA, USA
    2001-2002: Research Scientist, International Centre for Genetic Engineering &Biotechnology, India                  
    2000-2001: Postdoctoral Fellow, G.B. Pant University of Agriculture and Technology, India 
     
    Professional experience
    1. NIH Sponsored Human Embryonic Stem Cell training course- Children Hospital Orange County, CA, USA-2006
    2. Clinical Research Certification (CRC) - Collaborative Institutional Training Initiative (CITI), Member ID: 1811046- 2010
    1. SANBIO Cell preparation training for Thaw and Dosing for surgical implantation (GMP) – 2017
    2. GMP level cell manufacturing in Clinimac Prodigy and validation of manufactured products for startup company -Insysus– 2016 to present
    3. High dimensional flow cytometry: 14 color parameter for immune cells phenotyping using BD LSR Fortessa (X-20)
    SELECTED PUBLICATIONS
    Brile Chung, Ali Esmaeli, Sailesh Gopalakrishna-Pillai, John Murad, Emily Andersen, Naveen Kumar Reddy, Gayathri Srinivasan, Brian Armstrong, Young Kim, Tommy Tong, James Waisman, John Yim, Behnam Badie, Caleb Chu, Peter Lee. Human brain metastatic stroma recruits breast cancer cells via chemokines CXCL16 and CXCL12. npj Breast Cancer 3, Article number: 6 (2017) doi:10.1038/s41523-017-0008-8.

    Dobrin Draganov, Sailesh Gopalakrishna-Pillai, Yun-Ru Chen, Neta Zuckerman, Sara Moeller, Carrie Wang, David Ann, and Peter P. Lee. Modulation of P2X4/P2X7/Pannexin-1 sensitivity to extracellular ATP via Ivermectin induces a non-apoptotic and inflammatory form of cancer cell death. Scientific Reports. 2015; 5:16222.

    Ganlu Hu, Kevin Huang, Juehua Yu, Sailesh Gopalakrishna-Pillai, Jun Kong, He Xu, Zhenshan Liu, Kunshan Zhang, Jun Xu, Yuping Luo, Siguang Li, Yi E. Sun, Linda E Iverson, Zhigang Xue, Guoping Fan. Identification of miRNA signatures during the differentiation of hESCs into Retinal Pigment Epithelial Cells. PloS ONE 2012; 7(7) e37224

    Li Z. Luo#, Sailesh Gopalakrishna-Pillai#, Stephanie L. Nay#, Sang-Won Park, Steven E. Bates, Xianmin Zeng, Linda E. Iverson, Timothy R. O’Connor. DNA repair in human pluripotent stem cells is distinct from that in non-pluripotent human cells. PloS ONE 2012; 7(3): e30541 (#equal contribution) 

    Sailesh Gopalakrishna-Pillai and Linda Iverson. A DNMT3B alternatively spliced exon and encoded peptide are novel biomarkers of human pluripotent stem cells. PLoS ONE 2011; 6(6): e20663 

    Sailesh Gopalakrishna-Pillai and Linda Iverson. Astrocytes derived from trisomic human embryonic stem cells express markers of astrocytic cancer cells and premalignant stem-like progenitors. BMC Medical Genomics 2010; 3:12

    Dong-Suk Kim, Veronica Gusti, Sailesh G Pillai and Rajesh K. Gaur. An artificial riboswitch for controlling pre-mRNA splicing. RNA 2005; 11:1667-1677. 

    Sailesh Gopalakrishna, Veronica Gusti, Sethulekshmy Nair, Saurabh Sahar and Rajesh K. Gaur. 2004. Template-Dependent Incorporation of 8-N3AMP in to RNA with Bacteriophage T7 RNA Polymerase. RNA 2004; 10(11):1820-30.


    Publications:See a listing of publications on PubMed, a service of the National Library of Medicine.
  • Zhi-Xiang_Xu_webRank: Assistant Professor
    Division: Hematology/Oncology
    Campus Address: WTI 520D
    Office: 205-934-1868
    Fax: 205-934-1870
    Lab: 205-996-4085

    E-mail: zhixiangxu@uabmc.edu

    Departmental Affiliation(s):
    Primary: Medicine


    Biosketch

    2/2001-11/2004 Postdoctoral Fellow, Department Molecular Pathology, The University of Texas, M. D. Anderson Cancer Center, Houston, TX (Dr. Kun-Sang Chang)

    12/2004-11/2009 Assistant Professor (Research), Department of Molecular Therapeutics (Department of Systems Biology), The University of Texas M. D. Anderson Cancer Center, Houston, TX.

    11/2009-present Assistant Professor (tenure track), Division of Hematology / Oncology & Comprehensive Cancer Center, The University of Alabama at Birmingham, Birmingham, AL


    Research Description

    The objectives in Dr. Xu's lab are to identify the molecular mechanisms underlying tumor suppressor function and to develop pharmacological agents that can modulate or mimic tumor suppressors for cancer prevention and treatment. Specifically, the lab currently has three research directions:
    (1) Tumor suppressor and genomic stability: (A) To investigate mechanisms of how tumor suppressors, such as LKB1 (also known as serine/threonine kinase 11, STK11), PML, and p53, regulate genomic stability; (B) To determine LKB1-related protein signatures and signaling networks under stressed conditions and identify novel LKB1-interacting proteins; (C) To define LKB1 expression (mutation) in tumors and its relationship to patient outcomes and therapeutic response.
    (2) Cell death---Autophagy and Necrosis: (A) To determine the role of autophagy in LKB1-mediated genomic stabilization; (B) To screen and characterize genes that regulate autophagy and necrosis in mammalian cells; (C) To determine the role of autophagy and necrosis in tumorigenesis and targeted therapy.
    (3) Molecular therapeutics: To develop pharmacologic agents targeting the LKB1-AMPK-mTOR pathway for cancer prevention and treatment.

    Selected Publications


    1.    Xu HG, Zhai YX, Chen J, Lu Y, Wang JW, Quan CS, Zhao RX, Xiao X, He Q, Werle KD, Kim HG, Lopez R, Cui R, Liang J, Li YL, Xu ZX. LKB1 reduces ROS-mediated cell damage via activation of p38. Oncogene 2014 Sep 29. doi: 10.1038/onc.2014.315. [Epub ahead of print] PMID: 25263448

    2.    Jian W, Xu HG, Chen J, Xu ZX, Levitt JM, Stanley JA, Yang ES, Lerner SP, Sonpavde G. 2014. Activity of CEP-9722, a poly (ADP-ribose) polymerase inhibitor, in urothelial carcinoma correlates inversely with homologous recombination repair response to DNA damage. Anticancer Drugs 25: 878-886.

    3.    Werle KD, Chen J, Xu HG, Zhao RX, Cui R, Liang J, Xu ZX. Liver Kinase B1 regulates the centrosome via PLK1. Cell Death Disease 2014; 5: e1157

    4.    Lu C, Chen J, Xu HG, Zhou X, He Q, Li YL, Jiang G, Shan Y, Xue B, Zhao RX, Wang Y, Werle KD, Cui R, Liang J, Xu ZX. MIR106B and MIR93 Prevent Removal of Bacteria from Epithelial Cells by Disrupting ATG16L1-Mediated Autophagy. Gastroenterology 2014; 146 (1): 188-99.

    5.    Zhao RX, Xu ZX. Targeting the LKB1 Tumor Suppressor. Current Drug Targets 2014; 15(1): 32-52 

    6.    Wang Y, Wang JW, Xiao X, Shan Y, Xue B, Jiang G, He Q, Chen J, Xu HG, Zhao RX, Werle KD, Cui R, Liang J, Li YL, Xu ZX. Piperlongumine Induces Autophagy by Targeting p38 Signaling, Cell Death Disease 2013; 4: e824

    7.    Liu F, Cao J, Sullivian K, Shen J, Ryu B, Xu ZX, Liu X, Cui R. Stat3 targeted therapies overcome the acquired resistance to vemurafenib in melanomas. J Invest Dermatol 2013; 133(8): 2041-9. PMID: 23344460

    8.    Liu F, Cao J, Lv J, Dong L, Pier E, Xu GX, Wang RA, Xu ZX, Goding C, Cui R. TBX2 expression is regulated by PAX3 in the melanocyte lineage. Pigment Cell Melanoma Res 2013; 26(1): 67-77. PMID: PMC3527652 

    9.    Xiao XX, He Q, Lu C, Werle KD, Zhao RX, Chen J, Davis BC, Cui R, Liang J, Xu ZX. Metformin impairs the growth of LKB1-intact cervical cancer cells. Gynecol Oncol. 2012; 127(1): 249-55.

    10.    Miki T, Xu ZX, Chen-Goodspeed M, Liu MG, Van Oort-Jansen A, Rea MA, Zhao Z, Cheng CC, Chang KS. PML regulates PER2 nuclear localization and circadian function. EMBO J, 2012; 31(6): 1427-39.

    11.  Dong L, Li Y, Cao J, Liu F, Pier E, Chen J, Xu Z, Chen C, Wang RA, Cui R. FGF2 regulates melanocytes viability through the STAT3-transactivated PAX3 transcription. Cell Death Differ. 2012; 19(4): 616-22

    12.   Haridas V, Xu ZX, Kitchen D, Michels P, and Gutterman JU. The anticancer plant triterpenoid, Avicin D, regulates glucocorticoid receptor signaling: Implications for cellular metabolism. PLoS ONE, 2011, 6(11): e28037.

    13.   Wang S, Wang H, Davis BC, Liang J, Cui R, Chen SJ, Xu ZX. PARP1 inhibitors attenuate AKT phosphorylation via the upregulation of PHLPP1. Biochem Biophys Res Commun. 2011; 412(2): 379-84.

    14.   Wang H, Haridas V, Gutterman JU, and Xu ZX. Natural triterpenoid avicins selectively induce tumor cell death (Review). Communicative & Integrative Biology 2010; 3(3): 205-208

    15.   Xu ZX, Ding T, Haridas V, Connolly F, Gutterman JU. A plant triterpenoid, avicin D, induces cell apoptosis by recruitment of Fas and downstream signaling molecules into lipid rafts. PLoS ONE 2009; 4(12):e8532.

    16.   Haridas V, Nishimura G, Xu Z-X, Connolly F, Hanausek M, et al. Avicin D: A Protein Reactive Plant Isoprenoid Dephosphorylates Stat 3 by Regulating Both Kinase and Phosphatase Activities. PLoS ONE 2009; 4(5): e5578.

    17.   Pan J, Chen B, Su CH, Xu ZX, Sun L, Lee MH, Yeung SC. Autophagy induced by farnesyltransferase inhibitors in cancer cells. Cancer Biol Ther 2008; 7(10): 1679-1684

    18.   Zhang C, Li B, Gaikwad A, Haridas V, Xu ZX, Gutterman J, and Duvic M. Avicin D selectively induces apoptosis and downregulates p-STAT-3, bcl-2, and survivin in cutaneous T-cell lymphoma cells. J Invest Dermatol 2008; 128(11): 2728-35.

    19.   Xu ZX, Liang J, Haridas V, Gaikwad A, Connolly FP, Mills GB, Gutterman JU. A plant triterpenoid induces tumor cell autophagy by activation of AMPK. Cell Death and Differentiation 2007, 14: 1948-1957

    20.   Liang J, Shao S, Xu ZX, Hennessy B, Ding ZY, Kondo S, Dumont D, Gutterman JU, Walker CL, Slingerland JM, Mills GB. The energy sensing LKB1-AMPK pathway regulates p27(kip1) phosphorylation mediating the decision to enter autophagy or apoptosis. Nature Cell Biology 2007; 9: 218-224

    21.   Lin SY, Rai R, Li K, Xu ZX, Elledge SJ. BRIT1/MCPH1 is a DNA damage responsive protein that regulates the Brca1-Chk1 pathway, implicating checkpoint dysfunction in microcephaly. Proc Natl Acad Sci U S A 2005; 102: 15105-9

    22.   Pan J, She M, Xu ZX, Sun L, Yeung SCJ. Farnesyltransferase inhibitors induce DNA damage via reactive oxygen species in human cancer cells. Cancer Res 2005; 65(9): 3671-3681

    23.   Xu ZX, Zou WX, Lin P, Chang KS. A role for PML3 in centrosome duplication and genome stability. Mol Cell 2005; 17(5): 721-732

    24.   Xu ZX, Zhao RX, Ding T, Tran TT, Zhang W, Pandolfi PP, Chang KS. PML4 induces apoptosis by inhibition of Survivin expression. J Biol Chem 2004; 279(3): 1838-1844.

    25.   Wu WS, Xu ZX, Hittleman WN, Salomoni P, Pandolfi PP, Chang KS. Promyelocytic leukemia protein sensitizes tumor necrosis factor alpha-induced apoptosis by inhibition the NF-kappa B survival pathway. J Biol Chem 2003; 278(14): 12294-304.

    26.   Xu ZX, Timanova-Atanasova A, Zhao RX, Chang KS. PML colocalizes with and stabilizes the DNA damage response protein TopBP1. Mol Cell Biol 2003; 23(12): 4247-56.

    27.   Wu WS, Xu ZX, Ran RX, Feng M, Chang KS. Promyelocytic Leukemia Protein PML inhibits Nur77-mediated Transcription through Specific Functional Interaction. Oncogene 2002; 21(24): 3925-33.

    28.   Wu WS, Xu ZX, Chang KS. Promyelocytic leukemia protein represses A20-mediated transcription. J Biol Chem 2002; 277(35): 31734-9.