• Ochsenbauer C 2014Rank:
    Assistant Professor 


    Hematology & Oncology

    Campus Address:
    LHRB 611

    (205) 975-7872


    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


    Hematology & Oncology

    Campus Address:
    SHEL 420

    (205) 975-0963


    Departmental Affiliation(s):
    Primary: Medicine


    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’.


    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:
    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

    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

    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


    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


    • 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: Professordatta_pran and Director of Research
    Hematology & Oncology

    Campus Address:  WTI 520C

    Email: prandatta@uabmc.edu

    Departmental Affiliation(s):
    Primary: Medicine


    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 RobRobert S. Welner, PhD

    Assistant Professor

    Hematology & Oncology

    Campus Address:
    WTI 510D

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

    (205) 934-0439


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

    Harvard Medical School, Postdoc Fellowship

    American Society of Hematology (ASH)
    American Association of Immunologists

    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.

    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.

    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.

  • Lu 2019Rank:
    Assistant Professor

    Hematology & Oncology

    Campus Address:

    WTI 510G

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

    Phone: (205) 975-9878
    Fax: (205) 975-5745
    Lab: (205) 996-4085                

    E-mail Address:ruilu1@uabmc.edu

    Website: www.lu-lab.org

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

    Professional Experience and Education:
    2019 – present Assistant Professor
    University of Alabama at Birmingham, Birmingham, AL

    2017 – 2018 Research Associate
    University of North Carolina at Chapel Hill, Chapel Hill, NC

    2012 – 2017 Postdoctoral Fellow
    University of North Carolina at Chapel Hill, Chapel Hill, NC

    2005 – 2012 Ph.D. Developmental Biology
    Chinese Academy of Sciences, Shanghai, China

    Research/Interest Description:
    The overall goal of Dr. Lu’s laboratory is to better understand the epigenetic mechanisms that underlie cancer cell development, and to develop mechanism-based and targeted therapeutic approaches. His previous research has produced a series of important publications in the fields of epigenetics and cancer. Dr. Lu and colleagues have identified a novel reader for histone H3K36 methylation (Molecular Cell, 2013), revealed a new mechanism for DNMT3A mutations in acute myeloid leukemia (Cancer Cell, 2016), and discovered the molecular basis for DNMT3A-mediated substrate recognition (Nature, 2018). Building on the previous work and the strength of UAB Division of Hematology & Oncology, Dr. Lu’s lab currently is focusing on understanding various epigenetic regulations in the development of blood cancers. Recent projects in Dr. Lu’s lab include the following directions: (1) understanding the molecular basis of driver mutations in cancer; (2) discovery of novel targets for cancer epigenetic therapies; (3) development of new epigenome editing tools to study gene regulation in normal and cancer cells.    

    Selected Publications:
    1. Zhang ZM*, Lu R*, Wang P, Yu Y, Liu S, Ji D, Gao L, Rothbart SB, Wang Y, Wang GG, Song J: Structural basis for DNMT3A-mediated de novo DNA methylation. Nature 2018, 554(7692):387-391. (*equal contribution)

    2. Lu R, Wang P, Parton T, Zhou Y, Chrysovergis K, Rockowitz S, Chen W-Y, Abdel-Wahab O, Wade PA, Zheng D, Wang GG: Epigenetic Perturbations by Arg882-Mutated DNMT3A Potentiate Aberrant Stem Cell Gene-Expression Program and Acute Leukemia Development. Cancer Cell 2016, 30(1):92-107.

    3. Lu R, Wang GG: Pharmacologic Targeting of Chromatin Modulators as Therapeutics of Acute Myeloid Leukemia. Frontiers in Oncology 2017, 7:241.

    4. Lu R, Wang GG: Gene enhancer deregulation and epigenetic vulnerability. Oncoscience 2016, 3(11-12):299-301.

    5. Lu R, Wang GG: Tudor: a versatile family of histone methylation ‘readers’. Trends in Biochemical Sciences 2013, 38(11):546-555.

    6. Cai L*, Rothbart SB*, Lu R*, Xu B, Chen W-Y, Tripathy A, Rockowitz S, Zheng D, Patel DJ, Allis CD, Strahl BD, Song J, Wang GG: An H3K36 methylation-engaging Tudor motif of polycomb-like proteins mediates PRC2 complex targeting. Molecular Cell 2013, 49(3):571-582. (*equal contribution)

    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


    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.

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