Steve A. Maxwell, PhD

Steve A. Maxwell, PhD

Associate Professor

Department of Molecular and Cellular Medicine
Room 252 Reynolds Medical Building
College Station, TX   77843

Phone: 979.436.0804
Fax: 979.847.9481

Education and Post-Graduate Training

Dr. Steve Maxwell received his BA in chemistry and BS in biology in 1980 from Abilene Christian University. In 1985 he received a PhD in molecular virology from the University of Texas Graduate School of Biomedical Sciences where he worked with Dr. Ralph Arlinghaus. His postdoctoral training was in the Department of Molecular Virology at Baylor College of Medicine. Maxwell joined the faculty at Texas A&M in 1995. He is the coordinator for the Medical Sciences 602 Graduate course and has taught several medical pathology courses.

Research Interests

Primary interests include cancer; oncogenes; tumor suppressor; genes programmed cell death (apoptosis); chemoresistance, and angiogenesis

My laboratory studies mechanisms of evolution of chemoresistance in diffuse large B-cell lymphoma (DLBCL). The CHOPS drug regimen (doxorubicin/ cyclophosphamide/vincrinstine/prednisone) is currently the most effective treatment for DLBCL patients. Unfortunately, about one-half of DLBCL patients develop drug resistance leading to high mortality. As a model system, we generated CHOP-resistant DLBCL cell lines through repeated selections in the presence of CHOP. We have been using proteomics to investigate differences in protein expression between the CHOP-sensitive and –resistant DLBCL cells. One target of interest has been identified as the 14-3-3zeta protein, a known prosurvival gene product. CHOP-resistant cells overexpressed the 14-3-3zeta protein leading us to hypothesize that it might provide DLBCL cells with the selective advantage to survive CHOP treatment. We tested this hypothesis and showed that modulation of 14-3-3zeta, indeed, played a role in chemoresistance of DLBCL cells.

In collaboration with Dr. James Sacchettini at Texas A&M University, we utilized my chemoresistant cell lines in high-throughput screening and identified a member of the rifamycin family as a non-toxic compound that could restore chemosensitivity in lymphoma, breast, prostate, glioma, and pancreatic cancer cells. Medicinal chemistry in Sacchettini’s laboratory led to rifabutin derivatives that were ten-times more potent in chemosensitizing activity. Our lead compound, RTI-79, has been patented. One mode of action of RTI-79 is the induction of reactive oxygen species in cancer cells.

Our working model hypothesizes that acquired drug resistance in cancer involves the upregulation of anti-oxidant pathways like Nrf-2 that result in low oxidative stress. RTI-79 induces chemosensitization by upregulating both reactive oxygen species and downregulating anti-oxidant Nrf2 pathways. This two-pronged action results in a pronounced oxidative stress that re-sensitizes a broad range of cancer cells to chemotherapeutics. In support of our model, we have shown that RTI-79 not only induces superoxide, but downregulates the anti-oxidant Nrf-2 pathway and drug efflux. Current studies in my lab are focused on identifying the primary target of RTI-79 and conducting mechanistic studies into its mode of action.

One current primary objective is to conduct a Phase I study that (1) confirms RTI-79 safety in platinum-resistant/refractory ovarian cancer patients, and (2) demonstrates signals of efficacy in humans (ex: time-to-disease progression and changes in CA125 biomarker). A second objective is to better define the RTI-79 mechanism of action (“MOA”) by (1) determining how RTI-79 causes a rapid burst in superoxides, and (2) elucidating the basis of Nrf-2 pathway downregulation.

Graduate training is available through the Medical Science PhD program (College of Medicine), through the MD/PhD program (College of Medicine) and other programs that our faculty are affiliated with joint research.


  • Dave, JM, Kang, H, Abbey, CA, Maxwell, SA, and Bayless, KJ (2013) Proteomic profiling of endothelial invasion revealed receptor for activated C kinase 1 (RACK1) complexed with vimentin to regulate focal adhesion kinase (FAK). J. Biol Chem. 288(42):30720-33. PMID: 24005669.
  • Maxwell, SA and Mousavi-Fard, S (2013) Non-Hodgkin's B-cell lymphoma: advances in molecular strategies targeting drug resistance. Exp. Biol. Med. 238(9):971-90. PMID: 23986223.
  • Kwak, HI, Kang, H, Dave, JM, Mendoza, EA, Su, SC, Maxwell, SA, and Bayless KJ. (2012) Calpain-mediated vimentin cleavage occurs upstream of MT1-MMP membrane translocation to facilitate endothelial sprout initiation. Angiogenesis 15(2):287-303. PMID. 22407449.
  • Maxwell, SA, Cherry, E, and Bayless, KJ (2011) Akt, 14-3-3z, and Vimentin Mediate a Drug-Resistant Invasive Phenotype in Diffuse Large B-Cell Lymphoma. Leuk. Lymphoma, 52(5):849-864. PMID: 21323512.
  • Su, SC, Maxwell, SA, and Bayless, KJ. (2010) Annexin 2 regulates endothelial morphogenesis by controlling AKT activation and junctional integrity. J Biol Chem. 285(52):40624-40634. PMID: 20947498.
  • Maxwell, SA, Li, Z, Jaya, D, Ballard, S, Ferrell, J, and Fu, H. (2009) 14-3-3zeta mediates resistance of diffuse large B cell lymphoma to an anthracycline-based chemotherapeutic regimen. J. Biol. Chem. 284(33):22379-22389. PMID: 19525224.
  • Maxwell, SA, and Kochevar, GJ (2008) Identification of a p53-response element in the promoter of the proline oxidase gene. Biochem. Biophys. Res. Commun. 369(2): 308-813. PMID: 18279664.
  • Rivera A, Mavila A, Bayless KJ, Davis GE and Maxwell SA (2006) Cyclin A1 is a p53-Induced Gene That Mediates Apoptosis, G2/M Arrest, and Mitotic Catastrophe in Renal, Ovarian, and Lung Carcinoma Cells. Cell Mol. Life Sci. 63, 1425-1439. PMID: 16799873.
  • Rivera, A and Maxwell, SA (2005) The p53-induced gene-6 (proline oxidase) mediates apoptosis through a calcineurin-dependent pathway. J. Biol. Chem. 280, 29345-29354. PMID: 15914462.
  • Maxwell, SA and Davis, GE (2004) Gene expression profiling of p53-sensitive and-resistant tumor cells using DNA microarray. Apoptosis. 9, 171-179. PMID: 15004514.
  • Maxwell, SA and Rivera, A (2003) Proline oxidase induces apoptosis in tumor cells, and its expression is frequently absent or reduced in renal carcinomas. J. Biol. Chem. 278, 9784-9789. PMID: 12514185.
  • Bell, SE, Mavila, A, Salazar, R, Bayless, KJ, Kanagala, S, Maxwell, SA, and Davis GE. (2001) Differential gene expression during capillary morphogenesis in 3D collagen matrices: regulated expression of genes involved in basement membrane matrix assembly, cell cycle progression, cellular differentiation and G-protein signaling. J Cell Sci. 114(Pt 15):2755-73. PMID: 11683410.
  • Nelson, V, Davis, GE, and Maxwell SA. (2001) A putative protein inhibitor of activated STAT (PIASy) interacts with p53 and inhibits p53-mediated transactivation but not apoptosis. Apoptosis 6(3):221-34. PMID: 11388671.
  • Maxwell, SA and Davis GE. (2000) Biological and molecular characterization of an ECV-304-derived cell line resistant to p53-mediated apoptosis. Apoptosis 5(3):277-90. PMID: 11225849.
  • Davis, GE, Pintar, Allen, KA, Salazar, R, and Maxwell, SA (2001) Matrix metalloproteinase-1 and -9 activation by plasmin regulates a novel endothelial cell-mediated mechanism of collagen gel contraction and capillary tube regression in three-dimensional collagen matrices. .J Cell Sci. 114(Pt 5):917-30. PMID: 11181175.
  • Maxwell, SA and Davis, GE (2000) Differential gene expression in p53-mediated apoptosis-resistant vs. apoptosis-sensitive tumor cell lines. Proc. Natl. Acad. Sci. USA 97(24):13009-14. PMID: 11069295.