Signal Transduction and Cell Proliferation Research Program
Program Leaders: Al Reynolds, Ph.D., and Jeffrey Sosman, M.D.
The Signal Transduction and Cell Proliferation Program (ST) is focused on promoting basic and translational research in the area of cell growth control. In general, activities toward this end are aimed at two broadly defined objectives:
- To promote outstanding basic research, with an eye toward maintaining the strongest possible foundation of fundamental knowledge (including technology) in the relevant disciplines.
- To encourage and cultivate translational research through targeted recruitment of new faculty, selective funding of translational pilot projects, and other avenues aimed at leveraging the capabilities of outstanding basic and clinical research contingents at Vanderbilt.
The program leadership is equally committed to both goals and believes that together they comprise the most effective means of realizing translational objectives. Based on these goals, the formal aims for the program are: 1) to increase awareness of the research going on within each member’s laboratory and thereby encourage collaborative interactions within the program, and 2) to aggressively cultivate the cutting-edge basic science expertise required to foster and promote effective translational research within the Cancer Center. With respect to the latter, the program will continue to proactively build out translational capabilities by engaging specific opportunities – such as the recruitment of Dr. Stephen Fesik (highlighted later), who brings to the program worldclass expertise in drug discovery, and creation of the Translational Research Laboratory (TRL), spearheaded by Drs. Sosman and Hiebert, an expressly translation-oriented resource, now shared by all programs within the VICC. Thus, the ST program now encompasses basic science that focuses on some of the best therapeutic targets (signaling pathways), cancer drug discovery and medicinal chemistry, and translational research/clinical trials to attack these pathways.
Program Focus to Meet Scientific Goals
A common thread connecting all members of the ST program is an interest in cell growth control as it pertains to cancer. Dysregulation of cell growth is a hallmark of cancer and the pathways involved continue to be an important source of novel targets for cancer therapeutics. The underlying mechanisms, however, are diverse, as are the interests of the ST membership. The members of the program work in one or more broadly defined areas (i.e., Growth Factors and Receptors, Signaling Intermediates, and Gene Expression, Figure ST1). Within this general framework, however, the 49 ST program members bring to the table comprehensive expertise in nearly all aspects of signal transduction and cell proliferation, as described later in more detail.
An important goal for all programs in VICC is to determine how best to leverage the collective knowledge and expertise of their faculty. With this in mind, the ST leadership organizes and sponsors activities designed to promote intra- and inter-programmatic interaction as a means of encouraging information exchange and collaboration. These include seminars, quarterly mini-retreats, an annual retreat, mentorship of younger investigators via a T-32 training grant, contribution to cancer-related review panels and focus groups around specific research topics.
About the Program Leaders
In July 2008 Dr. Reynolds took over leadership of the program from Dr. Scott Hiebert, who had held the position since 2001. In this role, Dr. Reynolds organizes the program’s activities, as described in more detail above (see Program Features to Meet Scientific Goals). Currently, the main activities include the mini-retreat ‘research in progress’ series, the annual retreat, external seminars, and dissemination of information to the program’s members. On a more general level, he is responsible for guiding the evolution of the program, orchestrating changes in emphasis, as needed, and stimulating new initiatives.
Dr. Reynolds joined the Vanderbilt faculty in 1996 and is currently Professor of Cancer Biology. His training in the oncogene field was with Dr. J.T. Parsons at the University of Virginia, where he was instrumental in discovery of many of the first bone fide Src substrates, including Focal Adhesion Kinase (FAK), Cortactin, Actin Filament Associated Protein (AFAP) and p130CAS. He is best known for his discovery of another Src substrate, p120-catenin (p120), and its identification as a key regulator of the tumor and metastasis suppressor E-cadherin. His work at Vanderbilt has revealed that p120 is a master regulator of the turnover and stability of classical cadherins, including E-cadherin. Currently, his laboratory is interested in the signal transduction pathways linked to the role of p120 in oncogene-mediated cell transformation (e.g., by Src and/or Receptor Tyrosine Kinases), and the role of p120 as a tumor suppressor in the context of E-cadherin function and in relation to the colon tumor suppressor protein Adenomatous Polyposis Coli (APC). The laboratory is funded primarily by the GI-SPORE (Project 3) and two R01 grants.
Administratively, Dr. Reynolds is currently a permanent member of the NIH/NCI study section ‘Intercellular Interactions’ (ICI), and serves on the Board of Directors for the Ayers Institute. He also is Executive Director of the Vanderbilt Antibody Shared Resource (VASR), supported in part by the CCSG, and was instrumental in its recent restructuring. He has been a Project Leader in the Vanderbilt GI SPORE since its inception in 2002, and has prominent roles in the Epithelial Biology Center, the Breast Cancer SPORE, and the MMHCC (Mouse Models of Human Cancers Consortium), where he brings to the table several p120 conditional knockout mouse models and evidence that p120 plays a prominent role downstream of APC in the genesis of colon cancer. He is also co-founder and remains on the Board of Directors of Stovall Life Sciences Inc., which designs and constructs equipment for the biotech industry.
Dr. Sosman is a Professor of Medicine within the Division of Hematology/Oncology. Since his arrival at Vanderbilt in December 2001, he has taken on a number of responsibilities in addition to his leadership role in this program. Previously, these responsibilities included Medical Director of the VICC Clinical Trials Shared Resource. At present, he is Director of the Melanoma Group, and he works closely with the Phase I program in drug development in melanoma and renal cell carcinoma. He is a permanent member of the NIH/NCI study section for Cancer Immunology and Immunotherapy (CII) from 2006 - 2010. He is recognized nationally for his expertise in melanoma, clinical tumor immunology, and most recently targeted therapy for melanoma. He has been peer-review funded in the past for both immunotherapy trials and translational clinical trials in melanoma. Dr. Sosman recently was awarded a NCI K24 to support mentoring individuals in clinical investigations in melanoma. Most of his research has shifted focus from immunologic approaches in melanoma and renal cancer to clinical efforts utilizing inhibitors of tumor signaling pathways, surface growth factors, or vascular growth factors that target the cancer cell biology. As described above, he was an important force behind the development of the Translational Research Laboratory and is heavily involved in its activity. Dr. Sosman was recently named the Mary Hendrickson-Johnson American Cancer Society Melanoma Research Professor. He is the first honoree of this five-year award, which was awarded for his career achievements and new research initiatives in translational research in melanoma. He was also recently appointed as an Ingram Professor for Cancer Research. His translational activities are well matched to his role in ST, where his expertise in melanoma and clinical trials has been instrumental in facilitating trials led by other investigators in several other malignancies.
Areas Of Research Program Expertise
ST is a relatively large group connected by a common interest in cell proliferation as it relates to cancer. As one of its main goals, the program aims to promote outstanding basic research with an eye toward maintaining strong expertise in the diverse areas that collectively coordinate growth control. Thus, the 49 ST program members bring to the table comprehensive expertise in nearly all aspects of signal transduction and cell proliferation.
Growth Factors and Receptors
Our strength in growth factor and receptor signaling dates back to Stanley Cohen and his seminal work on epidermal growth factor (EGF). Cohen and Rita Levi-Mantalcini won the 1986 Nobel Prize for their discovery of cellular growth factors (EGF and NGF, respectively). EGF and NGF receptors were among the first discovered receptor tyrosine kinases (RTKs), and the first discovered RTK oncogenes. EGFR family members have been exploited extensively as therapeutic targets (e.g., Erbitux, Herceptin, small molecule EGFR inhibitors) and remain important areas of interest in ST. The Carpenter laboratory uses EGF stimulation of mammalian cells as a model system for identifying mechanisms by which growth factors regulate cell proliferation. Current areas of interest include endocytic trafficking of the different EGFR family members and a novel signaling mechanism involving the cleavage and nuclear translocation of the ErbB4 cytoplasmic domain. Dr. Carpenter is credited with discovery of phospholipase C-γ (PLCγ) as a key EGFR substrate.
Bruce Carter, Ph.D. is studying p75 neurotrophin receptor signaling mechanisms involved in context-dependent activation of survival or apoptosis. Data published recently in Neuron shows that the apoptotic pathway requires γ-secretase-dependent release of the intracellular domain and subsequent nuclear translocation of the DNA binding protein NRIF. Chin Chiang, Ph.D. and Ethan Lee, M.D., Ph.D. study signaling pathways stimulated by Wnt and Hedgehog, respectively. Both morphogens have prominent roles in development and cancer, and are important therapeutic intervention targets. A recent addition to ST, Stacey Huppert, Ph.D. is using mouse models to distinguish whether Notch is acting as a general tumor suppressor in the liver.
Several ST investigators study receptor signaling pathways involved in chronic inflammation, a phenomenon known to play a major role in tumorigenesis, tumor progression, and metastasis. Dr. Richmond investigates chemokine receptor signaling associated with chronic inflammation, wound healing, and tumorigenesis. The Richmond laboratory in collaboration with Dr. Sosman has integrated basic and clinical areas of expertise to study the efficacy of NFkB inhibition in mouse models of melanoma, and in related human clinical trials. Our Meharry colleague, Samuel Adunyah, Ph.D, is evaluating roles for other cytokines in immune function (e.g., IL-17), with emphasis on their roles in cancer susceptibility. Another cancer-associated mediator of inflammation is prostaglandin E2 (PGE2). The laboratory of Richard Breyer, Ph.D. is evaluating role(s) for the PGE2 receptor in colorectal tumorigenesis using a PGE2 receptor knockout mouse model. A very different approach in the Krezel laboratory relies on structural NMR studies to evaluate protein-protein and protein-DNA interactions involved in H. Pylori signaling. Inflammation associated with H. Pylori is strongly implicated in the genesis of stomach cancer. In related studies, the Reynolds and Peek laboratories have joined forces to show that p120-catenin, and its transcription factor binding partner Kaiso, are also modulators of H. Pylori-induced inflammation. Finally, an inter-institutional collaboration between Drs. Reynolds and Elaine Fuchs (NYU) has revealed that p120-catenin is a potent inflammation suppressor. Targeted p120 ablation in the skin induced cell autonomous activation of NFkB, resulting in a “cytokine storm” and dramatic inflammation.
A second broad area of expertise in ST involves signaling intermediates – comprising mostly downstream transducers of receptor signaling. Signaling intermediates in inflammation pathways have emerged as critical targets for pharmaceutical intervention and cancer prevention. Because most of these factors strongly influence cell proliferation, many are included in ST, recognizing that much of the work on inflammation also addresses other critical aspects of this phenomenon. The importance of prostaglandins to these processes is underlined by the efficacy of nonsteroidal anti-inflammatory drugs (NSAIDs), which inhibit prostaglandin synthesis via inactivation of the cyclooxygenases COX1 and COX2. Jacek Hawiger, M.D., Ph.D. is studying mechanisms associated with excessive and persistent cytokine production in response to bacterial lipopolysacharides (LPS) or super antigens. A critical consequence is signaling to the nucleus via NFkB or other stress-responsive transcription factors (SRTFs) that ultimately influence transcription of hundreds of genes encoding mediators of inflammation. The Hawiger laboratory has devised a cell-permeable peptide that antagonizes nuclear import of NFkB and other SRTFs. In mice, these peptides suppress systemic production of inflammatory cytokines (e.g., TNFα and interferon γ) and increase survival. Drs. Richmond, Sosman, and Reynolds also study signaling pathways linked to NFkB and inflammation, as described above. A frequent downstream consequence of this NFkB activity is inhibition of cell death. Elizabeth Yang, M.D., Ph.D. brings expertise in Bcl-2 and other pathway members associated with regulation of apoptosis. Dedicated efforts at clinical translation are well underway for several of the inflammation related discoveries.
A number of lipid intermediates are critical factors in pathways that directly modulate cell proliferation and/or tumorigenicity. Alex Brown, Ph.D. studies the role(s) of phospholipases and their lipid derivatives in a variety of cellular functions linked to cancer using a “lipidomics” mass spectrometry approach. One area of focus is the role of phospholipase D (PLD), a signaling intermediate responsible for the production of the lipid second messenger phosphatidic acid. In a multi-laboratory, intra- and inter-programmatic collaboration, Drs. Brown and Lindseyt have designed the first isoform-selective phospholipase D inhibitors and finds that a subset of these can block invasiveness in metastatic breast cancer models. These inhibitors will be important tools for evaluating the role(s) of PLD enzymes in tumor progression and metastasis. Even at this early phase both the TRL and the Phase I program is coordinating with the Brown laboratory to initate plans for clinical development.
Other work involves intermediate players in a variety of cell signaling pathways. The Colbran laboratory is interested in the structure, function and subcellular targeting of Ca2+/calmodulin-dependent protein kinase II (CaMKII), a ubiquitous integrator of the dynamics of calcium oscillations. CaMKII modulates multiple steps in pathways important for cell proliferation, cell death, and cell morphology. Pran Datta, Ph.D. has identified a novel WD-40 domain containing protein, STRAP (Serine Threonine Kinase Receptor Associated Protein), that negatively regulates TGF-β signaling via association with TGF-β type I and type II receptors. STRAP synergizes with Smad7, an inhibitory Smad, to inhibit TGF-β signaling and associated tumor suppressor functions. Biochemical, proteomic, and targeted gene ablation studies are underway to evaluate translational potential. Dr. Brash works on biosythesis and/or metabolism of cancer-relevant lipid intermediates, including eicosanoids, lipoxygenase, arachidonic acid, prostaglandins, and cyclooxygenases.
ST also supports work that fits the classic paradigm of basic science research having potential to provide novel insights into cancer cell growth. For example, control of gene expression and cell signaling is inherently dependent on nucleocytoplasmic transport. One focus of the Wente laboratory is the nuclear pore complex, including NUP98 and NUP214, both of which are linked to multiple chromosomal translocations associated with human leukemias. In addition, she reported recently on DEAD-box proteins, which are misexpressed in prostate, colon, and lung carcinomas. Dr. Wente discovered the inositol kinase pathway involved in inositol hexakisphosphate (IP-6) production, which may be involved in Hedgehog signaling. Dr. Wente also works on proteins that regulate translation. The translation initiation factor eIF4E is considered an oncogene, and eIF2a, eIF5A, and eIF3 are also linked to cancer. Andrew Link, Ph.D. has applied proteomics to identify a number of novel proteins involved in translation and protein synthesis.
Dr. Magnuson has developed a recombinase-mediated cassette exchange (RMCE) method to generate cassette acceptor alleles for in vivo structure-function experiments. He showed recently that Rictor (a component of the mTOR 2 complex (mTORC2), is a primary kinase for phosphorylation of Akt on ser473. Cells lacking Rictor exhibit low proliferation, impaired AKT activity, and diminished metabolic activity. As leader of the newly established Vanderbilt Stem Cell Biology Center, Dr. Magnuson brings both embryonic and adult stem cell expertise to the program.
Of note, several ST members bring to the table important cutting-edge technologies. For example, Dan Leibler, Ph.D. (Director of the Ayers Institute) uses mass spectrometry to identify early markers for colon cancer. A key technical objective is to boost the sensitivity of liquid chromatograph-tandem mass spectrometry (LC-MS-MS) technology. David Tabb, Ph.D. dedicates part of his effort to improvement of proteomic tools. He has developed information analysis software for mass spectrometry that has been adopted by most if not all of the mass spec resources at Vanderbilt. Similarly, Dr. Link brought shotgun proteomics to Vanderbilt, Dr. Magnuson has been instrumental in advancing technology in the transgenic mouse shared resource, and Dr. Reynolds recently took over and restructured the Vanderbilt Antibody Shared Resource to increase productivity and throughput. As mentioned previously, we are especially excited to recruit Dr. Thomson – one of the country’s foremost experts in miRNA biology. His technical expertise has made it practical and straightforward for ST and VICC members to ask fundamental questions as to whether and how their research is related to regulation by miRNAs. Thomas Andl, Ph.D. also is focused on the role of miRNAs in melanoma development.
Dr. Lee is interested in Wnt signal transduction pathways and the development of novel therapeutics aimed at blocking the pathway downstream of the colon cancer tumor suppressor APC. Using an assay based on Xenopus egg extracts, he devised a novel high-throughput screen to identify compounds that suppress the Wnt signaling pathway at the level of Axin. Interestingly, the most promising hit is a compound already approved by the FDA for treatment of an intestinal parasite. In its current form, it is not sufficiently soluble for systemic use, but we (and others) are very excited about its therapeutic potential in colon cancer. The ST leadership has been instrumental in guiding Dr. Lee to critical Vanderbilt resources. Through new alignments with ST members Craig Lindsley and Alex Waterson of the Vanderbilt Institute for Chemical Biology (VICB), Dr. Lee has identified an impressive pipeline of suitable high-affinity derivatives, which are now under testing in APC-based mouse models for efficacy in colon cancer. This work illustrates several important intra- and inter-programmatic interactions, as well as impressive coordination with other Vanderbilt entities such as the VICB and the GI Program, including support from the GI SPORE.
The Lee project and others like it highlight the need to establish bona fide experience in drug discovery and development. To that end, Dr. Fesik was actively recruited by VICC (and several other interested entities) to Vanderbilt from Abott Laboratories, where he is credited with a long list of high-profile accomplishements in drug discovery and development. He has held multiple positions at Abbott, including Vice President of Cancer Research, where he was responsible for efficiently moving key compounds through clinical trials. His research focus is cancer drug discovery using fragment-based approaches and structure-based drug design. We are fortunate to add him to the ST program and anticipate the he will have an important impact in the areas of drug development that are not yet well represented at Vanderbilt.
Many important oncogenes and tumors suppressors are transcription factors. An overall focus of the Pietenpol laboratory is to elucidate role(s) of the p53 gene family (p53, p63, p73) in normal cell proliferation and cancer. A recent finding identified mTOR as a regulator of p73, opening a window of opportunity for therapeutic intervention. In collaboration with clinical investigators in the Breast Cancer (BC) program, these preclinical findings have been translated to Phase I and Phase II clinical trials as described in the BC program narrative. Mechanisms controlling c-Myc expression in cancer have been particularly elusive. In a high-impact report, the laboratory of Stephen Hann, Ph.D. has identified differential effects of the p14ARF tumor suppressor (referred to as ARF) on c-Myc function, suggesting that c-Myc-induced proliferation and apoptosis are mediated by separate molecular mechanisms. These data invoke a direct feedback mechanism representing a novel p53-independent checkpoint that prevents c-Myc-mediated tumorigenesis.
Several ST members study oncogenes or tumor suppressors associated with particular cancers. Dr. Brandt’s group is focused on the control of blood cell production and how it is subverted in hematologic malignancy. A particular interest is the TAL1 (or SCL) oncogene, whose abnormal expression constitutes the most frequent gain of function mutation in T-cell acute lymphoblastic leukemia (T-ALL). Dr. Eid uses SYT-SSX, the translocation product responsible for synovial sarcoma, as a model to study mechanisms of gene expression in cancer. One area of interest is the role of the proto-oncogene SYT and SYT-SSX in chromatin remodeling and polycomb repression. She has found that SYT-SSX activates the Wnt signaling pathway, resulting in nuclear translocation of β-catenin, and is examining the role of this event in the genesis of synovial sarcoma. Mark deCaestecker, Ph.D. and Harold Lovvorn, M.D. are interested in the role and regulation of the Cited family of transcriptional co-factors in Wilm’s tumorigenesis. Dr. Sealy has identified a role for the transcription factor CCAAT/Enhancer Binding Protein (C/EBPb) in epithelial to mesenchymal transition (EMT). Interestingly, forced expression of C/EBPb-2, but not C/EBPb-1 in MCF10A cells induces EMT and several other cancer-related changes. LaMonica Stewart, Ph.D., a Meharry colleague, is investigating the role of PPARγ in cellular and mouse models for prostate cancer. Dr. Matusik is widely recognized for development of several mouse models for prostate cancer, including LADY and TRAMP, as well as key transgenic models for targeting Cre-mediated gene ablation to the prostate.
Recent insights highlight increasingly important roles for histone modification in cancer. Dr. Hiebert studies the molecular mechanisms of acute leukemia, cell cycle control, and the action of tumor suppressors. One focus is determining the normal functions of the AML1/RUNX1 and ETO/MTG family transcription factors and mechanism(s) by which their various translocation fusion proteins give rise to leukemia. Recent efforts extend to enzymes recruited by AML1 and MTG family members, the histone deacetylases. The consequence of histone deacetylase 3 inactivation in mice has interesting translational implications and is featured in more detail later. Dr Sun uses budding yeast as a eukaryotic model to study histone ubiquitination and gene regulation. The Weil laboratory studies the structure-function relationships of the TFIID complex in the yeast model system. TFIID is an evolutionarily conserved 15-subunit protein complex that binds to the promoters of essentially all eukaryotic mRNA-encoding genes, including humans. TFIID plays a key role in control of cell differentiation, growth and response to DNA damage. Roland Stein, Ph.D. has identified a novel transcription factor important in pancreatic development. Dr. Andl is examining the role of Dicer and miRNAs in squamous epithelial carcinogenesis and melanoma. He has demonstrated recently that Dicer is essential for hair follicle morphogenesis.
- Adunyah, Samuel E., Ph.D.
Professor and Chair of Cancer Biology, Meharry Medical College; Researcher
- Andl, Thomas, Ph.D.
Assistant Professor of Medicine (Dermatology); Researcher
- Arildsen, Mary Ann Thompson, M.D., Ph.D.
Associate Professor of Pathology, Microbiology and Immunology; Researcher
- Aune, Thomas M., Ph.D.
Professor of Medicine (Rheumatology); Associate Professor of Pathology, Microbiology and Immunology; Researcher
- Brandt, Stephen J., M.D.
Professor of Medicine (Hematology/Oncology); Professor of Cell and Developmental Biology; Professor of Cancer Biology; Researcher
- Brash, Alan R., Ph.D.
Professor of Pharmacology; Researcher
- Breyer, Richard M., Ph.D.
Ruth King Scoville Professor of Medicine (Nephrology) ; Researcher
- Brown, H. Alex, Ph.D.
Bixler-Johnson-Mayes Professor of Pharmacology; Researcher
- Carpenter, Graham F., Ph.D.
Professor of Biochemistry, Emeritus; Researcher
- Carter, Bruce D., Ph.D.
Professor of Biochemistry; Investigator, Center for Molecular Neuroscience ; Investigator, Kennedy Center for Research & Humanities; Researcher
- Chiang, Chin, Ph.D.
Professor of Cell and Developmental Biology; Researcher
- Colbran, Roger J., Ph.D.
Professor of Molecular Physiology and Biophysics; Researcher
- Cooper, Michael K., M.D.
Associate Professor of Neurology; Researcher
- Crispens, Marta Ann, M.D.
Associate Professor of Obstetrics and Gynecology; Gynecological Oncologist
- Davé, Utpal P., M.D.
Assistant Professor of Medicine (Hematology/Oncology); Assistant Professor of Cancer Biology; Hematologist/Oncologist
- deCaestecker, Mark P., M.D., Ph.D.
Assistant Professor of Medicine; Researcher
- Fesik, Stephen W., Ph.D.
Orrin H. Ingram, II Professor of Cancer Research; Professor of Biochemistry, Pharmacology and Chemistry; Researcher
- Hann, Stephen R., Ph.D.
Professor of Cell and Developmental Biology; Researcher
- Hawiger, Jack Jacek, M.D., Ph.D.
Distinguished Professor of Medicine (Allergy, Pulmonary, and Critical Care); Louise B. McGavock Endowed Chair; Professor of Physiology and Molecular Biophysics; Researcher
- Hiebert, Scott W., Ph.D.
Associate Director for Basic Research; Hortense B. Ingram Professor of Cancer Research; Professor of Biochemistry; Associate Professor of Medicine; Researcher
- Ho, Richard, M.D., MSCI
Assistant Professor of Pediatrics (Pediatric Hematology and Oncology); Pediatric Hematologist/Oncologist
- Ihrie, Rebecca A., Ph.D.
Assistant Professor of Cancer Biology; Assistant Professor of Neurological Surgery
- Irish, Jonathan M., Ph.D.
Assistant Professor of Cancer Biology; Assistant Professor of Pathology, Microbiology and Immunology
- Jagasia, Madan, M.B.B.S., M.S.
Professor of Medicine (Hematology/Oncology); Director, Outpatient Transplant Program; Section Chief, Hematology and Stem Cell Transplant; Hematologist/Oncologist
- Lee, Ethan, M.D., Ph.D.
Associate Professor of Cell and Development Biology; Researcher
- Liebler, Daniel (Dan) C., Ph.D.
Professor of Biochemistry, Pharmacology, Biomedical Informatics; Director, Center in Molecular Biology; Director, Ayers Institute; Researcher
- Lindsley, Craig W., Ph.D.
William K. Warren, Jr. Professor of Medicine; Professor of Pharmacology, Chemistry; Researcher
- Link, Andrew J., Ph.D.
Associate Professor of Pathology, Microbiology and Immunology; Assistant Professor of Biochemistry; Researcher
- Lopez, Carlos F., Ph.D.
Assistant Professor of Cancer Biology; Researcher
- Lovvorn, Harold N. (Bo), III, M.D.
Assistant Professor of Pediatrics; Assistant Professor of Pediatrics Surgery; Pediatric Surgeon
- Magnuson, Mark A., M.D.
Louise B. McGavock Professor of Molecular Physiology and Biophysics, ; Medicine, Cell and Developmental Biology; Researcher
- Matusik, Robert J., Ph.D.
William L. Bray Professor of Urologic Surgery; Professor of Cell & Developmental Biology, Cancer Biology; Director of Urologic Surgery Research; Researcher
- Pietenpol, Jennifer A., Ph.D.
Benjamin F. Byrd, Jr. Professor of Oncology Director; Professor of Biochemistry, Otolaryngology, Cancer Biology; Vanderbilt-Ingram Cancer Center; Administrator and Researcher
- Puzanov, Igor, M.D.
Associate Professor of Medicine; Medical Oncologist
- Reynolds, Albert B., Ph.D.
Ingram Professor of Cancer Research; Professor of Cancer Biology; Executive Director, Vanderbilt Antibody and Protein Resource (VAPR) ; Program Director, VICC Signal Transduction & Cell Proliferation Research Program; Researcher
- Sealy, Linda J., Ph.D.
Associate Professor of Cancer Biology, Cell and Developmental Biology, Molecular Physiology and Biophysics; Researcher
- Sosman, Jeffrey A., M.D.
Professor of Medicine; Director, Melanoma & Tumor Immunotherapy Program; Co-Leader, VICC Signal Transduction & Cell Proliferation Research Program; Medical Oncologist
- Stein, Roland W., Ph.D.
Mark Collie Chair in Diabetes Resesarch; Professor of Molecular Physiology and Biophysics, Cell and Developmental Biology; Researcher
- Stewart, LaMonica V., Ph.D.
Assistant Professor of Cancer Biology, Meharry Medical College; Researcher
- Strickland, Stephen A., Jr., M.D., MSCI
Assistant Professor of Medicine; Hematologist/Oncologist
- Sun, Zu-Wen, Ph.D.
Assistant Professor of Biochemistry; Researcher
- Tabb, David L., Ph.D.
Associate Professor of Biochemistry, Biomedical Informatics ; Mass Spectrometry Bioinformaticist
- Wang, Jialiang, Ph.D.
Assistant Professor of Cancer Biology; Director, Neurosurgical Oncology Laboratory
- Waterson, Alex G., Ph.D.
Research Assistant Professor of Pharmacology, Chemistry; Researcher
- Weil, P. Anthony, Ph.D.
Professor of Molecular Physiology & Biophysics; Researcher
- Wente, Susan R., Ph.D.
Associate Vice Chancellor for Research; Senior Associate Dean for Biomedical Sciences; Professor of Cell and Developmental Biology ; Researcher