Rutgers NJMS Logo

Department of Pharmacology, Physiology & Neuroscience

Teresa Wood, Ph.D.

Rena Warshow Endowed Chair in Multiple Sclerosis
Dept. Pharmacology, Physiology & Neuroscience

Department of Pharmacology, Physiology & Neuroscience

Cancer Research Center (CANCT)
195 South Orange Avenue Room H1200

Phone: (973) 972-6529
Fax: (973) 972-0008



Lab Members

Terri L. Wood, PhD

Research: The Wood laboratory is focused on determining how growth factors and signaling pathways
interact to promote growth, survival and differentiation of breast epithelial and neural progenitor cells. We
conduct both in vitro and in vivo studies and make use of mouse models carrying genetic alterations in
genes of interest, particularly in the insulin-like growth factor family of ligands and receptors and in the
mTOR signaling pathway. These studies are designed to reveal normal functions of these signaling systems
in growth and development as well as abnormal functions in cancer and neurological disorders.

Isis Ornelas, Postdoctoral Researcher

Alison Obr, Postdoctoral Researcher

Aminat Saliu, Grad Student

Virginia Ciliento, Grad Student

Luipa Khandker, Grad Student

Angelina Evangelou, Grad Student

Marisa Jeffries, Grad Student

Quan Shang, Research Associate



Ph.D., 1987, University of California, Los Angeles


Curriculum Vitae

View CV




Relevant Publications:

Flannery, C.A., Rowzee, A.M., Choe, G., Saleh, F., Taylor, H.S. and Wood, T.L. (2016) Development of a quantitative PCR assay for detection of human insulin-like growth factor receptor and insulin receptor isoforms. Endocrinology 157:1702-8.
Rota, L.M. and Wood, T.L. (2015) Crosstalk of the insulin-like growth factor receptor with the Wnt signaling pathway in breast cancer. (invited mini-review) Frontiers in Endocrinology, section Cancer Endocrinology Jun 9;6:92. doi: 10.3389/fendo.2015.00092. eCollection 2015. Review.
Wahl, S.E., McLane, L.E., Bercury, K.K., Macklin, W.B. and Wood, T.L. (2014) Mammalian target of rapamycin promotes oligodendrocyte differentiation, initiation and extent of CNS myelination. J. Neurosci. 34:4453-4465.
Rota, L.M., Albanito, L., Shin, M.E., Goyeneche, C.L., Shushanov, S., Gallagher, E.J., LeRoith, D., Lazzarino, D.A.* and Wood, T.L.* (2014) Inhibiting insulin-like growth factor receptor in mammary epithelium accelerates Wnt1-mediated tumorigenesis, canonical Wnt signaling and IGF-II/insulin receptor-A expression. Cancer Research 74(19): 1-12. *co-senior authors
Ziegler, A.N., Chidambaram, S., Forbes, B.E., *Wood, T.L. and *Levison, S.W. (2014) IGF-II and IGF-II analogs with enhanced insulin receptor-A binding affinity promote neural stem cell expansion. J. Biol. Chem. 289:4626-4633. *co-senior authors.
Ziegler, A.N., Levison, S.W. and Wood, T.L. (2014) Insulin and IGF receptor signaling in neural stem cell homeostasis. Nature Reviews Endocrinology, advance online publication 2 December 2014; doi:10.1038/nrendo.2014.208.
Wood, T.L., Bercury, K.K., Cifelli, S.E., Mursch, L.E., Min, J., Dai, J. and Macklin, W.B. (2013) mTOR: A link from the extracellular milieu to transcriptional regulation of oligodendrocyte development. ASN Neuro 5(1):63-79.
Simonishvili, S., Jain, M., Li, H., Levison, S.W. and Wood, T.L. (2013) Mechanisms for Bax-mediated death of oligodendrocyte progenitors in glutamate excitotoxicity and after perinatal hypoxia-ischemia. ASN- Neuro, Dec 23;5(5):e00131.
Min, J. and Wood, T.L. (2012) IGF-1 enhances S and G2/M phase progression in coordination with FGF-2 in oligodendrocyte progenitor cells. GLIA 60:1684-1695.
Ziegler, A.N., Schneider, J.S., Qin, M., Tyler, W.A., Pintar, J.E., Fraidenraich, D., *Wood, T.L. and *Levison, S.W. (2012) IGF-II promotes stemness of neural restricted precursors. Stem Cells 30:1265-1276. *co-senior authors.


Current Research

A major focus of my laboratory is in determining how hormones and peptide growth factors interact to promote growth, survival and differentiation of breast epithelial cells. These studies have provided new information on a role for the IGFs in hormone-mediated growth of the developing mammary gland. We have demonstrated expression of the IGFs and the IGF binding proteins during the major postnatal growth stages of mammary epithelium. Results from these studies demonstrated that the both IGF-I and IGF-II as well as the IGF-IR are expressed in cells of the mammary gland throughout postnatal growth including during pubertal-induced ductal growth and pregnancy-induced alveolar differentiation. We also demonstrated that IGF-I and IGF-II are expressed in both the stromal and epithelial compartments of the developing mammary gland and are distinctly regulated in their expression patterns. Insulin-like growth factor-I (IGF-I) and the epidermal growth factor (EGF)-related ligands are demonstrated mitogens for mammary epithelial cells in vitro and are essential for growth of the mammary epithelium during development. We have investigated the role of IGF-I and EGF in mediating proliferation and cell cycle progression in mammary epithelial cells in an ex vivo culture system. We demonstrated that IGF-I and EGF are synergistic in promoting DNA synthesis in mammary epithelial cells in the intact mammary gland. Moreover, we demonstrated that IGF-I and EGF induce expression of early G1 cyclins in mammary epithelial cells. IGF-I, but not EGF, induces late G1 and G2 cyclins and is required for mammary epithelial cells to overcome the G1-S checkpoint. These data demonstrate that in the intact mammary gland, IGF-I is essential for cell cycle progression and that it is required for EGF-mediated progression past the G1-S checkpoint in mammary epithelial cells.
Regulation of cell proliferation and cyclin expression has been of particular interest in the developing mammary gland as well as in breast cancer. In order to extend our studies to normal mammary development and mammary tumor formation in vivo, we have established or collected various mouse lines with genetic alterations in the IGF ligands, the IGFBPs or the IGF-IR. In my laboratory, we have established two lines of mice that overexpress a dominant-negative form of the IGF-IR from either the MMTV or WAP (milk protein) promoter. The expression of the dominant-negative IGF-IR is expected to produce functional deletion of signaling through the IGF-IR in mammary tissue during the major growth phases of pubertal ductal growth and pregnancy-induced alveolar growth. Analyses of these mouse lines show that decreased IGF-IR signaling results in decreased mammary epithelial growth and altered parameters of differentiation. Ongoing analyses of these and other mutant mouse lines will provide the basis to define the function of the IGFs in mammary epithelial growth and to discern the role of circulating versus local IGFs in growth and function of this tissue. Further, studies are currently in



Everything A Medical School Should Be - And More

© 2014, Rutgers, The State University of New Jersey. All rights reserved.

185 South Orange Avenue, Newark, New Jersey 07101