Lisa J. Wood, Ph.D., R.N.
Associate Professor
Oregon Health & Science University
School of Nursing Portland Campus
3455 SW US Veterans Hospital Road, SN-ORD
Portland, Ore. 97239
Phone: 503 494-3431
FAX: 503 494-3688
E-mail: woodl@ohsu.edu
Dual appointment with Radiation Medicine Web page
The long-range goal of our research is to effectively treat and manage the most common symptom experienced by cancer patients undergoing chemotherapy, radiation therapy or both; fatigue. To date the molecular mechanisms underlying the initiation and perpetuation of CTRF are not well established, and, the precise role of inflammatory cytokines, if any, in CTRF remains unclear. Our research program utilizes a pre-clinical and clinical approach to examine the relationship between cancer treatment, inflammatory cytokines and CTRF. This “bench to bedside” approach to understanding the cause of CTRF arises from a unique interdisciplinary collaboration among molecular, behavioral, and clinical investigators all working at various points within the spectrum of cancer research at our institution and hence, represents a major innovation in cancer symptom research.
EDUCATION
1994 Ph.D. Major: Molecular Biology - University of Glasgow, Glasgow, Scotland, UK.
2000 B.S. Major: Nursing - Johns Hopkins University School of Nursing, Baltimore, Md.
Nursing License: Maryland R150273
Community service
2006 Manuscript reviewer for British Journal of Cancer.2007 Manuscript reviewer for Journal of Experimental Therapeutics and Oncology.
2007 Ad-hoc grant reviewer for the American Society for Clinical Oncology Foundation Grant Program
2008 Grant reviewer Thrasher Research Fund
2008 Manuscript reviewer for Therapeutics & Clinical Risk Management
2007-2010 OHSU School of Medicine Research Committee
2005-2007 Member, OHSU School of Nursing, Curriculum Committee
2007-Present Chair, OHSU School of Nursing, Curriculum Committee
Research Support (active)
(Wood, PI) 7/1/2005 – 6/30/2009
American Cancer Society
The Role of Cytokine Deregulation in Cancer Treatment Related Fatigue
Our long-range goal of this program of research is to develop targeted therapies to effectively treat and manage cancer related symptoms, including fatigue. To this end, we have developed an innovative murine model to experimentally evaluate the associations among cancer and its treatment.
(Wood, PI) 7/1/2007-6/30/2009
R21: The National Institute of Nursing Research
The Role of Inflammatory Cytokines in Fatigue Associated with External Beam Radiation Therapy for Prostate Cancer. Using a translational research approach to determine the relationship between treatment-related inflammatory cytokine production and treatment related fatigue.
(Wood, PI) 3/1/2007-2/28/2009
Oregon Clinical & Translational Research Institute
The Role of IL-6 in Breast Cancer Treatment Associated Loss of Lean Body Mass. Our preclinical data implicates IL-6 in the loss of lean body mass in women undergoing systemic antineoplastic chemotherapy for breast cancer. The purpose of this one-year study is to examine this relationship in a clinical setting.
Publications
Wood LJ, Baxter MK, Plafker SM, Gibson W. Human cytomegalovirus capsid assembly protein precursor interacts with itself and with the major capsid protein through two different domains. J. Virology 1997;71:179-190.
Wood, LJ, Maher JF, Bunton TE, Resar LM. The Oncogenic properties of the HMGI gene family. Cancer Research 2000, 60:4256-61.
Wood LJ, Mukherjee M, Dolde CE, Xu Y, Maher JF, Bunton TE, Williams JB, Resar LM. HMG-I/Y, a new c-Myc target gene and potential oncogene. Mol. Cell Biol. 2000;20:5490-502.
Dinulescu D, Wood LJ, Loriaux M, Shen L, Corless CL, Jauron-Mills L, Gross AL, Ren R, Deininger MW, Druker BJ. C-CBL is not required for leukemia induction by Bcr-Abl in mice. Oncogene 2003; 22:8852-60.
Xu Y, Bhattacharya R, Tesfaye A, Felder T, Wood LJ, Huso D, Resar, LMS. Transgenic mice overexpressing HMG-I in lymphoid tissue develop lymphoid hyperplasia and malignancy. Cancer Research; 2004, 64: 3371-3375.
Wood LJ, Nail LM, Perrin NA, Elsea CR, Fischer A, & Druker BJ. The cancer chemotherapy drug etoposide (VP-16) induces pro-inflammatory cytokine production and sickness behavior-like symptoms in a mouse model of cancer chemotherapy related symptoms. Biological Research for Nursing, 2006; 8:157-169.
Wood LJ, Nail LM, Glister A, Winters KA & Elsea CR. Cancer Chemotherapy Related Symptoms: Evidence to Suggest a Role for Pro-Inflammatory Cytokines. Oncology Nursing Forum, 2006; 33:535-542.
Griswold IJ, Bumm T, O’Hare T, Corbin AS, Stoffregen E, Moseson E, Wood LJ, Druker BJ and Deininger MW. Kinase domain mutants of BCR-ABL: altered transformation potency irrespective of sensitivity to imatinib. Molecular & Cellular Biology, 2006, 26:6082-93.
Bumm TGP, Elsea CR, Corbin AS, Loriaux M, Sherbenou D, Wood LJ, Deininger J, Silver RT, Druker BJ & Deininger MWN. Characterization of Murine JAK2V617F-Positive Myeloproliferative Disease. Cancer Research, 2006; 66: 11156-11165.
Ross AM, Hurn P, Perrin N, Wood LJ, Carlini W, Potempa K. Evidence of the Peripheral Inflammatory Response in Transient Ischemic Attack Patients. Journal of Stroke and Cerebrovascular Disease 2008 (In Press).
Di Cello F, Hillion J, Hristov A, Wood LJ, Mukherjee M, Schuldenfrei A, Kowalski J, Bhattacharya R, Ashfaq R, and Resar LMS. HMGA2 participates in neoplastic transformation in human lung cancer. Molecular Cancer Research 2008 (In press).
Elsea CR, Roberts D, Errington DM, Druker BJ, & Wood LJ. Inhibition of p38 MAPK suppresses inflammatory cytokine induction by etoposide, 5-fluorouracil, and doxorubicin without affecting tumoricidal activity. PLoS ONE (In Press).
Wood LJ, Winters-Stone K, Nail LM. Does muscle-derived interleukin-6 mediate some of the beneficial effects of exercise on cancer treatment related fatigue? Oncology Nursing Forum (In Review).
Elsea CR, Roberts D, Druker BJ, & Wood LJ. AMPK induces IL-6 production in murine skeletal muscle in a TNF-α- independent manner. (In preparation).
Elsea CR, Roberts D, Ward AM, Druker BJ, & Wood LJ. Induction of interleukin-6 by doxorubicin-containing breast cancer chemotherapy regimen decreases hepatic IGF-1 production and contributes to loss of fat free mass in mice. (In preparation).
