Lisa J. Wood, Ph.D., R.N.
Oregon Health & Science University
School of Nursing Portland Campus
3455 SW US Veterans Hospital Road, SN-ORD
Portland, Ore. 97239
Phone: 503 494-3859
FAX: 503 494-3688
Dual appointment with Radiation Medicine
Co-director of The Healthy Aging Alliance at OHSU
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.This research is funded by the following grants:
(Wood/ Hill, MPI) 7/1/11-6/30/13
Department of Defense Breast Cancer Research Program, Collaborative Idea Award
Cytokine response to subclinical cytomegalovirus reactivation as a cause of severe fatigue in women undergoing chemotherapy for breast cancer.
(Wood, PI) 9/28/10-6/30/15
5R01NR012479-02, The National Institute for Nursing Research, Mechanisms of Cancer Treatment Related Symptoms.
(Winters-Stone/Wood, MPI) 2/1/12-8/31/13
1R21CA164661-01, National Cancer Institute
Influence of physical exercise on inflammatory biomarkers and adiposity in cancer survivors.
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
PublicationsSauter AD, Wood LJ, Wong J, Iordanov M, and Magun BE. Doxorubicin and daunorubicin induce processing and release of interleukin-1β through activation of the NLRP3 inflammasome. Cancer Biol Ther. 2011 Jun 15;11(12). [Epub ahead of print]
Farley S., Wood LJ & Iordanov M. An Epidermotypic Model of Interface Dermatitis Reveals Individual Functions of Fas Ligand and Gamma Interferon in Hypergranulosis, Cytoid Body Formation, and Gene Expression. Am. J Dermatopathol. 2011 Mar 11. [Epub ahead of print]
Seo JH, Wood LJ, Agarwal A, O'Hare T, Elsea CR, Griswold IJ, Deininger MW, Imamoto A, Druker BJ. A specific need for CRKL in p210BCR-ABL-induced transformation of mouse hematopoietic progenitors. Cancer Research, 2010 70:7325-35.
Ross RL, Jones KD, Ward RL, Wood LJ & Bennett RM. Atypical depression is more common than melancholic in fibromyalgia: an observational cohort study. BMC Musculoskeletal Disorders, 2010 11:120.
Ross RL, Jones KD, Bennett RM, Ward RL, Druker BJ, & Wood LJ. Preliminary Evidence of Increased Pain and Elevated Cytokines in Fibromyalgia Patients with Defective Growth Hormone Response to Exercise. The Open Immunology Journal, 2010, (3), 9-18.
Tyner JW, Bumm TG, Deininger J, Wood L, Aichberger KJ, Loriaux MM, Druker BJ, , Burns CJ, Fantino E, Deininger MW. CYT387, a novel JAK2 inhibitor, induces hematologic responses and normalizes inflammatory cytokines in murine myeloproliferative disorder. Blood, 2010 Apr 12 (Epub ahead of print).
Hillion J., Wood LJ., Mukherjee M., Bhattacharya R., di Cello F, Kowalski J., Elbahloul O., Segal J., Poirier J., Rudin C., Dhara S., Belton B., Joseph B., Zucker S., and Resar L.M. Up-regulation of MMP-2 by HMGA1 promotes transformation in undifferentiated, large cell lung cancer. Molecular Cancer Research, 2009, (7), 1803-12.
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. 2009, 36(5):519-24.
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 2008, 3(6):e2355.
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, 6(5):743-50.
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 2007, 16(5):203-7
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.
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.
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.
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.
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.
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.
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.
Wood, LJ, Maher JF, Bunton TE, Resar LM. The Oncogenic properties of the HMGI gene family. Cancer Research 2000, 60:4256-61.
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.