Photo of Lisa J Wood, Ph.D., R.N.

Lisa J Wood Ph.D., R.N.

  • (503) 494-3859

    Portland Campus

    • Associate Professor School of Nursing

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.

Education

  • B.S.N., Johns Hopkins University School of Nursing, Baltimore Maryland United States 2000
  • Ph.D., University of Glasgow, Glasgow United Kingdom 1995

Publications

  • "Lung inflammation caused by inhaled toxicants : A review." International Journal of COPD In: , Vol. 11, No. 1, 23.06.2016, p. 1391-1401.
  • "Localized External Beam Radiation Therapy (EBRT) to the Pelvis Induces Systemic IL-1Beta and TNF-Alpha Production : Role of the TNF-Alpha Signaling in EBRT-Induced Fatigue." Radiation Research In: , Vol. 185, No. 1, 01.01.2016, p. 4-12.
  • "Relationship between fatigue, sleep quality and inflammatory cytokines during external beam radiation therapy for prostate cancer : A prospective study." Radiotherapy and Oncology In: , Vol. 118, No. 1, 01.01.2016, p. 105-111.
  • "Induction of IL-6 by Cytotoxic Chemotherapy Is Associated With Loss of Lean Body and Fat Mass in Tumor-free Female Mice." Biological Research for Nursing In: , Vol. 17, No. 5, 08.10.2015, p. 549-557.
  • "Increased Th17/Treg Ratio in Poststroke Fatigue." Mediators of Inflammation  In: , Vol. 2015, 931398, 2015.
  • "Preliminary evidence of a blunted anti-inflammatory response to exhaustive exercise in fibromyalgia." Journal of Neuroimmunology In: , Vol. 277, No. 1-2, 15.12.2014, p. 160-167.
  • "Proinflammatory cytokines and DHEA-S in women with fibromyalgia : Impact of psychological distress and menopausal status." Journal of Pain Research In: , Vol. 7, 04.12.2014, p. 707-716.
  • "Preliminary differences in peripheral immune markers and brain metabolites between fatigued and non-fatigued breast cancer survivors : a pilot study." Brain Imaging and Behavior  In: , Vol. 8, No. 4, 23.11.2014, p. 506-516.
  • "Production of IL-1β by bone marrow-derived macrophages in response to chemotherapeutic drugs : Synergistic effects of doxorubicin and vincristine." Cancer Biology and Therapy In: , Vol. 15, No. 10, 01.10.2014, p. 1395-1403.
  • "A role for orexin in cytotoxic chemotherapy-induced fatigue." Brain, Behavior, and Immunity In: , Vol. 37, 03.2014, p. 84-94.
  • "The role of IL-1β and TNF-α signaling in the genesis of cancer treatment related symptoms (CTRS) : A study using cytokine receptor-deficient mice." Brain, Behavior, and Immunity In: , Vol. 38, 2014, p. 66-76.
  • "Inflammation and neural signaling : Etiologic mechanisms of the cancer treatment-related symptom cluster." Current Opinion in Supportive and Palliative Care  In: , Vol. 7, No. 1, 03.2013, p. 54-59.
  • "Small molecule kinase inhibitors block the ZAK-dependent inflammatory effects of Doxorubicin." Cancer Biology and Therapy In: , Vol. 14, No. 1, 01.2013, p. 56-63.
  • "Doxorubicin and daunorubicin induce processing and release of interleukin-1β through activation of the NLRP3 inflammasome." Cancer Biology and Therapy In: , Vol. 11, No. 12, 15.06.2011, p. 1008-1016.
  • "An epidermotypic model of interface dermatitis reveals individual functions of fas ligand and gamma interferon in hypergranulosis, cytoid body formation, and gene expression." American Journal of Dermatopathology In: , Vol. 33, No. 3, 05.2011, p. 244-250.
  • "A specific need for CRKL in p210BCR-ABL - Induced transformation of mouse hematopoietic progenitors." Cancer Research In: , Vol. 70, No. 18, 15.09.2010, p. 7325-7335.
  • "CYT387, a novel JAK2 inhibitor, induces hematologic responses and normalizes inflammatory cytokines in murine myeloproliferative neoplasms." Blood In: , Vol. 115, No. 25, 24.06.2010, p. 5232-5240.
  • "Atypical depression is more common than melancholic in fibromyalgia : An observational cohort study." BMC Musculoskeletal Disorders In: , Vol. 11, 120, 2010.
  • "Upregulation of MMP-2 by HMGA1 promotes transformation in undifferentiated, large-cell lung cancer." Molecular Cancer Research  In: , Vol. 7, No. 11, 11.2009, p. 1803-1812.
  • "Does muscle-derived interleukin-6 mediate some of the beneficial effects of exercise on cancer treatment-related fatigue." Oncology Nursing Forum In: , Vol. 36, No. 5, 09.2009, p. 519-524.
  • "Inhibition of p38 MAPK suppresses inflammatory cytokine induction by etoposide, 5-fluorouracil, and doxorubicin without affecting tumoricidal activity." PLoS One In: , Vol. 3, No. 6, e2355, 04.06.2008.
  • "HMGA2 participates in transformation in human lung cancer." Molecular Cancer Research  In: , Vol. 6, No. 5, 01.05.2008, p. 743-750.
  • "Evidence of the Peripheral Inflammatory Response in Patients With Transient Ischemic Attack." Journal of Stroke and Cerebrovascular Diseases  In: , Vol. 16, No. 5, 09.2007, p. 203-207.
  • "Characterization of murine JAK2V617F-positive myeloproliferative disease." Cancer Research  In: , Vol. 66, No. 23, 01.12.2006, p. 11156-11165.
  • "The cancer chemotherapy drug etoposide (VP-16) induces proinflammatory cytokine production and sickness behavior-like symptoms in a mouse model of cancer chemotherapy-related symptoms." Biological Research for Nursing In: , Vol. 8, No. 2, 10.2006, p. 157-169.
  • "Kinase domain mutants of Bcr-Abl exhibit altered transformation potency, kinase activity, and substrate utilization, irrespective of sensitivity to imatinib." Molecular and Cellular Biology In: , Vol. 26, No. 16, 08.2006, p. 6082-6093.
  • "Cancer chemotherapy-related symptoms : Evidence to suggest a role for proinflammatory cytokines." Oncology Nursing Forum In: , Vol. 33, No. 3, 2006, p. 535-542.
  • "The HMG-I oncogene causes highly penetrant, aggressive lymphoid malignancy in transgenic mice and is overexpressed in human leukemia." Cancer Research  In: , Vol. 64, No. 10, 15.05.2004, p. 3371-3375.
  • "c-CBL is not required for leukemia induction by Bcr-Abl in mice." Oncogene In: , Vol. 22, No. 55, 04.12.2003, p. 8852-8860.
  • "HMG-I/Y, a new c-Myc target gene and potential oncogene." Molecular and Cellular Biology  In: , Vol. 20, No. 15, 08.2000, p. 5490-5502.

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