The authors

suggest early life stress as a plausible risk factor for inflammation that undergirds cancer-related fatigue. The empirical paper by Witek-Jansek et al. in this volume explores whether childhood adversity is associated with vulnerability for intense sustained behavioral symptoms, including fatigue and depressive symptoms, and quality of life and immune dysregulation (Witek Janusek et al., 2012). Irwin and colleagues describe the common presentation of sleep disturbance and depression in cancer survivors (Irwin et al., 2012). The authors outline a model in which sleep disturbance drives alterations in inflammatory biology, which result in of depressive symptoms and in clinical depression for some. The model acknowledges depression history and other psychosocial, biobehavioral, and medical factors that might act as moderators. The Lutgendorf BIBW2992 nmr laboratory contributes an analysis of associations between cortisol, interleukin-6, BMS-354825 mw depression, fatigue, and disability in ovarian cancer patients followed prospectively from pre-surgical baseline to one-year post surgery, and illustrates how chemotherapy acts to normalize these biological markers (Schrepf et al., 2012). Although challenges exist, the review by Costanzo et al. identifies opportunities to explore clinically significant PNI relationships

in a hematopoietic stem cell transplantation context (HSCT) (Costanzo et al., 2012). Improved understanding of the factors that moderate timely immune recovery and optimal immune

regulation might confer improved short- and long-term Avelestat (AZD9668) outcomes for HSCT recipients. Noted as challenges for PNI researchers working in a HSCT context are the pace of change and evolution in HSCT medicine and associated technical innovations. The secondary data analysis by McGregor et al. investigating the effect of pre-transplantation distress on white blood cell count among autologous hematopoietic cell transplantation patients, highlights these challenges (McGregor et al., 2012). Within the last decade, exercise has been established as an effective adjuvant therapy to control adverse consequences associated with cancer treatment. Jones et al. comprehensively reviews extant evidence linking exercise behavior, functional capacity/exercise capacity, disease recurrence, and cancer-specific and all-cause mortality (Betof et al., 2012). Further, the authors outline host and tumor-related mechanisms underlying the exercise/fitness and prognosis relationship and review evidence from pre-clinical animal models of cancer. This exciting work highlights exercise as one critical component of energy balance influences on cancer etiology, progression, and outcome (Hursting et al., 2012).