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Stress, Immunity, and Cervical Cancer: Biobehavioral Outcomes of a Randomized Clinical Trail

Authors' Affiliations: Departments of ¹ Medicine, ² Obstetrics and Gynecology, ³ Psychiatry, and ⁴ Molecular Biology and Biochemistry, ⁵ Center for Health Policy Research, ⁶ Center for Immunology, and ⁷ Chao Family Comprehensive Cancer Center, University of California, Irvine, California

Requests for reprints: Lari Wenzel, Center for Health Policy and Research, University of California, Irvine, 111 Academy Way, Suite 220, Irvine, CA 92697. Phone: 949-824-3926; Fax: 949-824-3388; E-mail: lwenzel{at}uci.edu and Edward L. Nelson, Division of Hematology/Oncology, Center for Immunology University of California, Irvine, Hewitt Hall, Room 3032, Irvine, CA 92697. Phone: 949-824-2860; Fax: 949-824-2305; E-mail: enelson{at}uci.edu.

Purpose: Cancer diagnosis and treatment imparts chronic stressors affecting quality of life (QOL) and basic physiology. However, the capacity to increase survival by improving QOL is controversial. Patients with cervical cancer, in particular, have severely compromised QOL, providing a population well-suited for the evaluation of novel psychosocial interventions and the exploration of mechanisms by which modulation of the psychoneuroimmune axis might result in improved clinical outcomes.

Experimental Design: A randomized clinical trial was conducted in cervical cancer survivors that were enrolled at 13 and <22 months after diagnosis (n = 50), comparing a unique psychosocial telephone counseling (PTC) intervention to usual care. QOL and biological specimens (saliva and blood) were collected at baseline and 4 months post-enrollment.

Results: The PTC intervention yielded significantly improved QOL (P = 0.011). Changes in QOL were significantly associated with a shift of immune system T helper type 1 and 2 (Th1/Th2) bias, as measured by IFN-/interleukin-5 ELISpot T lymphocyte precursor frequency; improved QOL being associated with increased Th1 bias (P = 0.012). Serum interleukin-10 and the neuroendocrine variables of cortisol and dehydroepiandrosterone revealed trends supporting this shift in immunologic stance and suggested a PTC-mediated decrease of the subject's chronic stress response.

Conclusions: This study documents the utility of a unique PTC intervention and an association between changes in QOL and adaptive immunity (T helper class). These data support the integration of the chronic stress response into biobehavioral models of cancer survivorship and suggests a novel mechanistic hypotheses by which interventions leading to enhanced QOL could result in improved clinical outcome including survival.