Michael H Antoni1, Laura C Bouchard2, Jamie M Jacobs3, Suzanne C Lechner4, Devika R Jutagir2, Lisa M Gudenkauf2, Charles S Carver5, Susan Lutgendorf6, Steven W Cole7, Marc Lippman8, Bonnie B Blomberg9. 1. Dept. of Psychology, University of Miami, 5665 Ponce de Leon Blvd, Coral Gables, FL 33124, USA; Dept. of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, 1120 NW 14th St., Miami, FL 33136, USA; Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, 1475 NW 12th Ave., Miami, FL 33136, USA. Electronic address: mantoni@miami.edu. 2. Dept. of Psychology, University of Miami, 5665 Ponce de Leon Blvd, Coral Gables, FL 33124, USA. 3. Center for Psychiatric Oncology and Behavioral Sciences, Dept. of Psychiatry, Massachusetts General Hospital Cancer Center, 55 Fruit St., Boston, MA 02114, USA. 4. Dept. of Psychiatry and Behavioral Sciences, University of Miami Miller School of Medicine, 1120 NW 14th St., Miami, FL 33136, USA; Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, 1475 NW 12th Ave., Miami, FL 33136, USA. 5. Dept. of Psychology, University of Miami, 5665 Ponce de Leon Blvd, Coral Gables, FL 33124, USA; Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, 1475 NW 12th Ave., Miami, FL 33136, USA. 6. Dept. of Psychological and Brain Sciences, University of Iowa, E 11 Seashore Hall, Iowa City, IA 52242, USA. 7. Dept. of Medicine, Division of Hematology-Oncology, University of California - Los Angeles School of Medicine, 11-934 Factor Bldg, Los Angeles, CA 90095, USA; Dept. of Psychiatry and Biobehavioral Sciences, University of California - Los Angeles School of Medicine, 11-934 Factor Bldg, Los Angeles, CA 90095, USA; Norman Cousins Center, University of California - Los Angeles, 11-934 Factor Bldg, Los Angeles, CA 90095, USA. 8. Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, 1475 NW 12th Ave., Miami, FL 33136, USA; Dept. of Medicine, University of Miami Miller School of Medicine, 1600 NW 10th Ave., RMSB 3146A, Miami, FL 33136, USA. 9. Sylvester Comprehensive Cancer Center, University of Miami Miller School of Medicine, 1475 NW 12th Ave., Miami, FL 33136, USA; Dept. of Microbiology and Immunology, University of Miami Miller School of Medicine, 1600 NW 10th Ave., RMSB 3146A, Miami, FL 33136, USA.
Abstract
PURPOSE:Cognitive behavioral stress management (CBSM) is an empirically-validated group-based psychosocial intervention. CBSM is related to decreased self-reported indicators of psychological adversity during breast cancer treatment and greater disease-free survival (DFS) vs. a control condition. This study examined relationships between CBSM, DFS, and a potential biobehavioral pathway linking these variables in breast cancer patients through a gene expression composite representing the leukocyte conserved transcriptional response to adversity (CTRA). DESIGN:Women with stage 0-IIIb breast cancer completed questionnaires and provided blood samples post-surgery. Participants were randomized to 10-week group-based CBSM or a psychoeducation control group and followed at 6 months, 12 months, and median 11 years. In total, 51 participants provided blood data for longitudinal analyses (CBSM n=28; Control n=23). Mixed model analyses examined CBSM effects on 6-12 month changes in CTRA expression (53 indicator genes representing pro-inflammatory, anti-viral and antibody production signaling). Cox regression models assessed the relationship between 6 and 12 month changes in CTRA expression and 11-year DFS. RESULTS: Patients randomized to CBSM showed attenuated 6-12 month change in CTRA gene expression, whereas patients randomized to control showed increased CTRA expression (p=0.014). Average DFS was 5.92 years (SD=3.90). Greater 6-12 month CTRA increases predicted shorter 11-year DFS controlling for covariates (p=0.007). CONCLUSIONS:CBSM attenuated CTRA gene expression during the initial year of breast cancer treatment. In turn, greater increases in CTRA gene expression predicted shorter long-term DFS. These findings identify a biobehavioral oncology pathway to examine in future work.
RCT Entities:
PURPOSE: Cognitive behavioral stress management (CBSM) is an empirically-validated group-based psychosocial intervention. CBSM is related to decreased self-reported indicators of psychological adversity during breast cancer treatment and greater disease-free survival (DFS) vs. a control condition. This study examined relationships between CBSM, DFS, and a potential biobehavioral pathway linking these variables in breast cancerpatients through a gene expression composite representing the leukocyte conserved transcriptional response to adversity (CTRA). DESIGN:Women with stage 0-IIIb breast cancer completed questionnaires and provided blood samples post-surgery. Participants were randomized to 10-week group-based CBSM or a psychoeducation control group and followed at 6 months, 12 months, and median 11 years. In total, 51 participants provided blood data for longitudinal analyses (CBSM n=28; Control n=23). Mixed model analyses examined CBSM effects on 6-12 month changes in CTRA expression (53 indicator genes representing pro-inflammatory, anti-viral and antibody production signaling). Cox regression models assessed the relationship between 6 and 12 month changes in CTRA expression and 11-year DFS. RESULTS:Patients randomized to CBSM showed attenuated 6-12 month change in CTRA gene expression, whereas patients randomized to control showed increased CTRA expression (p=0.014). Average DFS was 5.92 years (SD=3.90). Greater 6-12 month CTRA increases predicted shorter 11-year DFS controlling for covariates (p=0.007). CONCLUSIONS: CBSM attenuated CTRA gene expression during the initial year of breast cancer treatment. In turn, greater increases in CTRA gene expression predicted shorter long-term DFS. These findings identify a biobehavioral oncology pathway to examine in future work.
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