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Abstract：
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).
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.
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).
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.
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.
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).
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.
摘要：
认知行为压力管理（CBSM）是一种经验验证的基于群体的心理社会干预措施。CBSM与乳腺癌治疗期间自我报告的心理逆境指标减少以及无病生存率（DFS）和控制条件。这项研究检查了CBSM之间的关系，DFS,和潜在的生物行为途径通过代表白细胞保守的逆境转录反应（CTRA）的基因表达复合物将乳腺癌患者的这些变量联系起来。
患有0-IIIb期乳腺癌的妇女完成了问卷调查，并在术后提供了血液样本。参与者被随机分为10周组CBSM或心理教育对照组，并在6个月时进行随访。12个月,和中位数11年。总的来说,51名参与者提供了血液数据进行纵向分析(CBSMn=28；对照n=23)。混合模型分析检查了CBSM对CTRA表达6-12个月变化的影响（53个指示基因代表促炎，抗病毒和抗体产生信号)。Cox回归模型评估了CTRA表达的6和12个月变化与11年DFS之间的关系。
随机接受CBSM的患者显示CTRA基因表达的6-12个月变化减弱，而随机分组至对照的患者显示CTRA表达增加(p=0.014)。平均DFS为5.92年(SD=3.90)。更大的6-12个月CTRA增加预测的11年DFS控制协变量(p=0.007)。
在乳腺癌治疗的最初一年，CBSM减弱了CTRA基因的表达。反过来,CTRA基因表达的增加预示着较短的长期DFS。这些发现确定了生物行为肿瘤学途径，以在未来的工作中进行检查。
患有0-IIIb期乳腺癌的妇女完成了问卷调查，并在术后提供了血液样本。参与者被随机分为10周组CBSM或心理教育对照组，并在6个月时进行随访。12个月,和中位数11年。总的来说,51名参与者提供了血液数据进行纵向分析(CBSMn=28；对照n=23)。混合模型分析检查了CBSM对CTRA表达6-12个月变化的影响（53个指示基因代表促炎，抗病毒和抗体产生信号)。Cox回归模型评估了CTRA表达的6和12个月变化与11年DFS之间的关系。
随机接受CBSM的患者显示CTRA基因表达的6-12个月变化减弱，而随机分组至对照的患者显示CTRA表达增加(p=0.014)。平均DFS为5.92年(SD=3.90)。更大的6-12个月CTRA增加预测的11年DFS控制协变量(p=0.007)。
在乳腺癌治疗的最初一年，CBSM减弱了CTRA基因的表达。反过来,CTRA基因表达的增加预示着较短的长期DFS。这些发现确定了生物行为肿瘤学途径，以在未来的工作中进行检查。
