Objective: We report results of a community-based multisite, randomized controlled trial of Nuevo Amanecer (NA-II), a 10-week stress management program for rural, low literacy Latina breast cancer survivors. Methods: Trained peers delivered NA-II to Spanish-speaking Latinas with nonmetastatic breast cancer in three rural communities. Women were randomized to receive the program immediately or wait 6 months. Assessments were conducted at baseline, 3 months, and 6 months. Primary outcomes were breast cancer-specific quality of life domains; secondary outcomes included general distress symptoms and stress management skills. Intention-to-treat analyses using repeated-measures linear regression models estimated changes in slope between groups. Results: Of 153 participants (76 randomized to intervention, 77 to control group), 92% were retained at 6 months. Mean age was 54.8 years (SD = 10.5); 80% had less than high school education. There were no statistically significant treatment × time effects on quality of life. Compared to women in the control group, intervention group women reported greater improvements in anxiety at 6 months (−0.20 vs −0.02, P = .049; range 0-4) as well as three stress management skills: relaxation at 3 months (+0.98 vs −0.07, P < .0001; range 0-4) and 6 months (+0.82 vs +0.04, P < .001), awareness of tension at 3 months (+0.31 vs −0.19, P < .01; range 0-4) and 6 months (+0.29 vs −0.11, P < .05), and coping confidence at 3 months (+0.12 vs −0.23, P < .01; range 0-4). Conclusions: Stress management programs delivered by trained peers in rural community settings can reduce anxiety and improve stress management skills among Latina breast cancer survivors. Trial registration: http://www.ClinicalTrials.gov identifier NCT02931552.

Evaluation of BIRADS 0, 4, or 5 abnormal mammograms was completed in most women within the recommended 60 days. Even within effective systems, correctible communication factors may adversely affect time to diagnosis.

Estrogen receptor coregulator over-expression promotes carcinogenesis and/or progression of endocrine related-cancers in which steroid hormones are powerful mitogenic agents. Recent studies in our laboratory, as well as others, demonstrated that the estrogen receptor coregulator PELP1 is a proto-oncogene. PELP1 interactions with histone demethylase KDM1 play a critical role in its oncogenic functions and PELP1 is a prognostic indicator of decreased survival in breast cancer patients. However, the in vivo significance of PELP1 deregulation during initiation and progression of breast cancer remains unknown. We generated an inducible, mammary gland–specific PELP1-expressing transgenic (Tg) mouse (MMTVrtTA-TetOPELP1). We found more proliferation, extensive side branching and precocious differentiation in PELP1-overexpressing mammary glands than in control glands. Aged MMTVrtTA-TetOPELP1 bitransgenic mice had hyperplasia and preneoplastic changes as early as 12 weeks, and ER-positive mammary tumors occurred at a latency of 14–16 months. Mechanistic studies revealed that PELP1 deregulation altered expression of a number of known ER target genes involved in cellular proliferation (such as cyclin D1, CDKs) and morphogenesis (EGFR, MMPs) and such changes facilitated altered mammary gland morphogenesis and tumor progression. Further, PELP1 was hyper-phosphorylated at its CDK phosphorylation site, suggesting an autocrine loop involving the CDK–cyclin D1–PELP1 axis in promoting mammary tumorigenesis. Treatment of PELP1 Tg mice with a KDM1 inhibitor significantly reduced PELP1 driven hyper branching, reversed alterations in cyclin D1 expression levels and reduced CDK-driven PELP1 phosphorylation. These results further support the hypothesis that PELP1 deregulation has the potential to promote breast tumorigenesis in vivo and represent a novel model for future investigation into molecular mechanisms of PELP1-mediated tumorigenesis.