Dataset Information

Affect regulation as a moderator of intentions for breast cancer chemoprevention.

ABSTRACT: Women at high risk for breast cancer (BC) may consider chemoprevention for risk reduction, but uptake is low. This study examined the role of affect regulation (the attempt to alter or control one's emotions) in decision-making about BC chemoprevention. A cross-sectional, single group design was used. High-risk women (N = 81) were surveyed. Moderation analyses specified cancer-specific distress as the independent variable, affect regulation (cognitive reappraisal or expressive suppression) as the moderator, and chemoprevention intentions (yes = 1, unsure = 0, no = -1) as the dependent variable. Cognitive reappraisal significantly moderated the relationship between cancer-specific distress and chemoprevention intentions (p = 0.03), but expressive suppression did not (p = 0.31). For the 44% of participants who were highest on reappraisal, higher cancer-specific distress was associated with greater intentions for chemoprevention. For the remaining 56%, there was no relationship between cancer-specific distress and chemoprevention intentions. Cognitive reappraisal may play an important role in decisions regarding uptake of chemoprevention.

SUBMITTER: Conley CC

PROVIDER: S-EPMC9167227 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature

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Affect regulation as a moderator of intentions for breast cancer chemoprevention.

Conley Claire C CC Agnese Doreen M DM Vadaparampil Susan T ST O'Neill Suzanne C SC Andersen Barbara L BL

Journal of behavioral medicine 20220203 3

Women at high risk for breast cancer (BC) may consider chemoprevention for risk reduction, but uptake is low. This study examined the role of affect regulation (the attempt to alter or control one's emotions) in decision-making about BC chemoprevention. A cross-sectional, single group design was used. High-risk women (N = 81) were surveyed. Moderation analyses specified cancer-specific distress as the independent variable, affect regulation (cognitive reappraisal or expressive suppression) as th ...[more]

PMID: 35113300

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Project description:BackgroundWhile negative affect (NA) typically increases risk for binge eating, the ultimate impact of NA may depend on a person's ability to regulate their emotions. In this daily, longitudinal study, we examined whether emotion regulation (ER) modified the strength of NA-dysregulated eating associations.MethodsWomen (N = 311) from the Michigan State University Twin Registry first reported dimensional binge eating symptoms and broad ER difficulties (e.g., limited emotional awareness, difficulty controlling emotional impulses). Participants then rated use of adaptive (cognitive reappraisal, social sharing, situation modification, and acceptance) and maladaptive (rumination, expressive suppression, and self-criticism) ER strategies, emotional eating (EE), objective binge eating (OBE), and NA once daily for 49 consecutive days.ResultsThere were several main effects of ER on binge-eating pathology in both between-person (i.e., comparing women who differed on average) and within-person (i.e., examining fluctuations in variables day-to-day) analyses. Between-person, greater broad ER difficulties, greater maladaptive strategy use, and lower adaptive strategy use were all associated with greater binge-eating pathology. Within-person, greater maladaptive strategy use was associated with greater odds of OBE on that day and on the following day. However, neither broad ER difficulties nor use of specific strategies moderated associations between NA and dysregulated eating in between- or within-person analyses.ConclusionsWhile ER is independently associated with risk for dysregulated eating, it may not fully mitigate the impact of NA. Additional strategies (e.g., decreasing environmental stressors and increasing social support) may be needed to minimize NA and its impact on dysregulated eating.Public significanceNegative affect (NA; e.g., sadness, guilt) increases dysregulated eating risk. Because NA is sometimes unavoidable, we examined whether emotion regulation (ER; i.e., how a person responds to their emotions) might impact whether NA leads to dysregulated eating. Although more effective ER was associated with less dysregulated eating overall, ER did not impact the association between NA and dysregulated eating. Other approaches may therefore be needed to mitigate NA-dysregulated eating associations.

Project description:BackgroundAlthough targeting of the cholesterol pathway by statins prevents breast cancer development in mouse models, efficacy is not absolute. Therefore, the goal of this study is to investigate if the upregulation in the cholesterol biosynthesis pathway genes associates with response to statin chemoprevention and may potentially be used as response biomarkers.MethodsExpression of cholesterol biosynthesis pathway genes was initially derived from the RNA sequencing of MCF10A cell line- based breast cancer progression model system and subsequently validated by quantitative PCR assay. Response to fluvastatin was assessed in vitro using the MCF10A cell line model system, including a statin resistant cell line that was generated (MCF10.AT1-R), and measured using colony forming assays. In vivo efficacy of statin for chemoprevention was assessed in the SV40C3 TAg mouse model. Mammary tumors were identified by histologic analysis of the mammary glands. Mammary glands without histologic evidence of high-grade lesions (in situ and/or invasive carcinoma) were considered responsive to statin treatment.ResultsWe found more than 70% of a published multi-gene fluvastatin resistance signature to be significantly upregulated during breast cancer progression and inversely correlated with statin inhibition of cellular growth and proliferation. This inherent statin resistance gene signature was also largely shared with the signature of acquired resistance to fluvastatin in MCF10.AT1-R cell line model of acquired statin resistance. These inherent resistance genes and genes exclusive to acquired statin resistance map to steroid-, and terpenoid backbone- biosynthesis pathway. We found upregulation of ~ 80% of cholesterol biosynthesis pathway genes in the tumor bearing mammary glands of SV40 C3TAg transgenic mouse model of TNBC, suggesting the involvement of cholesterol biosynthesis pathway in resistance to statin chemoprevention in vivo. A panel of 13-genes from the pathway significantly associated with response to statin treatment, as did the expression level of HMGCR alone in a mouse model of breast cancer suggesting their utility to predict the efficacy of statin chemoprevention.ConclusionsHigh basal level, or restorative upregulation, in the cholesterol biosynthesis pathway genes appear to be strongly associated with resistance to statin chemoprevention for breast cancer and may serve as a biomarker to tailor statin treatment to individuals who are most likely to benefit.

Dataset Information

Affect regulation as a moderator of intentions for breast cancer chemoprevention.

Publications

Affect regulation as a moderator of intentions for breast cancer chemoprevention.

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