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Objective: This study aimed to determine whether invisible social control provided by a romantic partner is associated with improved objective glucose outcomes for patients with Type 2 diabetes. Social control reflects a partner's attempt to modify or influence a patient's health behaviors. We hypothesized that the best outcome for all continuous glucose monitoring measures would be captured by an interaction condition reflecting invisible social control., Method: Patients with Type 2 diabetes and their partners ( N = 63 couples) completed an 8-day daily diary period between 2016 and 2017. Self-report measures of social control receipt and provision were obtained each evening from patients and partners and patients wore a continuous glucose monitor throughout the diary period. Outcomes of daily glucose mean, standard deviation, time in range, and coefficient of variation were computed and two-way interactions between social control receipt and social control provision were probed and plotted., Results: The two-way interaction significantly predicted daily glucose mean, standard deviation, and time in range, such that when patients reported no social control receipt, but partners reported social control provision, patients showed improvements in objective glucose measures. We found no significant effect for coefficient of variation., Conclusions: This study was the first to use an invisible social control framework to examine the daily dyadic associations between partner social control provision, patient social control receipt, and four objectively measured continuous glucose monitoring outcomes. Findings suggest that the visibility of social control provided by a romantic partner may be predictive of glycemic control in patients with Type 2 diabetes. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Purpose: Partners of breast cancer (BC) survivors report high rates of psychological distress including fear of cancer recurrence (FCR). Research suggests that partners may have poorer physical health outcomes than the general population, but little research has examined the physiological biomarkers by which distress may impact partner health outcomes. The current study examined the associations between FCR and changes in hair cortisol among BC partners., Methods: Male partners (N = 73) of early-stage BC survivors provided hair samples during two visits, one after completion of survivors' adjuvant treatment (T1) and again 6 months later (T2). Two subscales from the Fear of Cancer Recurrence Inventory and one subscale from the Concerns about Recurrence Scale comprised a latent FCR factor at T1. A latent change score model was used to examine change in cortisol as a function of FCR., Results: Partners were on average 59.65 years of age (SD = 10.53) and non-Hispanic White (83%). Latent FCR at T1 was positively associated (b = 0.08, SE = 0.03, p = .004, standardized β = .45) with change in latent hair cortisol from T1 to T2., Conclusions: Results indicated that greater FCR was associated with increases in hair cortisol in the months following adjuvant treatment. This is one of the first studies to examine the physiological correlates of FCR that may impact health outcomes in BC partners., Implications for Cancer Survivors: Findings highlight the need for further research into the relationship between FCR and its physiological consequences. Interventions to address partner FCR are needed and may aid in improving downstream physical health outcomes., (© 2024. The Author(s).)

Purpose: Breast cancer (BC) survivors and their intimate partners face several adverse consequences from the cancer experience, including sleep disturbance, which is a common side effect of BC and its treatment. Sleep has been conceptualized and examined as an individual phenomenon despite most adults sharing a bed/room with a partner. Limited research has examined the associations between daily relationship processes and sleep in couples coping with cancer. Using an intensive longitudinal design, the present study examined the daily, within-person links between attempted and perceived partner responsiveness and subjective sleep., Methods: Immediately following adjuvant treatment, 72 early-stage BC survivors and their intimate partners (144 paired individuals) reported on daily attempted and perceived partner responsiveness each evening and subjective sleep each morning for 21 consecutive days., Results: Survivor and partner reports of partner responsiveness were associated with their own subjective sleep, such that greater attempted and perceived partner responsiveness were associated with improvements in one's own subjective sleep. Effects of one participant's partner responsiveness on their partner's sleep were not observed., Conclusions: Findings suggest that among couples coping with early-stage BC, increased partner responsiveness is associated with subsequent improvements in subjective sleep., Implications for Cancer Survivors: Sleep disturbance is a serious concern for BC survivors and their intimate partners. Future research should assess intimacy processes as a potential method to improve BC survivor and partner sleep., (© 2022. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.)

Since the identification of the human breast and ovarian cancer gene, BRCA1, a large spectrum of germline mutations has been characterized that predispose women to developing these diseases. We have determined the complete coding sequence for the rat BRCA1 homolog and compared it with those of the mouse, dog, and human to help identify the important functional domains of the BRCA1 protein. The overall rat Brcal amino acid identity compared with the predicted mouse, dog, and human gene products is 81%, 69%, and 58%, respectively. In spite of this low overall homology, the amino terminal RING finger domain and one of two nuclear localization signals are highly conserved among these species. In addition, two BRCT domains at the carboxy terminus and a highly acidic region are relatively well conserved. We have also identified several putative regulatory elements through comparison of the bidirectional BRCA1 promoter regions among the rat, mouse, and human genes. These include motifs for CCAAT and G/C boxes, as well as potential SP1, CREB, and NFkB transcription factor binding sites. Finally, analysis of splice variants from rat mammary gland, ovary, testis, spleen, and liver tissues revealed that, while alternative transcripts are detectable, full-length transcripts are the predominant steady-state form.

Inherited BRCA2 mutations confer profound susceptibility to human breast and ovarian cancer. The rat and mouse Brca2 homologues share 58% and 59% identity (72% similarity), respectively, with the human BRCA2 protein. The Brca2 proteins also share a potential nuclear localization signal (human codons 3263-3269) and a highly conserved large carboxyl region (77% identity, 86% similarity between human and rodents) that may represent important functional domains. At least six of eight previously described BRC repeats have been highly conserved in rats and mice. Expression studies demonstrate an 11-12 Kb transcript with rodent tissue-specific patterns of expression consistent with human BRCA2. These results will facilitate studies of Brca2 function during normal and neoplastic development.

BRCA1 mutations lead to cancer susceptibility in hormonally dependent tissues such as the ovary and breast. To test the hypothesis that Brca1 expression in the ovary is hormonally regulated and specifically regulated by a functional estrogen receptor, we examined its expression by in situ hybridization in ovaries from virgin, pregnant, and lactating mice, in hypophysectomized mice treated with hormones, and in estrogen-receptor-deficient mice. To determine the relationship between Brca1 expression and cell cycle, serial and adjacent sections of ovary were evaluated for proliferating cell nuclear antigen by immunohistochemistry. Regardless of the model, Brca1 was consistently expressed in granulosa and thecal cells of follicle populations that proliferate independently of hormonal stimulation. Expression was similar in these same follicle populations in the ovaries of estrogen-receptor-deficient mice, in which the lack of this estrogen receptor results in abnormal and incomplete follicular development. Brca1 expression was diminished in the granulosa and thecal cells of hormonally dependent antral follicles. Brca1 expression was also localized to luteal cells of recently formed corpora lutea and corpora lutea associated with pregnancy, but it was greatly diminished in regressing corpora lutea in cycling mice. In all cases, Brca1 expression correlated to S-phase proliferating cell nuclear antigen nuclear staining. Thus, Brca1 expression in the mouse ovary occurs independently of hormonal status and in the absence of a major estrogen receptor-mediated pathway; it is, however, closely correlated with cell cycle in mouse ovarian granulosa, thecal, and luteal cell.

Microsomal epoxide hydrolase (EPHX) is one of many enzymes involved in the metabolism of endogenous and exogenous toxicants. Polymorphic forms of the human EPHX gene have been described that vary in enzymatic activity, and one, Tyr113His, has been associated with hepatocellular carcinoma susceptibility. We demonstrated that EPHX was highly expressed in the human ovary, and investigated whether specific EPHX genotypes are associated with ovarian cancer susceptibility. Seventy-three Caucasian patients with ovarian cancer and 75 Caucasian-female controls without cancer were genotyped for the Tyr113His polymorphism by a polymerase chain reaction-restriction fragment length polymorphism assay. The frequency of the homozygous high-activity genotype was 41% in the control population and 64% in the ovarian cancer patients. The odds ratio for ovarian cancer with this genotype was 2.6 (95% confidence interval 1.3, 5.0; P < 0.01). The increased ovarian cancer risk associated with the high-activity genotype could reflect differences in metabolic activation of endogenous or exogenous carcinogens.

The BRCA1 gene is in large part responsible for hereditary human breast and ovarian cancer. Here we report the isolation of the murine Brca1 homologue cDNA clones. In addition, we identified genomic P1 clones that contain most, if not all, of the mouse Brca1 locus. DNA sequence analysis revealed that the mouse and human coding regions are 75% identical at the nucleotide level while the predicted amino acid identity is only 58%. A DNA sequence variant in the Brca1 locus was identified and used to map this gene on a (Mus m. musculus Czech II x C57BL/KsJ)F1 x C57BL/KsJ intersubspecific backcross to distal mouse chromosome 11. The mapping of this gene to a region highly syntenic with human chromosome 17, coupled with Southern and Northern analyses, confirms that we isolated the murine Brca1 homologue rather than a related RING finger gene. The isolation of the mouse Brca1 homologue will facilitate the creation of mouse models for germline BRCA1 defects.