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The contribution of germline copy number variants (CNVs) to risk of developing cancer in individuals with pathogenic BRCA1 or BRCA2 variants remains relatively unknown. We conducted the largest genome-wide analysis of CNVs in 15,342 BRCA1 and 10,740 BRCA2 pathogenic variant carriers. We used these results to prioritise a candidate breast cancer risk-modifier gene for laboratory analysis and biological validation. Notably, the HR for deletions in BRCA1 suggested an elevated breast cancer risk estimate (hazard ratio (HR) = 1.21), 95% confidence interval (95% CI = 1.09-1.35) compared with non-CNV pathogenic variants. In contrast, deletions overlapping SULT1A1 suggested a decreased breast cancer risk (HR = 0.73, 95% CI 0.59-0.91) in BRCA1 pathogenic variant carriers. Functional analyses of SULT1A1 showed that reduced mRNA expression in pathogenic BRCA1 variant cells was associated with reduced cellular proliferation and reduced DNA damage after treatment with DNA damaging agents. These data provide evidence that deleterious variants in BRCA1 plus SULT1A1 deletions contribute to variable breast cancer risk in BRCA1 carriers., (© 2022. The Author(s).)

Purpose: To provide precise age-specific risk estimates of cancers other than female breast and ovarian cancers associated with pathogenic variants (PVs) in BRCA1 and BRCA2 for effective cancer risk management., Methods: We used data from 3,184 BRCA1 and 2,157 BRCA2 families in the Consortium of Investigators of Modifiers of BRCA1/2 to estimate age-specific relative (RR) and absolute risks for 22 first primary cancer types adjusting for family ascertainment., Results: BRCA1 PVs were associated with risks of male breast (RR = 4.30; 95% CI, 1.09 to 16.96), pancreatic (RR = 2.36; 95% CI, 1.51 to 3.68), and stomach (RR = 2.17; 95% CI, 1.25 to 3.77) cancers. Associations with colorectal and gallbladder cancers were also suggested. BRCA2 PVs were associated with risks of male breast (RR = 44.0; 95% CI, 21.3 to 90.9), stomach (RR = 3.69; 95% CI, 2.40 to 5.67), pancreatic (RR = 3.34; 95% CI, 2.21 to 5.06), and prostate (RR = 2.22; 95% CI, 1.63 to 3.03) cancers. The stomach cancer RR was higher for females than males (6.89 v 2.76; P = .04). The absolute risks to age 80 years ranged from 0.4% for male breast cancer to approximately 2.5% for pancreatic cancer for BRCA1 carriers and from approximately 2.5% for pancreatic cancer to 27% for prostate cancer for BRCA2 carriers., Conclusion: In addition to female breast and ovarian cancers, BRCA1 and BRCA2 PVs are associated with increased risks of male breast, pancreatic, stomach, and prostate (only BRCA2 PVs) cancers, but not with the risks of other previously suggested cancers. The estimated age-specific risks will refine cancer risk management in men and women with BRCA1/2 PVs., Competing Interests: Timothy R. RebbeckHonoraria: AstraZeneca (I)Consulting or Advisory Role: AstraZeneca (I) Andrew LeeEmployment: IlluminaPatents, Royalties, Other Intellectual Property: I am an inventor of the BOADICEA model that is licensed to Cambridge Enterprise (part of the University of Cambridge) for commercialization. I have received royalties from Cambridge Enterprise. Norbert ArnoldHonoraria: AstraZeneca Åke BorgHonoraria: Roche, AstraZenecaTravel, Accommodations, Expenses: Roche, AstraZeneca Sandrine CaputoResearch Funding: AstraZeneca/France (Inst) Wendy K. ChungConsulting or Advisory Role: RegeneronResearch Funding: Biogen Chrystelle ColasConsulting or Advisory Role: AstraZeneca/Merck, Pfizer Miguel de la HoyaConsulting or Advisory Role: AstraZenecaResearch Funding: AstraZeneca D. Gareth EvansHonoraria: AstraZeneca Tanja N. FehmConsulting or Advisory Role: Roche, Novartis, Pfizer, AstraZeneca, Daiichi Sankyo, MSD OncologyTravel, Accommodations, Expenses: Roche George FountzilasStock and Other Ownership Interests: GENPREX Inc (I), ARIAD (I), Deciphera Pharmaceuticals Inc (I), Daiichi Sankyo, RFL Holdings, FORMYCONHonoraria: AstraZenecaConsulting or Advisory Role: Pfizer, Roche, NovartisSpeakers' Bureau: Roche (I), LEO Pharma (I), Pfizer (I)Travel, Accommodations, Expenses: Merck (I), Pfizer (I), K.A.M Oncology/Hematology (I) Megan FronePatents, Royalties, Other Intellectual Property: Receive royalties for being a codeveloper of CancerGene Connect Eric HahnenConsulting or Advisory Role: AstraZeneca Helen HansonHonoraria: Pfizer Beth Y. KarlanConsulting or Advisory Role: Roche Pharma AG, Merck, Mercy Bioanalytics, GRAILResearch Funding: GOG Foundation (Inst), NCI-NRG Oncology (Inst), Genentech/Roche (Inst)Patents, Royalties, Other Intellectual Property: US and EU patent on gene signatureOther Relationship: Elsevier Irene KonstantopoulouSpeakers' Bureau: AstraZenecaResearch Funding: AstraZeneca Ava KwongHonoraria: Stryker, AstraZeneca Taiwan Limited, Roche Singapore, Pfizer, AstraZeneca Hong Kong Ltd Joanne Ngeow Yuen YieResearch Funding: AstraZeneca Rita K. SchmutzlerHonoraria: AstraZeneca, Clovis, MSD/AstraZenecaConsulting or Advisory Role: AstraZeneca, MSD/AstraZenecaResearch Funding: Amgen Leigha SenterConsulting or Advisory Role: AstraZeneca/MerckSpeakers' Bureau: AstraZeneca/Merck Christian F. SingerHonoraria: Novartis, AstraZeneca/MedImmune, Daiichi Sankyo Europe GmbHConsulting or Advisory Role: AstraZeneca/MedImmune, Daiichi-Sankyo, Gilead Sciences, Sanofi/Aventis, NovartisSpeakers' Bureau: Novartis, AstraZeneca/MedImmuneResearch Funding: Novartis, Sanofi, Myriad Genetics, Roche, AstraZeneca/MedImmuneTravel, Accommodations, Expenses: Roche, Novartis Dominique Stoppa-LyonnetHonoraria: AstraZeneca/Merck (Inst) Soo Hwang TeoSpeakers' Bureau: AstraZeneca, Pfizer, Roche Sebastian A. WagnerConsulting or Advisory Role: Bayer Antonis C. AntoniouPatents, Royalties, Other Intellectual Property: Inventor of the BOADICEA model, which has been licensed to Cambridge Enterprise for commercialization. May receive royalties if commercialization is realized.No other potential conflicts of interest were reported.

Background: Recent population-based female breast cancer and prostate cancer polygenic risk scores (PRS) have been developed. We assessed the associations of these PRS with breast and prostate cancer risks for male BRCA1 and BRCA2 pathogenic variant carriers., Methods: 483 BRCA1 and 1318 BRCA2 European ancestry male carriers were available from the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). A 147-single nucleotide polymorphism (SNP) prostate cancer PRS (PRSPC) and a 313-SNP breast cancer PRS were evaluated. There were 3 versions of the breast cancer PRS, optimized to predict overall (PRSBC), estrogen receptor (ER)-negative (PRSER-), or ER-positive (PRSER+) breast cancer risk., Results: PRSER+ yielded the strongest association with breast cancer risk. The odds ratios (ORs) per PRSER+ standard deviation estimates were 1.40 (95% confidence interval [CI] =1.07 to 1.83) for BRCA1 and 1.33 (95% CI = 1.16 to 1.52) for BRCA2 carriers. PRSPC was associated with prostate cancer risk for BRCA1 (OR = 1.73, 95% CI = 1.28 to 2.33) and BRCA2 (OR = 1.60, 95% CI = 1.34 to 1.91) carriers. The estimated breast cancer odds ratios were larger after adjusting for female relative breast cancer family history. By age 85 years, for BRCA2 carriers, the breast cancer risk varied from 7.7% to 18.4% and prostate cancer risk from 34.1% to 87.6% between the 5th and 95th percentiles of the PRS distributions., Conclusions: Population-based prostate and female breast cancer PRS are associated with a wide range of absolute breast and prostate cancer risks for male BRCA1 and BRCA2 carriers. These findings warrant further investigation aimed at providing personalized cancer risks for male carriers and informing clinical management., (© The Author(s) 2021. Published by Oxford University Press.)

Purpose: Mutations in hereditary breast cancer genes play an important role in the risk for cancer., Methods: Cancer susceptibility genes were sequenced in 664 unselected breast cancer cases from Guatemala. Variants were annotated with ClinVar and VarSome., Results: A total of 73 out of 664 subjects (11%) had a pathogenic variant in a high or moderate penetrance gene. The most frequently mutated genes were BRCA1 (37/664, 5.6%) followed by BRCA2 (15/664, 2.3%), PALB2 (5/664, 0.8%), and TP53 (5/664, 0.8%). Pathogenic variants were also detected in the moderate penetrance genes ATM, BARD1, CHEK2, and MSH6. The high ratio of BRCA1/BRCA2 mutations is due to two potential founder mutations: BRCA1 c.212 + 1G > A splice mutation (15 cases) and BRCA1 c.799delT (9 cases). Cases with pathogenic mutations had a significantly earlier age at diagnosis (45 vs 51 years, P < 0.001), are more likely to have had diagnosis before menopause, and a higher percentage had a relative with any cancer (51% vs 37%, P = 0.038) or breast cancer (33% vs 15%, P < 0.001)., Conclusions: Hereditary breast cancer mutations were observed among Guatemalan women, and these women are more likely to have early age at diagnosis and family history of cancer. These data suggest the use of genetic testing in breast cancer patients and those at high risk as part of a strategy to reduce breast cancer mortality in Guatemala., (© 2021. This is a U.S. government work and not under copyright protection in the U.S.; foreign copyright protection may apply.)

RASopathies caused by germline pathogenic variants in genes that encode RAS pathway proteins. These disorders include neurofibromatosis type 1 (NF1), Noonan syndrome (NS), cardiofaciocutaneous syndrome (CFC), and Costello syndrome (CS), and others. RASopathies are characterized by heterogenous manifestations, including congenital heart disease, failure to thrive, and increased risk of cancers. Previous work led by the NCI Pediatric Oncology Branch has altered the natural course of one of the key manifestations of the RASopathy NF1. Through the conduct of a longitudinal cohort study and early phase clinical trials, the MEK inhibitor selumetinib was identified as the first active therapy for the NF1-related peripheral nerve sheath tumors called plexiform neurofibromas (PNs). As a result, selumetinib was granted breakthrough therapy designation by the FDA for the treatment of PN. Other RASopathy manifestations may also benefit from RAS targeted therapies. The overall goal of Advancing RAS/RASopathy Therapies (ART), a new NCI initiative, is to develop effective therapies and prevention strategies for the clinical manifestations of the non-NF1 RASopathies and for tumors characterized by somatic RAS mutations. This report reflects discussions from a February 2019 initiation meeting for this project, which had broad international collaboration from basic and clinical researchers and patient advocates., (Published 2020. This article is a U.S. Government work and is in the public domain in the USA.)

Objective: To describe a patient with a germline succinate dehydrogenase (SDHC) gene mutation presenting with primary hyperparathyroidism and a large catecholamine-producing temporal bone paraganglioma (PGL)., Methods: Evaluation of a SDHC mutation-positive PGL tumor biology using staining for tyrosine hydroxylase (TH), hypoxia-inducible factors 1α (HIF-1α) and 2α (HIF-2α)., Results: A 66-year-old man was noted to have a lytic skull base mass during work-up for his primary hyperparathyroidism. Biochemical evaluation with 24-hour urine catecholamines and metanephrines revealed marked elevation of norepinephrine and normetanephrine. Genetic testing revealed a germline SDHC mutation. A partial excision of skull base tumor was performed, which upon further examination revealed PGL. Immunohistochemistry of skull base PGL demonstrated heavy expression of TH and HIF-2α but reduced expression of HIF-1α. The remaining skull base PGL was treated with adjuvant radiation therapy. The patient's normetanephrine levels significantly decreased after surgery and radiation., Conclusion: Here, we report an unusual case of a patient presenting with a germline SDHC mutation-related functional PGL along with concomitant primary hyperparathyroidism. The present case illustrates that overexpression of HIF-2α but not of HIF-1α is linked to the pathogenesis of SDHC mutation-related PGL, and it may be responsible for the aggressive clinical behavior of a usually indolent course of SDHC-related PGLs.

This study examined the relation between work-family conflict and several types of psychiatric disorders: mood, anxiety, substance dependence, and substance abuse. Survey data were obtained from a representative national sample of 2,700 employed adults who were either married or the parent of a child 18 years old or younger. Hierarchical logistic regression analyses revealed that both work-to-family and family-to-work conflict were positively related to having a mood, anxiety, and substance dependence disorder. Depending on the type of work-family conflict and type of disorder, employees who reported experiencing work-family conflict often were 1.99-29.66 times more likely than were employees who reported no work-family conflict to experience a clinically significant mental health problem. No support was found for gender differences.

On the basis of A. P. Fiske's (1992) general theory of social relations, a model of interpersonal conflict at work was developed and tested in a sample of young workers. The model predicts that conflict with supervisors is predictive of organizationally relevant psychological outcomes (job satisfaction, organizational commitment, and turnover intentions), whereas conflict with coworkers is predictive of personally relevant psychological outcomes (depression, self-esteem, and somatic symptoms). Data were obtained from a sample of 319 individuals ages 16 to 19 years. Structural equation modeling results supported the hypothesized relations. Secondary regression analysis of 2 data sets from M. A. Donovan, F. Drasgow, and L. J. Munson (1998) provides initial support for the generalizability of the hypothesized model to older employees.

The longitudinal relations among contact with one's social network (social contact), perceived social support, depression, and alcohol use were examined. An integrative model was developed from affect regulation theory and theories of social support and dysfunctional drinking. Data were obtained from a random sample of 1,192 adults. The 3-wave panel model was tested using structural equation modeling analysis. Results revealed that (a) social contact was positively related to perceived social support; (b) perceived social support was, in turn, negatively related to depression; and (c) depression was, in turn, positively related to alcohol use for 1 of 2 longitudinal lags. There was partial support for the feedback hypothesis that increased alcohol use leads to decreased contact with family and friends. Although the results generally supported the authors' hypotheses, the significant coefficients in the model were generally small in size.

Employees who drink heavily or who abuse or are dependent on alcohol can undermine a workforce's overall health and productivity. To better understand the reasons behind employee abusive drinking and to develop more effective ways of preventing problem drinking in the workforce, researchers have developed a number of paradigms that guide their research. One such paradigm is the alienation/stress paradigm, which suggests that employee alcohol use may be a direct or indirect response to physical and psychosocial qualities of the work environment. Although in the alcohol literature, work alienation and work stress traditionally have been treated as separate paradigms, compelling reasons support subsuming the work-alienation paradigm under a general work-stress paradigm. Researchers have developed several models to explain the relationship between work stress and alcohol consumption: the simple cause-effect model, the mediation model, the moderation model, and the moderated mediation model. Of these, the moderated mediation model particularly stands out, because it simultaneously addresses the two fundamental issues of how and when work stressors are related to alcohol use. Recent research supports a relation of work-related stressors to elevated alcohol consumption and problem drinking. Future research should focus on the relation between work stressors and alcohol use among adolescents and young adults, because they are just entering the workforce and are the most likely to engage in heavy drinking. Longitudinal studies also are needed to better explain the relation between work stress and alcohol use.

Both alcohol use and stress appear to increase blood pressure. In addition, stress is associated with increased alcohol use. To investigate these relationships, researchers interviewed representative samples of the black and non-black adult household populations in Erie County, New York, in 1986, 1989, and 1993. The results support a causal relationship between stress and alcohol use and point to a number of factors that influence this relationship. Significant relationships between changes in alcohol use and blood pressure were also found. Although the researchers found little evidence for a direct effect of stress on blood pressure, stress related to family life, anxiety, and depression was associated with an increased risk for hypertension.

Predictors of work injuries were studied in a sample of employed adolescents. The 20 predictors comprise 5 general categories of risk factors: demographic, personality, employment, health, and substance use. Data were obtained from a sample of 319 individuals ages 16 to 19. Hierarchical regression analysis revealed that all 5 categories of risk factors were related to job injuries. The significant predictors of work injuries among adolescents were gender, negative affectivity, job tenure, exposure to physical hazards, excessive workloads, job boredom, poor physical health, and on-the-job substance use.

A conceptual model of work-school conflict was developed and tested. This study extends prior adolescent employment research by investigating the process by which job characteristics are associated with school outcomes. Data were obtained from a sample of 319 adolescents (16 to 19 years old) who were full-time students and part-time workers. The model was tested using structural equation modeling techniques. Results supported the hypothesized path model. Job characteristics (workload, number of work hours, and job dissatisfaction) were positively related to work-school conflict. Work-school conflict was negatively related to school readiness. School readiness was positively related to school performance, which was negatively associated with school dissatisfaction. In addition, results support a feedback relation, such that school dissatisfaction is negatively related to school readiness.

This study extends prior stress-coping-substance use research among adolescents by examining the employment context. Specifically, this study examines the relation of job dissatisfaction to substance use and the potential moderating influence of active and avoidant coping styles. Data were obtained from 446 employed high school students. Ordered-probit regression analyses reveal that job dissatisfaction is positively related to cigarette and alcohol use, but not to illicit drug use. Coping styles do not moderate the relation between job dissatisfaction and substance use. Nonetheless, coping styles have significant main-effect relations to substance use. Active coping is negatively related and avoidant coping is positively related to both cigarette and alcohol use. Neither coping style is related to illicit drug use.

On the basis of identity theory and research on sex role socialization, it was predicted that both work interfering with family (W-->F conflict) and family interfering with work (F-->W conflict) are uniquely related to depression, poor physical health, and heavy alcohol use (Hypothesis 1). It also was predicted that gender would moderate these relationships, such that W-->F conflict is more strongly related to the outcomes among women (Hypothesis 2a) and F-->W conflict is more strongly related to the outcomes among men (Hypothesis 2b). Survey data were obtained from 2 random community samples of employed parents (Ns = 496 and 605). Hierarchical regression analyses supported Hypothesis 1 but failed to support Hypotheses 2a and 2b.

This study examined whether specific facets of social support (tangible assistance, appraisal, and belonging) moderate the relationship between a specific type of stress (financial stress) and alcohol involvement (drinking to cope, heavy drinking, and alcohol problems). Data were derived from a community sample stratified by education and race. Respondents (N = 1,040) were interviewed in 1986 and 1989 and had drunk alcohol during the year preceding both interviews. Results supported the buffering influence of tangible support on the financial stress-alcohol involvement relationship. In contrast, neither appraisal nor belonging support consistently revealed a buffering pattern. These findings indicate the importance of taking into account specific components of social support when examining the relationship between specific sources of life stress and alcohol involvement.

The present study proposed and tested a motivational model of alcohol use in which people are hypothesized to use alcohol to regulate both positive and negative emotions. Two central premises underpin this model: (a) that enhancement and coping motives for alcohol use are proximal determinants of alcohol use and abuse through which the influence of expectancies, emotions, and other individual differences are mediated and (b) that enhancement and coping motives represent phenomenologically distinct behaviors having both unique antecedents and consequences. This model was tested in 2 random samples (1 of adults, 1 of adolescents) using a combination of moderated regression and path analysis corrected for measurement error. Results revealed strong support for the hypothesized model in both samples and indicate the importance of distinguishing psychological motives for alcohol use.

Limited research has examined the relationship between financial strain and alcohol use and abuse. Building on affect regulation theory and recent research in the stress and alcohol literatures, this study developed and tested a model relating financial strain, social resources, personal resources, depression, and drinking to cope to alcohol use and abuse. Data were obtained from a random sample of 1,424 adults who indicated that they had drunk alcohol in the previous year. We tested and then revised our model using structural equation modeling analysis. Results supported the affect regulation model of financial strain and alcohol use and abuse. Generally, depression mediated the relationship between financial strain and drinking to cope, and drinking to cope mediated the relationship between depression and alcohol use and abuse. In addition, both gender and race moderated six of the relationships in our revised model.

Prior research indicates that alcohol-related outcome expectancies represent important etiological factors in the understanding of alcohol use/abuse. Although current multidimensional measures assess several substantively different domains of alcohol-related outcome expectancies, there is growing evidence that they may not possess adequate levels of discriminant validity. Therefore, the present study sought to examine whether reliable between-person differences exist in the ability to differentiate among alcohol expectancy domains. The focus of the study was on three sets of intrapersonal characteristics: cognitive resources, cognitive constraints, and alcohol-related experience. Data were collected via household interviews with a random sample of 1125 adults. Multiple regression analysis revealed that higher levels of cognitive resources were associated with increasing levels of differentiation among alcohol expectancy domains. Results are discussed in terms of implications for the development of new or revised multidimensional alcohol expectancy questionnaires. Directions for future research are also discussed.

A stressor vulnerability model of stress-induced drinking was tested in a stratified random sample of 1,316 Black and White adult drinkers. Stressors were highly predictive of both alcohol use and drinking problems among men who relied on avoidant forms of emotion coping or held strong positive expectancies for alcohol's effects and accounted for more than 35% of the variance in alcohol use among the subgroup of men who were high in both vulnerability factors. In contrast, stressors were negatively related among men who were low in both and were unrelated among women regardless of their coping or expectancies. These findings suggest that tension reduction theories of alcohol use are overly broad and that individual characteristics must be considered to account for stress-related effects on alcohol use and abuse.

A comprehensive model of the work-family interface was developed and tested. The proposed model extended prior research by explicitly distinguishing between work interfering with family and family interfering with work. This distinction allowed testing of hypotheses concerning the unique antecedents and outcomes of both forms of work-family conflict and a reciprocal relationship between them. The influence of gender, race, and job type on the generalizability of the model was also examined. Data were obtained through household interviews with a random sample of 631 individuals. The model was tested with structural equation modeling techniques. Results were strongly supportive. In addition, although the model was invariant across gender and race, there were differences across blue- and white-collar workers. Implications for future research on the work-family interface are discussed.

Correlates of abstention and heavier drinking were examined among 654 African-American and 474 white women, aged 19-70+, from a representative sample of households in Erie County, New York. Discriminant function analysis was employed to investigate the relationship between alcohol consumption and race, age, church attendance, family history of alcohol problems, household density, marriage, socioeconomic status (SES), employment and parity. Abstention was compared with drinking, and light/moderate drinking was compared with heavier drinking in the total sample and within each race. Compared to drinkers, abstainers were older, more religious, more likely to be African-American, or to be of lower SES. Racial differences in the correlates of abstention were found with respect to church attendance (positive association in African-Americans only), SES (negative association in African-Americans only), and household density (positive association in whites only). Compared to light/moderate drinkers, heavier drinking women were younger, less religious, more likely to be white, to have a positive family history, or to live in less crowded households. Racial differences in the correlates of heavier drinking were found with respect to church attendance (negative association in African-Americans only), parity (positive association in African-Americans only), and marital status (more heavier drinking among unmarried white women). Racial differences in the correlates of alcohol consumption document the need for further examination of the culture-specific determinants of women's drinking patterns.

Drawing on both tension reduction and social learning theories, we hypothesized that work stressors lead to increased distress, which in turn promotes problematic alcohol use among vulnerable individuals. Vulnerable individuals are hypothesized to possess few personal and social resources for responding adaptively to work-related stressors and distress and to hold positive expectancies for alcohol's effects. We tested our model in a random sample of 574 employed adults, using a combination of path analytic and hierarchical moderated regression techniques. Results revealed no support for a simple tension reduction model of work stress-induced drinking and only limited support for a social learning model. We conclude that a much more circumscribed view of the etiologic role of work stress in problematic alcohol use is indicated.

The moderating influence of race (black versus white), age, sex, and socioeconomic status on the relationship between alcohol abuse/dependence in offspring and a family history of alcoholism/problem drinking was investigated in a representative general population sample (N = 1659). Significant family history by race by age and family history by race by sex interactions were observed when predicting lifetime risk of alcohol abuse/dependence in offspring. Socioeconomic status did not moderate the effect of familial alcoholism/problem drinking on offspring alcohol abuse/dependence. Relative odds ratios indicated that the risk of alcohol abuse/dependence associated with a positive family history increased with increasing age among whites; whereas, it decreased with increasing age among blacks. Among whites, the relative odds ratio for the effect of family history was higher for females than for males; however, among blacks it was higher for males than females. Although these findings need to be replicated in other populations, they suggest that it is important to take race, age, and sex into consideration when investigating familial alcohol problems.

By using a cybernetic approach to occupational stress, it was hypothesized that the relationship between chronic work stressors and strain would be stronger among individuals high in private self-consciousness than among individuals low in private self-consciousness. Moderated regression analyses, using a sample of 135 blue-collar workers, revealed strong support for this hypothesis. This finding is antithetical to prior research showing that self-focused attention may buffer the effect of acute life events (Mullen & Suls, 1982; Suls & Fletcher, 1985). The results of the present study in conjunction with prior research suggest that the type of stressor (acute vs. chronic) examined may be a boundary condition influencing the direction of Stressor X Self-Focused Attention interactions. Implications for future research and stress management are discussed.