No abstract

Research in marketing often begins with two assumptions: that consumers are able to choose among desirable products, and that they have sufficient resources to buy them. However, many consumer decision journeys are constrained by a scarcity of products and/or a scarcity of resources. We review research in marketing, psychology, economics and sociology to construct an integrative framework outlining how these different types of scarcity individually and jointly influence consumers at various stages of their decision journeys. We outline avenues for future research and discuss implications for developing consumer-based marketing strategies.

Academics have shown a growing interest in the effects of resource scarcity—a discrepancy between one's current resource levels and a higher, more desirable reference point. However, the existing literature lacks an overarching theory to explain the breadth of findings across different types of resources. To address this, we introduce a self‐regulatory model of resource scarcity. In it, we propose that consumers respond to resource scarcity through two distinct psychological pathways: a scarcity‐reduction route aimed at reducing the discrepancy in resources and a control‐restoration route aimed at reestablishing diminished personal control by attaining security in other domains. We explain how a key determinant of which route the consumer will pursue is the perceived mutability of the resource discrepancy. We also specify moderators, based on our proposed model, to identify when each of the two routes is pursued. This model is assessed in the context of alternative theoretical perspectives, including commodity theory, life history theory, and models of compensatory behavior. Finally, we provide a research agenda for those interested in studying the psychology of resource scarcity from a self‐regulatory perspective.

Many consumer promotions involve uncertainty (e.g., purchase incentives offering the chance to receive one of several rewards). Despite retailers' heavy reliance on such promotions, much academic research on uncertainty has demonstrated examples of consumers avoiding and/or disliking uncertainty, implying that promotions involving uncertainty may not be as effective for retailers as promotions offering certain rewards. In an effort to reconcile the prevalence of uncertain promotions with the existing research, this article explores the conditions under which uncertain promotions may be effective for retailers. The article concludes with a discussion of the theoretical and practical implications for these findings.

Neuroblastoma is a childhood tumor in which transient therapeutic responses are typically followed by recurrence with lethal chemoresistant disease. In this study, we characterized the apoptotic responses in diverse neuroblastomas using an unbiased mitochondrial functional assay. We defined the apoptotic set-point of neuroblastomas using responses to distinct BH3 death domains providing a BH3 response profile, and directly confirmed survival dependencies. We found that viable neuroblastoma cells and primary tumors are primed for death with tonic sequestration of Bim, a direct activator of apoptosis, by either Bcl-2 or Mcl-1, providing a survival dependency that predicts the activity of Bcl-2 antagonists. The Bcl-2/Bcl-xL/Bcl-w inhibitor ABT-737 showed single agent activity against only Bim:Bcl-2 primed tumor xenografts. Durable complete regressions were achieved in combination with non-curative chemotherapy even for highest-risk molecular subtypes with MYCN amplification and activating ALK mutations. Furthermore, the use of unique isogenic cell lines from patients at diagnosis and at the time of relapse showed that therapy resistance was not mediated by upregulation of Bcl-2 homologues or loss of Bim priming, but by repressed Bak/Bax activation. Together, our findings provide a classification system that identifies tumors with clinical responses to Bcl-2 antagonists, defines Mcl-1 as the principal mediator of Bcl-2 antagonist resistance at diagnosis, and isolates the therapy resistant phenotype to the mitochondria.