A New Way to Reflect the IS Identity? Uncovering the Intellectual Core of Podcasts

The information systems (IS) discipline has long been critically questioning its identity to determine its central research avenues, its distinction from other disciplines, and the future directions for the field. Although this question is central to all stakeholders of the IS field, so far the debates have been conducted primarily in research papers, editorial commentaries, and opinion pieces published by influential IS scholars. Our study explores how the broader IS community engages in the discourse about IS identity by examining podcasts as an increasingly popular means of communicating IS viewpoints. We apply a podcast ethnography to study the IS podcast universe, consisting of 51 shows with 660 episodes. Our preliminary findings offer insights about the stakeholders, podcast topics, and intellectual core of the audio tracks that shed light on the role of podcasts in constructing and reflecting on IS identity

Trust Recipes for Enhancing the Intention to Adopt Conversational Agents for Disease Diagnosis: An fsQCA Approach

In this study, we examine the configurations of trust-enhancing factors that determine the intention to adopt conversational agents (CAs) for disease diagnosis. After identifying trust factors influencing the behavioral intent to adopt CAs based on the information systems acceptance research field, we assigned 201 participants to use the mobile Ada application and surveyed them about their experience. Ada is a medical diagnostic CA that combines patients’ symptoms with their medical history and provides diagnostic suggestions. The collected data was analyzed using a fuzzy set qualitative comparative analysis to capture the causal complexity of trust. We identified several configurations of trust-enhancing factors affecting the intention to adopt the CA. In particular, our results show that the adoption intentions are strongly determined by trust factors associated with the performance dimension. Furthermore, we derived two propositions for the development of CAs for healthcare purposes and elaborated implications for research and practice

Painting A Holistic Picture of Trust in and Adoption of Conversational Agents: A Meta-Analytic Structural Equation Modeling Approach

With their human-like nature, conversational agents (CAs) introduce a social component to human-computer interaction. Numerous studies have previously attempted to integrate this social component by incorporating trust into models such as the technology acceptance model (TAM) to decipher the adoption mechanisms related to CAs. Given the heterogeneity of these previous works, the aim of this paper is to integrate empirical evidence on the role and influence of trust within the nomological network of the TAM. For this purpose, we conduct a meta-analytic structural equation modeling approach based on 45 studies comprising k = 155 correlations, and N = 13,786 observations. Our findings highlight the multifaceted role of trust as a mediator transmitting the effects of the technology-related perceptions that drive the intention to use CAs. Our results present a comprehensive overview in a thriving research field that can guide both future theory building and the designs of more trustworthy CAs

Beyond Digital Data and Information Technology: Conceptualizing Data-Driven Culture

Background: The role of a data-driven culture in improving organizational performance is widely recognized, but its conceptual definition lacks uniformity, leading to the existence of various constructs. This paper proposes a guiding framework for a data-driven culture, aiming to foster a unified understanding that aids both researchers and practitioners in the information systems (IS) field. Method: Adopting a qualitative research approach, this study conducts a systematic literature review to discern the breadth and depth of data-driven culture as portrayed in previous works. Alongside this, ten interviews were carried out with professionals well-versed in the application of data-driven strategies. Results: The study uncovers the multifaceted nature of a data-driven culture, highlighting its influence on decision-making practices within organizations. It identifies a range of characteristics relevant to the construct and consolidates these into an integrative framework, thereby developing a conceptual definition for data-driven culture. Conclusion: The paper contributes to the IS field by providing a framework that illuminates the concept of data-driven culture. This new understanding aids researchers in consistently theorizing the same phenomenon, supports the development of refined metrics for assessing data-driven culture, and paves the way for future research in this area. For practitioners, this framework delineates the characteristics of a data-driven culture and their interplay, enabling a more informed approach to cultural change efforts. Moreover, it highlights the importance of acknowledging the wider cultural context, and provides mechanisms to balance the emphasis on tools and values

Antagonizing CD105 enhances radiation sensitivity in prostate cancer.

Radiation therapy is the primary intervention for nearly half of the patients with localized advanced prostate cancer and standard of care for recurrent disease following surgery. The development of radiation-resistant disease is an obstacle for nearly 30-50% of patients undergoing radiotherapy. A better understanding of mechanisms that lead to radiation resistance could aid in the development of sensitizing agents to improve outcome. Here we identified a radiation-resistance pathway mediated by CD105, downstream of BMP and TGF-β signaling. Antagonizing CD105-dependent BMP signaling with a partially humanized monoclonal antibody, TRC105, resulted in a significant reduction in clonogenicity when combined with irradiation. In trying to better understand the mechanism for the radio-sensitization, we found that radiation-induced CD105/BMP signaling was sufficient and necessary for the upregulation of sirtuin 1 (SIRT1) in contributing to p53 stabilization and PGC-1α activation. Combining TRC105 with irradiation delayed DNA damage repair compared to irradiation alone. However, in the absence of p53 function, combining TRC105 and radiation resulted in no reduction in clonogenicity compared to radiation alone, despite similar reduction of DNA damage repair observed in p53-intact cells. This suggested DNA damage repair was not the sole determinant of CD105 radio-resistance. As cancer cells undergo an energy deficit following irradiation, due to the demands of DNA and organelle repair, we examined SIRT1's role on p53 and PGC-1α with respect to glycolysis and mitochondrial biogenesis, respectively. Consequently, blocking the CD105-SIRT1 axis was found to deplete the ATP stores of irradiated cells and cause G2 cell cycle arrest. Xenograft models supported these findings that combining TRC105 with irradiation significantly reduces tumor size over irradiation alone (p value = 10-9). We identified a novel synthetic lethality strategy of combining radiation and CD105 targeting to address the DNA repair and metabolic addiction induced by irradiation in p53-functional prostate cancers

Cancer epithelia-derived mitochondrial DNA is a targetable initiator of a paracrine signaling loop that confers taxane resistance.

Stromal-epithelial interactions dictate cancer progression and therapeutic response. Prostate cancer (PCa) cells were identified to secrete greater concentration of mitochondrial DNA (mtDNA) compared to noncancer epithelia. Based on the recognized coevolution of cancer-associated fibroblasts (CAF) with tumor progression, we tested the role of cancer-derived mtDNA in a mechanism of paracrine signaling. We found that prostatic CAF expressed DEC205, which was not expressed by normal tissue-associated fibroblasts. DEC205 is a transmembrane protein that bound mtDNA and contributed to pattern recognition by Toll-like receptor 9 (TLR9). Complement C3 was the dominant gene targeted by TLR9-induced NF-κB signaling in CAF. The subsequent maturation complement C3 maturation to anaphylatoxin C3a was dependent on PCa epithelial inhibition of catalase in CAF. In a syngeneic tissue recombination model of PCa and associated fibroblast, the antagonism of the C3a receptor and the fibroblastic knockout of TLR9 similarly resulted in immune suppression with a significant reduction in tumor progression, compared to saline-treated tumors associated with wild-type prostatic fibroblasts. Interestingly, docetaxel, a common therapy for advanced PCa, further promoted mtDNA secretion in cultured epithelia, mice, and PCa patients. The antiapoptotic signaling downstream of anaphylatoxin C3a signaling in tumor cells contributed to docetaxel resistance. The inhibition of C3a receptor sensitized PCa epithelia to docetaxel in a synergistic manner. Tumor models of human PCa epithelia with CAF expanded similarly in mice in the presence or absence of docetaxel. The combination therapy of docetaxel and C3 receptor antagonist disrupted the mtDNA/C3a paracrine loop and restored docetaxel sensitivity

Heterogeneous cancer-associated fibroblast population potentiates neuroendocrine differentiation and castrate resistance in a CD105-dependent manner.

Heterogeneous prostatic carcinoma-associated fibroblasts (CAF) contribute to tumor progression and resistance to androgen signaling deprivation therapy (ADT). CAF subjected to extended passaging, compared to low passage CAF, were found to lose tumor expansion potential and heterogeneity. Cell surface endoglin (CD105), known to be expressed on proliferative endothelia and mesenchymal stem cells, was diminished in high passage CAF. RNA-sequencing revealed SFRP1 to be distinctly expressed by tumor-inductive CAF, which was further demonstrated to occur in a CD105-dependent manner. Moreover, ADT resulted in further expansion of the CD105+ fibroblastic population and downstream SFRP1 in 3-dimensional cultures and patient-derived xenograft tissues. In patients, CD105+ fibroblasts were found to circumscribe epithelia with neuroendocrine differentiation. CAF-derived SFRP1, driven by CD105 signaling, was necessary and sufficient to induce prostate cancer neuroendocrine differentiation in a paracrine manner. A partially humanized CD105 neutralizing antibody, TRC105, inhibited fibroblastic SFRP1 expression and epithelial neuroendocrine differentiation. In a novel synthetic lethality paradigm, we found that simultaneously targeting the epithelia and its microenvironment with ADT and TRC105, respectively, reduced castrate-resistant tumor progression, in a model where either ADT or TRC105 alone had little effect