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STS theories of biocapital conceptualize how biomedical knowledge and capital form together. Though these formations of biocapital often are located in large urban centers, few scholars have attended to how they are transforming urban spaces and places. In this paper we argue that the twinned technological development of cells and cities concentrates economic and symbolic capital and sets in motion contentious practices we name urban biopolitics . We draw on archival research and a nearly decade-long ethnography of the expansion of biomedical campuses in a major American city to show how the speculative logics of land development and biomedical innovation become bound together in a process we describe as speculative revitalization . We examine how the logics of speculative revitalization imagine a future in which cities and biomedicine produce wealth and health harmoniously together. However, in practice-as buildings of new biomedical urban campuses get built-the dreams of billionaire philanthrocapitalists to create global cities clash with the plans of biomedical researchers to create global health. We document the reproduction of stratified and racialized biomedical exclusions that result while also highlighting the unlikely opportunities for creating alliances committed to creating equitable biomedical research and healthcare in urban communities.

Genomic Tumour Testing (GTT) is an emerging site of "experimental care" in oncology [Cambrosio, Alberto, Peter Keating, Etienne Vignola-Gagné, Sylvain Besle, and Pascale Bourret. 2018a. "Extending Experimentation: Oncology's Fading Boundary Bbetween Research and Care." New Genetics and Society 37 (3): 207-226. doi: 10.1080/14636778.2018.1487281]. Few efforts to implement GTT have reached community oncology practices or patients living in rural communities within the US. Drawing on interdisciplinary research on a state-wide cancer genomics initiative in the rural US state of Maine, this paper explores the valuation practices within community oncologist and cancer stakeholders accounts of "doing good" within genomic science and care. We contribute to STS literatures on the bio-economy by highlighting the affective dimensions of strategies for managing economic and non-economic values. Clinician and stakeholders negotiated de-economizing and capitalizing modes of doing good as they built local genomic platforms "for Maine." These situated modes of doing good and feeling good via cancer genomics shaped how they navigated the ethical ambiguities of US biomedical markets across the boundaries of research and care., Competing Interests: Disclosure statement No potential conflict of interest was reported by the author(s).

Humans are inextricably linked to each other and our natural world, and microorganisms lie at the nexus of those interactions. Microorganisms form genetically flexible, taxonomically diverse, and biochemically rich communities, i.e., microbiomes that are integral to the health and development of macroorganisms, societies, and ecosystems. Yet engagement with beneficial microbiomes is dictated by access to public resources, such as nutritious food, clean water and air, safe shelter, social interactions, and effective medicine. In this way, microbiomes have sociopolitical contexts that must be considered. The Microbes and Social Equity (MSE) Working Group connects microbiology with social equity research, education, policy, and practice to understand the interplay of microorganisms, individuals, societies, and ecosystems. Here, we outline opportunities for integrating microbiology and social equity work through broadening education and training; diversifying research topics, methods, and perspectives; and advocating for evidence-based public policy that supports sustainable, equitable, and microbial wealth for all.

Biomedical research is increasingly informed by expectations of "translation," which call for the production of scientific knowledge that can be used to create services and products that improve health outcomes. In this paper, we ask how translation, in particular the idea of social responsibility, is understood and enacted in the post-genomic life sciences. Drawing on theories examining what constitutes "good science," and interviews with 35 investigators who study the role of gene-environment interactions in the etiology of cancer, diabetes, and cardiovascular disease, we describe the dynamic and unsettled ethics of translational science through which the expected social value of scientific knowledge about complex disease causation is negotiated. To describe how this ethics is formed, we first discuss the politics of knowledge production in interdisciplinary research collectives. Researchers described a commitment to working across disciplines to examine a wide range of possible causes of disease, but they also pointed to persistent disciplinary and ontological divisions that rest on the dominance of molecular conceptions of disease risk. The privileging of molecular-level causation shapes and constrains the kinds of knowledge that can be created about gene-environment interactions. We then turn to scientists' ideas about how this knowledge should be used, including personalized prevention strategies, targeted therapeutics, and public policy interventions. Consensus about the relative value of these anticipated translations was elusive, and many scientists agreed that gene-environment interaction research is part of a shift in biomedical research away from considering important social, economic, political and historical causes of disease and disease disparities. We conclude by urging more explicit engagement with questions about the ethics of translational science in the post-genomic life sciences. This would include a consideration of who will benefit from emerging scientific knowledge, how benefits will accrue, and the ways in which normative assumptions about the public good come to be embedded in scientific objects and procedures.

Despite a proclaimed shift from 'nature versus nurture' to 'genes and environment' paradigms within biomedical and genomic science, capturing the environment and identifying gene-environment interactions (GEIs) has remained a challenge. What does 'the environment' mean in the post-genomic age? In this paper, we present qualitative data from a study of 33 principal investigators funded by the U.S. National Institutes of Health to conduct etiological research on three complex diseases (cancer, cardiovascular disease and diabetes). We examine their research practices and perspectives on the environment through the concept of molecularization: the social processes and transformations through which phenomena (diseases, identities, pollution, food, racial/ethnic classifications) are re-defined in terms of their molecular components and described in the language of molecular biology. We show how GEI researchers' expansive conceptualizations of the environment ultimately yield to the imperative to molecularize and personalize the environment. They seek to 'go into the body' and re-work the boundaries between bodies and environments. In the process, they create epistemic hinges to facilitate a turn from efforts to understand social and environmental exposures outside the body, to quantifying their effects inside the body. GEI researchers respond to these emergent imperatives with a mixture of excitement, ambivalence and frustration. We reflect on how GEI researchers struggle to make meaning of molecules in their work, and how they grapple with molecularization as a methodological and rhetorical imperative as well as a process transforming biomedical research practices., (Copyright © 2016 Elsevier Ltd. All rights reserved.)

Scientists now agree that common diseases arise through interactions of genetic and environmental factors, but there is less agreement about how scientific research should account for these interactions. This paper examines the politics of quantification in gene-environment interaction (GEI) research. Drawing on interviews and observations with GEI researchers who study common, complex diseases, we describe quantification as an unfolding moral economy of science, in which researchers collectively enact competing ''virtues.'' Dominant virtues include molecular precision, in which behavioral and social risk factors are moved into the body, and ''harmonization,'' in which scientists create large data sets and common interests in multisited consortia. We describe the negotiations and trade-offs scientists enact in order to produce credible knowledge and the forms of (self-)discipline that shape researchers, their practices, and objects of study. We describe how prevailing techniques of quantification are premised on the shrinking of the environment in the interest of producing harmonized data and harmonious scientists, leading some scientists to argue that social, economic, and political influences on disease patterns are sidelined in postgenomic research. We consider how a variety of GEI researchers navigate quantification's productive and limiting effects on the science of etiological complexity., Competing Interests: Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

The US National Institute of Health's Human Microbiome Project aims to use genomic techniques to understand the microbial communities that live on the human body. The emergent field of microbiome science brought together diverse disciplinary perspectives and technologies, thus facilitating the negotiation of differing values. Here, we describe how values are conceptualized and negotiated within microbiome research. Analyzing discussions from a series of interdisciplinary workshops conducted with microbiome researchers, we argue that negotiations of epistemic, social, and institutional values were inextricable from the reflective and strategic category work (i.e., the work of anticipating and strategizing around divergent sets of institutional categories) that defined and organized the microbiome as an object of study and a potential future site of biomedical intervention. Negotiating the divergence or tension between emerging scientific and regulatory classifications also activated "values levers" and opened up reflective discussions of how classifications embody values and how these values might differ across domains. These data suggest that scholars at the intersections of science and technology studies, ethics, and policy could leverage such openings to identify and intervene in the ways that ethical/regulatory and scientific/technical practices are coproduced within unfolding research., Competing Interests: Declaration of Conflicting Interests The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

This article examines how race and ancestry are taken up in gene-environment interaction (GEI) research on complex diseases such as heart disease, diabetes, and cancer. Using 54 in-depth interviews of 33 scientists and over 200 hours of observation at scientific conferences, we explore how GEI researchers use and interpret race, ethnicity, and ancestry in their work. We find that the use of self-identified race and ethnicity (SIRE) exists alongside ancestry informative markers (AIMs) to ascertain genetic ancestry. Our participants assess the utility of these two techniques in relative terms, downplaying the accuracy and value of SIRE compared to the precision and necessity of AIMs. In doing so, we argue that post-genomic scientists seeking to understand the interactions of genetic and environmental disease determinants actually undermine their ability to do so by valorizing precise characterizations of individuals' genetic ancestry over measurement of the social processes and relations that differentiate social groups., (© American Sociological Association 2014.)

In this article, we explore current thinking and practices around the logics of difference in gene-environment interaction research in the post-genomic era. We find that scientists conducting gene-environment interaction research continue to invoke well-worn notions of racial difference and diversity, but use them strategically to try to examine other kinds of etiologically significant differences among populations. Scientists do this by seeing populations not as inherently homogeneous or heterogeneous, but rather by actively working to produce homogeneity along some dimensions and heterogeneity along others in their study populations. Thus we argue that homogeneity and heterogeneity are situational properties--properties that scientists seek to achieve in their study populations, the available data, and other aspects of the research situation they are confronting, and then leverage to advance post-genomic science. Pointing to the situatedness of homogeneity and heterogeneity in gene-environment interaction research underscores the work that these properties do and the contingencies that shape decisions about research procedures. Through a focus on the situational production of homogeneity and heterogeneity more broadly, we find that gene-environment interaction research attempts to shift the logic of difference from solely racial terms as explanatory ends unto themselves, to racial and other dimensions of difference that may be important clues to the causes of complex diseases.

Background: Previously, we reported that prenatal exposures to polycyclic aromatic hydrocarbons (PAH) and postnatal environmental tobacco smoke (ETS) in combination were associated with respiratory symptoms at ages 1 and 2 years. Here, we hypothesized that children exposed to both prenatal PAH and ETS may be at greater risk of asthma and seroatopy at ages 5-6 years, after controlling for current pollution exposure., Methods: Prenatal PAH exposure was measured by personal air monitoring over 48 h. ETS exposure, respiratory symptoms and asthma at ages 5-6 years were assessed through questionnaire. Immunoglobulin (Ig) E was measured by Immunocap., Results: A significant interaction between prenatal PAH and prenatal (but not postnatal) ETS exposure on asthma (p < 0.05), but not IgE, was detected. Among children exposed to prenatal ETS, a positive nonsignificant association was found between prenatal PAH exposure and asthma (OR 1.96, 95% CI [0.95-4.05]). Among children without exposure to prenatal ETS, a negative nonsignificant association was found between prenatal PAH exposure and asthma (OR 0.65, 95% CI [0.41-1.01]). Prenatal PAH exposure was not associated with asthma or IgE at age 5-6 years., Conclusions: Combined prenatal exposure to PAH and ETS appears to be associated with asthma but not seroatopy at age 5-6. Exposure to PAH alone does not appear associated with either asthma or seroatopy at age 5-6 years. Discerning the differential effects between ETS exposed and ETS nonexposed children requires further study., (Copyright © 2010 Elsevier Ltd. All rights reserved.)