Surveys use questions to collect measurements from a sample in order to estimate characteristics of a population. The “objective” data obtained by survey interviews are achieved in the interaction between respondents and interviewers who have been trained to behave in a standardized manner. Over the years, both critics and practitioners of standardized survey interviewing have considered how the fundamentally social nature of the interview affects the data produced there. Both groups consider the interaction between the interviewer and respondent when they evaluate the quality of survey data. Critics present examples of interactions that depart from ordinary conversation as evidence that the resulting data cannot be valid. Practitioners suggest that surveys are about measurement rather than meaning in a conventional sense and view such individual incidents as leading to measurement error that results from unusual circumstances or “bad” survey questions. They also consider that adherence to rules of standardization improves the overall quality of the data in the aggregate by increasing reliability. We consider these issues by reviewing the meaning of standardization, the role of tacit knowledge for conducting and participating in the interview, and recent conversation analytic (CA) studies of interaction during survey calls.

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Habitat for Humanity (HFH)

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We previously reported that high numbers of mast cells in benign (extra-tumoral) regions of the prostate are associated with worse outcomes after radical prostatectomy including biochemical recurrence and the development of metastases. Herein, on a cohort of 384 men, we performed mast cell subtyping and report that higher minimum number of the tryptase-only (MCT) subset of extra-tumoral mast cells is associated with increased risk of biochemical recurrence (comparing highest to lowest tertiles: HR 2.20, 95% CI 1.32-3.65; P-trend 0.004), metastases (HR 3.60, 95% CI 1.77-7.36; P-trend 0.001), and death from prostate cancer (HR 2.96, 95% CI 1.23-7.08; P-trend 0.02). RNAsequencing of benign versus cancer tissue mast cells revealed differential expression of additional site-specific genes. We demonstrate that genes more highly expressed in tumor-infiltrating mast cells, such as CXCR4 and TFE3, represent an altered tumor microenvironment. C-kit variants were also differentially expressed in benign versus cancer tissue mast cells, with C-kit variant 1 (GNNK+) mast cells identified as more prevalent in extra-tumoral regions of the prostate. Finally, using an established mouse model, we found that mast cells do not infiltrate Hi-Myc tumors, providing a model to specifically examine the role of extra-tumoral mast cells in tumorigenesis. Hi-Myc mice crossed to mast cell knockout (Wsh) mice and aged to one year revealed a higher degree of pre-invasive lesions and invasive cancer in wildtype mice versus heterozygous and knockout mice. This suggests a dosage effect where higher numbers of extra-tumoral mast cells resulted in higher cancer invasion. Overall, our studies provide further evidence for a role of extra-tumoral mast cells in driving adverse prostate cancer outcomes.