Proactive Recruitment Strategy for Patient Identification for Lung Cancer Screening.

PURPOSE: We assessed low-dose computed tomography (LDCT) screening for lung cancer using a proactive patient education/recruitment program. METHODS: We identified patients aged 55-80 years from a family medicine group. In the retrospective phase (March-August, 2019), patients were categorized as current/former/never smokers, and screening eligibility was determined. Patients who underwent LDCT in the past year, along with outcomes, were documented. In the prospective phase (2020), patients in the same cohort who did not undergo LDCT were proactively contacted by a nurse navigator to discuss eligibility and prescreening. Eligible and willing patients were referred to their primary care physician. RESULTS: In the retrospective phase, of 451 current/former smokers, 184 (40.8%) were eligible for LDCT, 104 (23.1%) were ineligible, and 163 (36.1%) had an incomplete smoking history. Of those eligible, 34 (18.5%) had LDCT ordered. In the prospective phase, 189 (41.9%) were eligible for LDCT (150 [79.4%] of whom had no prior LDCT or diagnostic CT), 106 (23.5%) were ineligible, and 156 (34.6%) had an incomplete smoking history. The nurse navigator identified an additional 56/451 (12.4%) patients as eligible after contacting patients with incomplete smoking history. In total, 206 patients (45.7%) were eligible, an increase of 37.3% compared with the retrospective phase (150). Of these, 122 (59.2%) verbally agreed to screening, 94 (45.6%) met with their physician, and 42 (20.4%) were prescribed LDCT. CONCLUSIONS: A proactive education/recruitment model increased eligible patients for LDCT by 37.3%. Proactive identification/education of patients desiring to pursue LDCT was 59.2%. It is essential to identify strategies that will increase and deliver LDCT screening among eligible and willing patients.

Colonic Epithelial-Derived Selenoprotein P Is the Source for Antioxidant-Mediated Protection in Colitis-Associated Cancer.

BACKGROUND & AIMS: Patients with inflammatory bowel disease (IBD) demonstrate nutritional selenium deficiencies and are at greater risk of developing colon cancer. Previously, we determined that global reduction of the secreted antioxidant selenium-containing protein, selenoprotein P (SELENOP), substantially increased tumor development in an experimental colitis-associated cancer (CAC) model. We next sought to delineate tissue-specific contributions of SELENOP to intestinal inflammatory carcinogenesis and define clinical context. METHODS: Selenop floxed mice crossed with Cre driver lines to delete Selenop from the liver, myeloid lineages, or intestinal epithelium were placed on an azoxymethane/dextran sodium sulfate experimental CAC protocol. SELENOP loss was assessed in human ulcerative colitis (UC) organoids, and expression was queried in human and adult UC samples. RESULTS: Although large sources of SELENOP, both liver- and myeloid-specific Selenop deletion failed to modify azoxymethane/dextran sodium sulfate-mediated tumorigenesis. Instead, epithelial-specific deletion increased CAC tumorigenesis, likely due to elevated oxidative stress with a resulting increase in genomic instability and augmented tumor initiation. SELENOP was down-regulated in UC colon biopsies and levels were inversely correlated with endoscopic disease severity and tissue S100A8 (calprotectin) gene expression. CONCLUSIONS: Although global selenium status is typically assessed by measuring liver-derived plasma SELENOP levels, our results indicate that the peripheral SELENOP pool is dispensable for CAC. Colonic epithelial SELENOP is the main contributor to local antioxidant capabilities. Thus, colonic SELENOP is the most informative means to assess selenium levels and activity in IBD patients and may serve as a novel biomarker for UC disease severity and identify patients most predisposed to CAC development.