Salivary agglutinin/DMBT1(SAG) expression is up-regulated in the presence of salivary gland tumors

Salivary agglutinin (SAG) is encoded by the gene Deleted in Malignant Brain Tumors 1 (DMBT1) and represents the salivary variant of DMBT1 (DMBT1SAG). While SAG is a bona fide anti-caries factor, DMBT1 was proposed as a candidate tumor-suppressor for brain, digestive tract, and lung cancer. Though DMBT1SAG is expressed in the salivary glands, its expression in salivary gland tumors is unknown. Here we analyzed DMBT1SAG expression in 20 salivary gland tumors and 14 tumor-flanking tissues by immunohistochemistry. DMBT1SAG in salivary gland tumors resembles the changes of expression levels known from DMBT1 in tumors in other cancer types. Particularly, DMBT1SAG was up-regulated in 10/14 tumor-flanking tissues, and a strong staining of the luminal content in the tumor and/or the tumor-flanking tissue was observed in 14/20 cases. This suggests that, in addition to its role in caries defense, SAG may serve as a potential tumor indicator and/or tumor suppressor in salivary gland tissue

Communicating clinical trial results to research participants

Background: Communicating clinical trial results to research participants is seldom accomplished in a timely or an effective manner. Objective: To evaluate the effectiveness of a plan to communicate results in an industry-sponsored randomized controlled trial for Huntington disease. Design, Setting, and Participants: Postal survey to research participants at 28 of 41 research sites (including 217 of 316 participants) in Canada and the United States. Intervention: We communicated trial results by means of (1) a media release from the investigators within a day after a sponsor-issued press release; (2) a subsequent telephone call from the site staff to the participants; and (3) a conference call for research participants 2 weeks after the results were released. Main Outcome Measures: Source and timing for learning study results and satisfaction with their communication. Results: Of the 217 study participants surveyed, 114 (52.5%) responded. Most (73.1%) firstlearned the study results from their site\u27s telephone call, and 46.3% learned the results within 1 day of the sponsor\u27s press release. Participants reported high or complete satisfaction with the site telephone call (89.3%) and conference call (82.1%) but relatively low satisfaction with the sponsor\u27s press release (50.0%). Most respondents reported good understanding of the risks and benefits of the experimental treatment and the next steps for their participation. Conclusion: Surveyed research participants learned of the clinical trial results soon after public release and highly valued the personalized and accurate communication efforts by the study investigators. © 2008 American Medical Association. All rights reserved

Randomized controlled trial of ethyl-eicosapentaenoic acid in huntington disease

Objective: To determine whether ethyl-eicosapentaenoic acid (ethyl-EPA), an ω-3 fatty acid, improves the motor features of Huntington disease. Design: Six-monthmulticenter,randomized,double-blind, placebo-controlled trial followed by a 6-month open-label phase without disclosing initial treatment assignments. Setting: Forty-one research sites in the United States and Canada. Patients: Three hundred sixteen adults with Huntington disease, enriched for a population with shorter trinucleotide (cytosine-adenine-guanine) repeat length expansions. Interventions: Random assignment to placebo or ethyl- EPA, 1 g twice a day, followed by open-label treatment with ethyl-EPA. Main Outcome Measures: Six-month change in the Total Motor Score 4 component of the Unified Huntington’s Disease Rating Scale analyzed for all research participants and those with shorter cytosine-adenineguanine repeat length expansions (\u3c 45). Results: At 6 months, the Total Motor Score 4 point change for patients receiving ethyl-EPA did not differ from that for those receiving placebo. No differences were found in measures of function, cognition, or global impression. Before public disclosure of the 6-month placebo-controlled results, 192 individuals completed the open-label phase. The Total Motor Score 4 change did not worsen for those who received active treatment for 12 continuous months compared with those who received active treatment for only 6 months (2.0-point worsening; P=.02). Conclusion: Ethyl-EPA was not beneficial in patients with Huntington disease during 6 months of placebocontrolled evaluation