ABSTRACT
Passive consent, which is ethically questionable, requires parents to sign and return a form if they refuse to allow their child to participate in research. Active consent requires parents to sign and return a form if they consent for their child to participate. To compare passive and active consent research projects, we evaluated 15 published examples (since 1995) of passive consent and the adjacent experimental article (active consent). Passive consent projects involved significantly higher response rates, more subjects, greater likelihood of being conducted in school rather than in clinical settings, but about the same age of participants as active consent projects. We recommend that: (a) Institutional Review Boards scrutinize all passive consent projects and consider whether the consent procedure is ethical for the research sample; (b) editors and reviewers examine all manuscripts for the consent procedure used; and (c) ethicists and researchers debate the appropriateness/ethics of passive consent.
Subject(s)
Behavioral Research/ethics , Behavioral Research/standards , Child , Parental Consent/ethics , Parental Consent/psychology , Patient Selection/ethics , Presumed Consent/ethics , Adolescent , Child, Preschool , Consent Forms , Editorial Policies , Ethics Committees, Research , Humans , Refusal to Participate/psychology , Refusal to Participate/statistics & numerical data , SchoolsABSTRACT
Mouse skin tumors, benign papillomas, and squamous cell carcinomas (SCCs) were initiated by a single topical application of urethane followed by repeated promotion with 12-O-tetradecanoylphorbol-13-acetate (TPA). Using the NIH 3T3 focus forming assay, dominant transforming activity was detected in DNA isolated from SCC samples. Rearranged and amplified copies of the c-Ha-ras gene were detected in NIH 3T3 transformant cell lines, indicating that an activated Ha-ras gene had been transferred to the NIH 3T3 recipient cells. Analysis of p21ras from the transformant cell lines suggested that the activating ras mutation was present in codon 61. Ultimately, the Ha-ras gene was shown to be activated by a specific A----T transversion at the second position of codon 61. This mutation was detected in both benign papillomas and SCCs, suggesting the activation occurred early in tumor development. The results demonstrate a highly consistent activation of the Ha-ras oncogene by a specific point mutation, suggesting a functional role for an activated ras gene in the initiation of mouse skin tumors by urethane.
