Search PubMedSearch

PubMed · 9544521

A Bayesian framework for intent-to-treat analysis with missing data.

Abstract

In longitudinal clinical trials, one analysis of interest is an intention-to-treat analysis, which groups subjects according to the randomized treatment regardless of whether they stayed on that treatment or not. When in addition to going off the randomized treatment subjects may also drop out of the study and be lost to follow-up, it is unclear what an intention-to-treat analysis should be. If measurements are made after treatment drop-out on a random sample of subjects who drop the treatment, then Hogan and Laird (1996, Biometrics 52, 1002-1017) present a random effects model, well suited to this type of analysis, which fits a two-piece linear spline to the data with the knot at the time the assigned treatment is dropped. This article presents a Bayesian approach to fitting a similar two-piece linear spline model and shows how the model can be applied to data that have no off-treatment observations.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

K P Kleinman, J G Ibrahim, N M Laird. 1998. A Bayesian framework for intent-to-treat analysis with missing data.. https://pubmed.ncbi.nlm.nih.gov/9544521/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Regulatory functions of Cdk9 and of cyclin T1 in HIV tat transactivation pathway gene expression.

HIV-1 gene expression relies upon a complex machinery that is primarily controlled by two viral regulatory proteins, Tat and Rev. Rev is involved in regulating post-transcriptional events of HIV-1 gene expression. The Tat protein transactivates transcription from the HIV-1 5' long terminal repeat (LTR) and acts in synergy with specific cellular factors. Recently, it has been shown that one set of these cellular factors is a protein kinase activity termed TAK (Tat-associated kinase), which activates transcription by hyperphosphorylation of the carboxyl-terminal domain (CTD) of the large subunit of RNA polymerase II. TAK also enhances transcription of HIV-2, together with the retroviral transactivator, Tat-2. The TAK activity appears to be related to the CTD kinase P-TEFb, which stabilizes transcription elongation of many genes and was originally isolated from Drosophila extracts. Both TAK and P-TEFb contain at least two subunits: the cyclin-dependent kinase, CDK9 (PITALRE), the catalytic subunit, and the regulatory subunit, cyclin T1. CDK9 and cyclin T1 are ubiquitous factors that affects many cellular processes, including cell differentiation and apoptosis. The involvement of TAK in HIV-1 and HIV-2 gene expression is an important aspect in the biology of these two retroviruses, and may lead to the development of novel antiretroviral drugs and/or gene therapy approaches for the treatment of patients with AIDS.

Acquired Immunodeficiency Syndrome