@article{lunceford_davidian_tsiatis_2002, title={Estimation of survival distributions of treatment policies in two-stage randomization designs in clinical trials}, volume={58}, ISSN={["0006-341X"]}, DOI={10.1111/j.0006-341X.2002.00048.x}, abstractNote={Summary.  Some clinical trials follow a design where patients are randomized to a primary therapy at entry followed by another randomization to maintenance therapy contingent upon disease remission. Ideally, analysis would allow different treatment policies, i.e., combinations of primary and maintenance therapy if specified up‐front, to be compared. Standard practice is to conduct separate analyses for the primary and follow‐up treatments, which does not address this issue directly. We propose consistent estimators for the survival distribution and mean restricted survival time for each treatment policy in such two‐stage studies and derive large‐sample properties. The methods are demonstrated on a leukemia clinical trial data set and through simulation.}, number={1}, journal={BIOMETRICS}, author={Lunceford, JK and Davidian, M and Tsiatis, AA}, year={2002}, month={Mar}, pages={48–57} }
 @article{meeker_stafford_lunceford_avner_ma_teuscher_1999, title={Physical mapping of the autoimmune disease susceptibility locus, Bphs: co-localization with a cluster of genes from the TNF receptor superfamily on mouse Chromosome 6}, volume={10}, ISSN={["0938-8990"]}, DOI={10.1007/s003359901104}, abstractNote={An important approach to understanding complex diseases is to reduce them into well-characterized subphenotypes that are under monogenic control. One such example is Bordetella pertussis toxin-induced histamine sensitization in mice, a subphenotype of experimental allergic encephalomyelitis and experimental allergic orchitis. This subphenotype is controlled by a single locus, Bphs, previously mapped to a 33 cM region on mouse Chromosome (Chr) 6. We achieved considerable reduction of this candidate region and constructed a YAC contig across the refined interval. Our results demonstrate that Bphs is located between D6Mit151 and a newly developed marker, EC108RR, a region containing a small cluster of genes belonging to the TNF receptor superfamily. Sequence and quantitative analysis of the candidate gene, tumor necrosis factor receptor 1 (Tnfr1, p55), indicates that it is unlikely to be Bphs. However, the location of Bphs, together with physiologic effects it shares with Tnfr1 activation, suggest that Bphs may prove to be another member of the TNF receptor superfamily.}, number={9}, journal={MAMMALIAN GENOME}, author={Meeker, ND and Stafford, AN and Lunceford, JK and Avner, P and Ma, RZ and Teuscher, G}, year={1999}, month={Sep}, pages={858–863} }