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Forrest Spencer

Researcher at Johns Hopkins University School of Medicine

Publications -  51
Citations -  8367

Forrest Spencer is an academic researcher from Johns Hopkins University School of Medicine. The author has contributed to research in topics: Saccharomyces cerevisiae & Gene. The author has an hindex of 31, co-authored 51 publications receiving 8164 citations. Previous affiliations of Forrest Spencer include Johns Hopkins University.

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A Model-Based Background Adjustment for Oligonucleotide Expression Arrays

TL;DR: The default ad hoc adjustment, provided as part of the Affymetrix system, can be improved through the use of estimators derived from a statistical model that uses probe sequence information, which greatly improves the performance of the technology in various practical applications.
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Multiple-laboratory comparison of microarray platforms

TL;DR: A consortium of ten laboratories from the Washington, DC–Baltimore, USA, area was formed to compare data obtained from three widely used platforms using identical RNA samples to demonstrate that there are relatively large differences in data obtained in labs using the same platform, but that the results from the best-performing labs agree rather well.
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Toward a Comprehensive Atlas of the Physical Interactome of Saccharomyces cerevisiae

TL;DR: A novel probabilistic metric is created that takes advantage of the high density of data, including both the presence and absence of individual associations, to provide a measure of the relative confidence of each potential protein-protein interaction and organized proteins into coherent multisubunit complexes using hierarchical clustering.
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Human T cell leukemia virus type 1 oncoprotein Tax targets the human mitotic checkpoint protein MAD1

TL;DR: A model of viral transformation in which Tax targets TXBP181, thereby abrogating a mitotic checkpoint is proposed, which proposes a phenotype consistent with a loss of HsMAD1 function.
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Chromatid cohesion defects may underlie chromosome instability in human colorectal cancers.

TL;DR: It is shown that down-regulation or genetic disruption of the two major candidate CIN genes identified in previous studies also resulted in abnormal sister chromatid cohesion in human cells, suggesting that defective sister chrom atid cohesion as a result of somatic mutations may represent a major cause of chromosome instability in human cancers.