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Todd R. Golub

Researcher at Harvard University

Publications -  454
Citations -  234100

Todd R. Golub is an academic researcher from Harvard University. The author has contributed to research in topics: Cancer & Gene expression profiling. The author has an hindex of 164, co-authored 422 publications receiving 201457 citations. Previous affiliations of Todd R. Golub include Rush University Medical Center & Boston Children's Hospital.

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Imaging of multiple mRNA targets using quantum dot based in situ hybridization and spectral deconvolution in clinical biopsies

TL;DR: A methodology of multiplexed in situ hybridization (ISH) using a novel combination of quantum dot (QD)-labeled oligonucleotide probes and spectral imaging analysis in routinely processed, formalin-fixed paraffin embedded human biopsies is described.
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Occurrence of TEL-AML1 fusion resulting from (12;21) translocation in human early B-lineage leukemia cell lines

TL;DR: The recurrent (12;21)(p13;q22) translocation fuses the two genes TEL and AML1 that have previously been cloned from translocation breakpoints in myeloid leukemias and provides a further example of the paradigm of TEL-AML1 fusion accompanied by deletion of the residual TEL allele.
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Genome-wide views of cancer.

TL;DR: Nearly coincident with the publication of the article by Hedenfalk et al. in this issue of the Journal are reports of the complete DNA sequence of the human genome.
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Improved estimation of cancer dependencies from large-scale RNAi screens using model-based normalization and data integration

TL;DR: This model is applied to individual large-scale datasets and shows that it substantially improves estimates of gene dependency across a range of performance measures, including identification of gold-standard essential genes as well as agreement with CRISPR-Cas9-based viability screens.
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STK33 kinase inhibitor BRD-8899 has no effect on KRAS-dependent cancer cell viability

TL;DR: The development of selective, low nanomolar inhibitors of STK33’s kinase activity are described, which failed to kill KRAS-dependent cells and are most consistent with the view that inhibition of STk33‘sKinase activity does not represent a promising anti-KRAS therapeutic strategy.