BI 2536, a potent and selective inhibitor of polo-like kinase 1, inhibits tumor growth in vivo.

By M. Steegmaier, M. Hoffmann, A. Baum, P. Lénárt, M. Petronczki, Martin Krssák, U. Gürtler, P. Garin‐Chesa, Simone Lieb, Jens Quant and 5 more. Current Biology, 2007

859 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/26082266ac16a8a3de8909be703db9bc0680685f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cell Biology

1. Antonio Giordano
2. Ji Luo
3. Stephen J. Elledge
4. S. Lens
5. S. Lapenna
6. R. Medema
7. E. Voest

In Molecular Biology

1. P. McCray
2. Antonio Giordano
3. Chad Creighton
4. Ji Luo
5. Stephen J. Elledge
6. S. Lens
7. S. Lapenna
8. R. Medema

In Oncology

1. Stephen J. Elledge
2. Antonio Giordano
3. Ji Luo
4. S. Lapenna
5. Pengfei Lu

Citations in the corpus

• BIBF 1120: triple angiokinase inhibitor with sustained receptor blockade and good antitumor efficacy. (2008, methodology): “assay for proliferation analysis and apoptosis assay was performed as previously described ( 26 ).”
• Cell cycle kinases as therapeutic targets for cancer (2009, background): “Another compound that is currently in clinical testing, ON01910, was initially described as a PLK1 inhibitor, but subsequent studies found this not to be s”
• Shared and separate functions of polo-like kinases and aurora kinases in cancer (2010, background): “Inhibitors of PLK1 elicit a typical 'Polo' phenotype: cells arrest in mitosis with a monopolar or disorganized spindle and most eventually die from this mitotic arrest (mitotic cell death”
• Current prospects for RNA interference-based therapies (2011, methodology): “One study used SNALPs targeting PLK1, a cell cycle protein that is crucial for the activating phosphorylation of many cell cycle proteins; inhibition of PLK1 induces cell cycle arrest and tumour cell apoptosis 130 .”
• A genome-wide RNAi screen identifies multiple synthetic lethal interactions with the Ras oncogene. (2009, positive): “We have recently proposed the concept of ‘‘nononcogene addiction’’ (NOA) to describe the extensive dependency of cancer cells on the function of diverse networks of genes—many of which are neither mutated in cancer nor oncogenic—for their growth and survival ( Solimini et al., 2007; Luo et al., 200”