Indication

Target/marker/pathway

Summary

Licensing status

Publication and contact information

Cancer

Diffuse large B cell lymphoma (DLBCL)

Cyclin dependent kinase (CDK); p53

In vitro and mouse studies identified DLBCL gene signatures that could help predict prognosis and guide targeted therapy. In primary DLBCL samples, genotyping and analysis of transcriptional profiles and pathways identified a signature of copy number alterations that decreased p53 activity and increased cell cycle progression. In patients with the signature, the 5-year survival rate was 62%, whereas all patients without the signature survived. In mice implanted with cells from DLBCL patients containing the signature, pan-CDK inhibition decreased proliferation and tumor growth compared with no inhibition. Next steps include developing an assay to detect the gene signature.
At least five companies have CDK inhibitors in clinical and preclinical development to treat multiple types of cancer. At least four companies have p53-activating compounds in clinical and preclinical development to treat multiple types of cancer.

SciBX 5(39); doi:10.1038/scibx.2012.1028
Published online Oct. 4, 2012

Patent application filed; available for licensing

Monti, S. et al. Cancer Cell; published online Sept. 11, 2012;
doi:10.1016/j.ccr.2012.07.014
Contact: Margaret A. Shipp, Dana-Farber Cancer Institute, Boston, Mass.
e-mail:

margaret_shipp@dfci.harvard.edu