Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10909272 | Leukemia Research | 2012 | 7 Pages |
Abstract
Hedgehog (Hh) signaling pathway is activated in diffuse large B-cell lymphoma (DLBCL). Genetic abnormalities that explain activation of Hh signaling in DLBCL are unknown. We investigate the presence of amplifications of Hh genes that might result in activation of this pathway in DLBCL. Our data showed few extra copies of GLI1 and SMO due to chromosomal aneuploidies in a subset of DLBCL cell lines. We also showed that pharmacologic inhibition of PI3K/AKT and NF-κB pathways resulted in decreased expression of GLI1 and Hh ligands. In conclusion, our data support the hypothesis that aberrant activation of Hh signaling in DLBCL mainly results from integration of deregulated oncogenic signaling inputs converging into Hh signaling.
Related Topics
Life Sciences
Biochemistry, Genetics and Molecular Biology
Cancer Research
Authors
Elisa Ramirez, Rajesh R. Singh, Kranthi Kunkalla, Yadong Liu, Changju Qu, Christine Cain, Asha S. Multani, Patrick A. Lennon, Jared Jackacky, Michael Ho, Sity Dawud, Jun Gu, Su Yang, Peter C. Hu, Francisco Vega,