Defining causative factors contributing in the activation of hedgehog signaling in diffuse large B-cell lymphoma |
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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 |
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Institution: | Molecular Genetic Technology Program, School of Health Sciences, The University of Texas M. D. Anderson Cancer Center, Houston, TX, USA. |
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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. |
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