Defining causative factors contributing in the activation of hedgehog signaling in diffuse large B-cell lymphoma
| Autor: | Christine Cain, Changju Qu, Jared Jackacky, Jun Gu, Kranthi Kunkalla, Francisco Vega, Rajesh R. Singh, Su Yang, Peter Hu, Michael Ho, Asha S. Multani, Elisa Ramirez, Yadong Liu, Sity Dawud, Patrick A. Lennon |
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| Rok vydání: | 2012 |
| Předmět: |
Cancer Research
Blotting Western Real-Time Polymerase Chain Reaction Zinc Finger Protein GLI1 Article Receptors G-Protein-Coupled Phosphatidylinositol 3-Kinases immune system diseases GLI1 hemic and lymphatic diseases Biomarkers Tumor Tumor Cells Cultured medicine Humans Hedgehog Proteins RNA Messenger Hedgehog Protein kinase B In Situ Hybridization Fluorescence PI3K/AKT/mTOR pathway Cell Proliferation biology Reverse Transcriptase Polymerase Chain Reaction NF-kappa B Hematology medicine.disease Smoothened Receptor Hedgehog signaling pathway Lymphoma Oncology Immunology biology.protein Cancer research Lymphoma Large B-Cell Diffuse Signal transduction Proto-Oncogene Proteins c-akt Diffuse large B-cell lymphoma Signal Transduction Transcription Factors |
| Zdroj: | Leukemia Research. 36:1267-1273 |
| ISSN: | 0145-2126 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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