Human Glioblastoma (GBM)Dissecting the mechanisms causing the most malignant of human brain tumorsHuman Glioblastoma (GBM)Dissecting the mechanisms causing the most malignant of human brain tumors
Glioma Stem CellsDefining distinct phenotypes in clinically relevant subtypes of GBM cell linesGlioma Stem CellsDefining distinct phenotypes in clinically relevant subtypes of GBM cell lines
Molecular profilingCharacterizing the differential expression profiles in proneural vs mesenchymal GBM stem cellsMolecular profilingCharacterizing the differential expression profiles in proneural vs mesenchymal GBM stem cells
Our lab
The primary goals of research projects in Cheng laboratory is to improve our understanding of the molecular mechanisms and signaling pathways of human cancer initiation, tumorigenesis, invasion, metastases and angiogenesis, and to develop novel approaches for anti-cancer therapies by targeting molecular pathways by which human tumors develop and progress. Our approaches include molecular, cellular biology, histology, tumor xenografts in cell culture and animals model systems of human brain tumors (in particular, glioblastomas) and breast cancers.
News and Events
- Congratulations to Dr. Tianzhi Huang and the Cheng lab for their new publication in Autophagy! (Jan 2019)
- Congratulations to Ms. Namratha Sastry for receiving the NIH NRSA F31 Grant! (Sept 2018)
- Congratulations to Dr. Tianzhi Huang and the Cheng lab for their new publication in Autophagy! (Jan 2018)
Select Publications
- Huang, T., et al. (2017) "MST4 Phosphorylation of ATG4B Regulates Autophagic Activity, Tumorigenicity, and Radioresistance in Glioblastoma. Cancer Cell 32(6):840-855
- Huang, T., et al. (2016) “A Regulatory Circuit of miR-125b/miR-20b and Wnt Signaling Controls GBM Phenotypes through FZD6-Mediated Pathways.” Nat. Comm. 7:12885
- Feng, H., et al. (2012) “Phosphorylation of Dock180Y722 by Src Family Kinases Mediates EGFRvIII-driven Glioma Tumorigenesis.” PNAS, 109(8):3018-23
- Feng, H., et al. (2014) “EGFR Phosphorylation of DCBLD2 Recruits TRAF6 and Stimulates Akt-promoted Tumorigenesis.” J Clin. Invest. 124(9):3741-56
