Identification of genomic mutations associated with clinical outcomes of induction chemotherapy in patients with head and neck squamous cell carcinoma.
Seoul, South Korea. In J Cancer Res Clin Oncol, Jan 2016
Thirty-three mutations in TP53, NOTCH3, FGFR2, FGFR3, ATM, EGFR, MET, PTEN, FBXW7, SYNE1, and SUFU were frequently altered in poor responders.
Germline and somatic mutations in meningiomas.
Manchester, United Kingdom. In Cancer Genet, Apr 2015
The sonic hedgehog (SHH)-GLI1 signaling pathway gene, SUFU, has also been identified as the cause of hereditary multiple meningiomas in a large Finnish family.
Genomic analysis of smoothened inhibitor resistance in basal cell carcinoma.
San Francisco, United States. In Cancer Cell, Apr 2015
Genomic analysis of tumor biopsies revealed that vismodegib resistance is associated with Hedgehog (Hh) pathway reactivation, predominantly through mutation of the drug target SMO and to a lesser extent through concurrent copy number changes in SUFU and GLI2.
Epigenetic targeting of Hedgehog pathway transcriptional output through BET bromodomain inhibition.
Stanford, United States. In Nat Med, 2014
We show that BRD4 and other BET bromodomain proteins regulate GLI transcription downstream of SMO and suppressor of fused (SUFU), and chromatin immunoprecipitation studies reveal that BRD4 directly occupies GLI1 and GLI2 promoters, with a substantial decrease in engagement of these sites after treatment with JQ1, a small-molecule inhibitor targeting BRD4.
Small-molecule antagonists of Gli function
Bethesda, United States. In Unknown Journal, 2013
How Smo regulates Gli transcription factor function remains unclear, but this process involve the scaffolding protein Suppressor of Fused (Sufu), which can directly inhibit the Gli proteins and facilitate their proteolytic processing into N-terminal repressors.
Nevoid Basal Cell Carcinoma Syndrome
Seattle, United States. In Unknown Journal, 2002
The risk of developing medulloblastoma is substantially higher in individuals with an SUFU pathogenic variant (33%) than in those with a PTCH1 pathogenic variant (<2%).