| Literature DB >> 28469964 |
Jianman Guo1,2, Michael R Grovola1, Hong Xie1, Grace E Coggins1, Patrick Duggan1, Rukhsana Hasan3, Jiale Huang4, Danny W Lin1, Claire Song1, Gabriela M Witek1, Simon Berritt4, David C Schultz3, Jeffrey Field1.
Abstract
Patients with Neurofibromatosis type 1 (NF1) and Neurofibromatosis type 2 (NF2) are predisposed to tumors of the nervous system. NF1 patients predominantly develop neurofibromas, and Malignant Peripheral Nerve Sheath Tumors (MPNST) while NF2 patients develop schwannomas and meningiomas. Here we quantified the drug sensitivities of NF1 and NF2 tumor cell lines in a high throughput platform. The platform contained a comprehensive collection of inhibitors of MEK, RAF, RAS, farnesyl transferase, PAK and ERK, representative drugs against many other cancer pathways including Wnt, Hedgehog, p53, EGF, HDAC, as well as classical cytotoxic agents recommended for treating MPNST, such as doxorubicin and etoposide. We profiled seven NF1-associated MPNST cell lines (ST88-14, ST88-3, 90-8, sNF02.2, T265, S462TY, SNF96.2), one sporadic MPNST cell line (STS26), one schwannoma from a NF2 patient (HEI193), one NF2-deficient malignant meningioma (KT21-MG-Luc5D), one mouse NF2 schwannoma (SC4) and one sporadic rat schwannoma (RT4-67 or RT4). NF1 cells were primarily distinguished from NF2 cells and the sporadic MPNST cell line by their sensitivity to MEK and ERK inhibitors, and to a smaller extent their sensitivity to BH3 mimetics and farnesyl transferase inhibitors. The platform was highly successful in predicting the effects of clinical trials for Neurofibromas.Entities:
Keywords: HTS; Spearman’s rank correlation coefficient; heat map; high throughput screen; paradoxical activation; signal transduction; von Recklinghausen disease
Year: 2017 PMID: 28469964 PMCID: PMC5411799
Source DB: PubMed Journal: Am J Cancer Res ISSN: 2156-6976 Impact factor: 6.166