ArticlePloS one2013
ZNF-mediated resistance to imatinib mesylate in gastrointestinal stromal tumor.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
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- Systematic Investigation of DNA Methylation Associated With Platinum Chemotherapy Resistance Across 13 Cancer Types.Frontiers in pharmacology · 2021Article
- Analyses of germline variants associated with ovarian cancer survival identify functional candidates at the 1q22 and 19p12 outcome loci.Oncotarget · 2017Article
- Personalized medicine: a new option for nuclear medicine and molecular imaging in the third millennium.European journal of nuclear medicine and molecular imaging · 2017Article
- Successful establishment of patient-derived tumor xenografts from gastrointestinal stromal tumor-a single center experience.American journal of cancer research · 2016Article
- KAP1 promotes proliferation and metastatic progression of breast cancer cells.Cancer research · 2015Article
- Beyond standard therapy: drugs under investigation for the treatment of gastrointestinal stromal tumor.Expert opinion on investigational drugs · 2015Review
- Association of high expression of Groβ with clinical and pathological characteristics of unfavorable prognosis in gastrointestinal stromal tumors.Disease markers · 2015Article
- Drug repurposing identifies a synergistic combination therapy with imatinib mesylate for gastrointestinal stromal tumor.Molecular cancer therapeutics · 2014Article
- Best targeted sarcoma treatment: advances from the Musculoskeletal Tumor Society annual meeting.Clinical orthopaedics and related research · 2014Article
- GSTT1 copy number gain and ZNF overexpression are predictors of poor response to imatinib in gastrointestinal stromal tumors.PloS one · 2013Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
Abstract
Although imatinib mesylate (IM) has transformed the treatment of gastrointestinal stromal tumors (GIST), many patients experience primary/secondary drug resistance. In a previous study, we identified a gene signature, consisting mainly of Kruppel-associated box (KRAB) domain containing zinc finger (ZNF) transcriptional repressors that predict short-term response to IM. To determine if these genes have functional significance, a siRNA library targeting these genes was constructed and applied to GIST cells in vitro. These screens identified seventeen "IM sensitizing genes" in GIST cells (sensitization index (SI) <0.85 ratio of drug/vehicle) with a false discovery rate (FDR) <15%, including twelve ZNF genes, the majority of which are located within the HSA19p12-13.1 locus. These genes were shown to be highly specific to IM and another tyrosine kinase inhibitor (TKI), sunitinib, in GIST cells. In order to determine mechanistically how these ZNFs might be modulating response to IM, RNAi approaches were used to individually silence genes within the predictive signature in GIST cells and expression profiling was performed. Knockdown of the 14 IM-sensitizing genes (10 ZNFs) universally led to downregulation of six genes, including TGFb3, periostin, and NEDD9. These studies implicate a role of KRAB-ZNFs in modulating response to TKIs in GIST.
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Registered trials
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