Distinct classes of chromosomal rearrangements create oncogenic ETS gene fusions in prostate cancer

By S. Tomlins, B. Laxman, S. Dhanasekaran, Beth E. Helgeson, Xuhong Cao, David S. Morris, A. Menon, Xiaojun Jing, Q. Cao, B. Han and 10 more. Nature, 2007

891 citations recorded by the source corpus.

Subfields: Genetics, Molecular Biology, Pulmonary and Respiratory Medicine

View Paper: https://www.semanticscholar.org/paper/c55218203ef15143f687e15a248a8727fb74734d

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Citations in the corpus

Genomic Hallmarks and Structural Variation in Metastatic Prostate Cancer. (2018, positive): “Fusions between ETV1 and this region have been previously reported in the prostate cancer cell line MDA-PCa 2B (Tomlins et al., 2007) and in a single patient sample (Abeshouse et al.”
Next-generation transcriptome assembly (2011, background): “Detection of trans-spliced genes has been shown to be critical for understanding the genetic pathways involved in some cancers 56 , such as prostate cancer 57 .”
Emergence of FGFR family gene fusions as therapeutic targets in a wide spectrum of solid tumours (2014, background): “Another example in prostate cancer are fusions containing SLC45A3 fused to –ERG , –ETV1 , and –ETV4 [10,57].”
An Integrated Network of Androgen Receptor, Polycomb, and TMPRSS2-ERG Gene Fusions in Prostate Cancer Progression (2010, background): “The shared AR binding targets were further confirmed by the inclusion of previously reported androgen-sensitive 50 partners of gene fusions in prostate cancer such as TMPRSS2, SLC45A3, and C15ORF21 (Tomlins et al., 2007) (Figure S1C).”
Role of the TMPRSS2-ERG gene fusion in prostate cancer. (2008, neutral): “3 , C15ORF21 , and HNRPA2B1 [3,22].”
Genetics and biology of prostate cancer (2018, background): “Notably, prostate-specific transgene expression of the truncated human ERG yields only minimal or weak PIN in GEMMs (Tomlins et al. 2007; Klezovitch et al. 2008), but another recent report illustrates that ERG overexpression alone can generate prostate cancer when mice are as old as 26 mo of age…”
Genome-wide analysis of ETS-family DNA-binding in vitro and in vivo (2010, positive): “…a strong transcriptional activator domain to the ETS DBD (e.g. EWS fused to FLI1 or ERG in Ewing’s sarcoma; Delattre et al, 1992; Sorensen et al, 1994) and/or overexpression of an ETS-family member due to introduction of a strong cis-regulatory element up- stream of it (Tomlins et al, 2005, 2007).”
The genomic complexity of primary human prostate cancer (2011, positive): “This chain (found in sample PR-2832) contained breakpoint pairs at the following loci: (1) 60 bp from exon 6 of TANK binding kinase 1 (TBK1 or ‘NF-kB-activating kinase’)(29); (2) within the first intron of TP53 (7 kilobases (kb) upstream of translation start); (3) 51 kb from MAP2K4 (a kinase recentl”
Molecular genetics of prostate cancer: new prospects for old challenges. (2010, background): “…rearrangements that activate members of the ETS family of transcription factors (ERG, ETV1, and ETV4) in the majority of prostate carcinomas (Tomlins et al. 2005, 2007a; Iljin et al. 2006; Mehra et al. 2007b; Mosquera et al. 2007; Hu et al. 2008; Rouzier et al. 2008; Saramaki et al. 2008).”
The molecular taxonomy of primary prostate cancer (2015, background): “This event is similar to previously described ETV1 translocations in LNCaP andMDA-PCa2b cell lines and in patient samples (Tomlins et al., 2007; Gasi et al., 2011).”
Recurrent fusion of MYB and NFIB transcription factor genes in carcinomas of the breast and head and neck (2009, result): “The recent discovery that the majority of prostate cancers harbor ETS gene fusions (2) is in line with this reasoning.”