ライフサイエンスコーパス: gene fusion

1 the HlyIIC structure may have arisen through gene fusion.

2 that all were concordant for the TMPRSS2:ERG gene fusion.

3 that at least one of the CARPs arose from a gene fusion.

4 xpressed in prostate cancer as a result of a gene fusion.

5 in prostate cancer harboring the TMPRSS2-ERG gene fusion.

6 ll as 1 EML4-ALK gene fusion and 1 KIF5B-RET gene fusion.

7 ion, calling genetic variants, and detecting gene fusions.

8 PCR we validated all the reliable predicted gene fusions.

9 include EIF1AX, PPM1D, and CHEK2 and diverse gene fusions.

10 ular subtype of PCa that harbors TMPRSS2-ERG gene fusions.

11 -number aberrations, structural variants and gene fusions.

12 the expression of therapeutically actionable gene fusions.

13 al events including alternative splicing and gene fusions.

14 at is specifically tailored for prioritizing gene fusions.

15 hybridization demonstrated evidence of NTRK1 gene fusions.

16 o the scattered phyletic distribution of the gene fusions.

17 d identify individuals with rare, targetable gene fusions.

18 l breast cancers have a variety of expressed gene fusions.

19 chromosomal translocations that may lead to gene fusions.

20 -1 murine leukemia viral oncogene homolog-1) gene fusions.

21 sis, and unable to screen a large numbers of gene fusions.

22 load, and high prevalence (70%) of oncogenic gene fusions.

23 rearrangements, including a large number of gene fusions.

24 than 13 million non-coding mutations, 18 029 gene fusions, 187 429 genome rearrangements, 1 271 436 a

25 entified 11 additional tumors with KIF5B-RET gene fusions (2.0%; 95% CI 0.8-3.1%).

26 than six million noncoding mutations, 10,534 gene fusions, 61,299 genome rearrangements, 695,504 abno

27 ed by gene duplication, diversification, and gene fusion; a combination of events previously unknown

28 The EBF1-PDGFRB gene fusion accounts for <1% of B-cell precursor acute l

29 that contribute to carcinogenesis, including gene fusions, alternative splice isoforms, and somatic m

30 e present a systematic analysis of oncogenic gene fusions among a clinically well-characterized, pros

31 e MCF-7 using the SOLiD system, we called 40 gene fusions among over 120,000 splicing junctions.

32 h for identifying differentially distributed gene fusions among whole-genome datasets: fdfBLAST.

33 s include multiple cancer-driving mutations, gene fusions, amplification, deletion, and post-translat

34 uctural genomic rearrangements, resulting in gene fusions, amplifications, and deletions, are a criti

35 Gene fusion analyses found that expression of B. bronchi

36 Gene fusion analysis revealed that ftrABCD promoter acti

37 s, and 1 MET mutation, as well as 1 EML4-ALK gene fusion and 1 KIF5B-RET gene fusion.

38 The tumors contained the Dnajb1-Prkaca gene fusion and had histologic and cytologic features of

39 encing requires transcription of the trigger-gene fusion and is maintained despite loss of the trigge

40 tion, including induction of the TMPRSS2-ERG gene fusion and its oncogenic activity.

41 VCaP cells, which harbor the TMPRSS2-ERG gene fusion and PC3 cells that stably express a similar

42 transcripts implicated in cancer-associated gene fusions and chromosomal translocations.

43 Detection of gene fusions and differential expression of known diseas

44 Gene fusions and duplications have further shaped the co

45 atures including gene expression, mutations, gene fusions and expression of non-human sequences.

46 , somatic structural variants, including new gene fusions and focal deletions of MBNL1, ZEB2 and ELF1

47 Gene fusions and fusion products were thought to be uniq

48 sed methods, when orthology mapping involves gene fusions and horizontal gene transfers.

49 ent-negative prostate cancers for targetable gene fusions and identified the SLC45A3-BRAF (solute car

50 pressed candidate genes by promoter-reporter gene fusions and in situ hybridization.

51 orectal carcinoma that can lead to essential gene fusions and other oncogenic events.

52 rces, we analyse 753 lung cancer samples for gene fusions and other transcriptomic alterations.

53 over many novel alternative splicing events, gene fusions and other variations in RNA transcripts.

54 We also determined, using gene fusions and point mutations, that RhlR thermoregula

55 ging RNA-Seq technology enables us to detect gene fusions and profile their features.

56 However, TMPRSS2-ERG gene fusions and PTEN losses occurred in only 21% and 8%

57 The R-spondin gene fusions and several other gene mutations identified

58 Gene fusions and somatic genetic variations were identif

59 We found recurrent gene fusions and splice alterations to be frequent mecha

60 The EWS-ETS family of gene fusions and their downstream effects in Ewing's sar

61 Gene fusions and their encoded products (fusion RNAs and

62 Gene fusions and their products (RNA and protein) were o

63 Using reporter gene fusions and transcriptomics, here we report that Dn

64 ling (including previously undescribed EWSR1 gene fusions), and telomere maintenance.

65 f prostate tumours harbour at least one such gene fusion, and that the most common fusion event, betw

66 ed genetic alterations, including mutations, gene fusions, and copy number changes, within this well-

67 regulation, then via promoter mutations and gene fusions, and finally via activation by intragenic g

68 strong and weak promoters in the context of gene fusions, and find that this has a measurable global

69 To identify viral elements, gene fusions, and gene expression patterns associated wi

70 s of cell type-specific expression of tandem gene fusions, and we report the first cell type-specific

71 hanism to control catalytic function through gene fusion appears to be a general mechanism for provid

72 rotein domain components arranged as a novel gene fusion architecture and of distant evolutionary anc

73 Gene fusions are being discovered at an increasing rate

74 Gene fusions are common cancer-causing mutations, but th

75 nomic variations such as point mutations and gene fusions are directly or indirectly associated with

76 The novel gene fusions are found to be of low frequency, but, inte

77 Gene fusions are important genomic events in human cance

78 ALK, ROS1 and RET gene fusions are important predictive biomarkers for tyr

79 Gene fusions are known to play critical roles in tumor p

80 egies for simultaneous detection of multiple gene fusions are limited by tedious and prolonged experi

81 Gene fusions are the result of chromosomal aberrations a

82 ed to identify new therapeutically important gene fusions: ARHGEF2-NTRK1 and CHTOP-NTRK1 in glioblast

83 ive genomic analysis strongly indicates that gene fusions arose by merger of adjacent open reading fr

84 In particular, we observed RPS6KB1-VMP1 gene fusion as a recurrent event occurring in approximat

85 er region and deficiency in Keap1 instead of gene fusion as in colon cancer.

86 Considering the importance of gene fusions as driver alterations, we explored their re

87 Through RNA-Seq, we discovered similar gene fusions as those found in their human counterparts:

88 exon 2 of Prkaca to create the Dnajb1-Prkaca gene fusion associated with FL-HCC, or control Cas9 vect

89 rough triplosensitivity, gene disruption, or gene fusion at breakpoints.

90 -quality graphics focused on annotating each gene fusion at the transcript- and protein-level and ass

91 n is accomplished by the function of a novel gene fusion (BeGC1) of a type I (microbial) rhodopsin do

92 Here we report a cancer-specific gene fusion between BCAM, a membrane adhesion molecule,

93 earrangements, including the first case of a gene fusion between kinase insert domain receptor (KDR)

94 Here we report the discovery of a gene fusion between TBL1XR1 and TP63, the only recurrent

95 Half of prostate cancers harbor gene fusions between TMPRSS2 and members of the ETS tran

96 It will be fruitful to merge three camps of gene fusion bioinformatics that appear to rarely cross o

97 iven the vectors to induce the Dnajb1-Prkaca gene fusion, but none of the 11 mice given the control v

98 iral etiology of SS or recurrently expressed gene fusions, but it did identify 21 SC-associated annot

99 ation in 59% of the samples and revealed two gene fusions, C2orf44-ALK in a colorectal cancer sample

100 c rearrangements that give rise to oncogenic gene fusions can offer actionable targets for cancer the

101 quantity of tools for accurately predicting gene fusion candidates from sequencing data, we are stil

102 roach (FusionSeq) in order to identify novel gene fusion candidates with high confidence.

103 hese studies have also identified many novel gene fusion candidates with more detailed resolution tha

104 ng the biological consequence of top scoring gene fusion candidates.

105 Of the 2,200 gene fusions catalogued, 1,435 consist of genes not prev

106 ication of a rapidly growing number of novel gene fusions caused by tumour-specific chromosomal rearr

107 To investigate the fidelity of gene-fusion characters, we developed an approach for ide

108 This tool can detect gene fusions, construct the structures of chimerical tra

109 levance of the promoter region used in these gene fusion constructs was verified by the effective com

110 varieties of genetic abnormalities: chimeric gene fusions, copy number alterations, and single-nucleo

111 and representing the significant features of gene fusion data in an inter-operable and query-able fas

112 and representing the significant features of gene fusion data.

113 , alternative splicing, functional analysis, gene fusion detection and eQTL mapping.

114 fied in TNBC demonstrate the need to advance gene fusion detection for molecularly heterogeneous canc

115 Currently, the gold standard method for gene fusion detection is Fluorescence In Situ Hybridizat

116 However, current gene fusion detection methodologies are largely dependen

117 nscriptome studies have been widely used for gene fusion discoveries, the current non-standard mode o

118 cing (NGS) technologies have enabled de novo gene fusion discovery that could reveal candidates with

119 Therefore, we developed a gene fusion discovery tool, INTEGRATE, that leverages bo

120 EGRATE, we compared it with eight additional gene fusion discovery tools using the well-characterized

121 such genes by analyzing genomic context, and gene fusions, distributions and co-expression.

122 Oncogenic gene fusions drive many human cancers, but tools to more

123 ions involving horizontal gene transfers and gene fusion due to the lack of a sound basis when based

124 Previous methods to find gene fusions either ignored these reads or required addi

125 genetic material that forms the non-natural gene fusion EML4-ALK encoding a constitutively active ty

126 A reporter gene fusion, encoding GFP fused to the full-length CEH-6

127 all "driver" CNAs secondary to the prenatal gene fusion event and most probably postnatal in the seq

128 We demonstrate that this simple gene fusion event on its own is sufficient to confer fun

129 The second gene fusion event, a translocation between the CLPTM1L a

130 a user infer the potential consequence of a gene fusion event.

131 loid progenitor of polyploid wheat through a gene-fusion event that gave rise to its unique structure

132 IDP-fusion is the first method to study gene fusion events by integrating Third Generation Seque

133 Then, by mapping gene fusion events identified from fully sequenced genom

134 we develop heuristics for reliably detecting gene fusion events in RNA-seq data and apply them to nea

135 evious assumptions, there have been multiple gene fusion events that have generated the single-chain

136 seedlings as well as maize lineage specific gene fusion events.

137 c prostate cancers harboring the TMPRSS2-ERG gene fusions exhibited overexpression of wild-type ERG.

138 will enable biologically intuitive access to gene fusion findings and expedite functional characteriz

139 enes across 115 fungal genomes, testing each gene fusion for evidence of homoplasy, including gene fi

140 ory of how I became interested in the use of gene fusions for studying biological problems.

141 The T2E gene fusion, formed by fusion of the transmembrane prote

142 progress, computational tools that identify gene fusions from next-generation whole transcriptome se

143 s highly sensitive and specific detection of gene fusions from RNA-Seq data, including the highest Po

144 MEK inhibitors may be useful in a subset of gene fusion-harboring solid tumors and demonstrate that

145 However, the DNAJB1-PRKACA gene fusion has not been shown to induce liver tumorigen

146 The TMPRSS2-ERG gene fusion has provided insight into the early developm

147 naling, and overexpression of MAST1 or MAST2 gene fusions has a proliferative effect both in vitro an

148 erstanding of the prevalence and function of gene fusions has been revolutionized by the rise of next

149 The computational work on gene fusions has been vastly diverse, and the present st

150 Oncogenic gene fusions have been identified in many cancers and ma

151 Chromosomal rearrangements without gene fusions have been implicated in leukemogenesis by c

152 Although gene fusions have been recognized as important drivers o

153 at enhance Wnt signaling and RSPO2 and RSPO3 gene fusions have been reported in CRC.

154 Gene fusions have been suggested to be useful characters

155 currently mutated, deleted or amplified, but gene fusions have not been characterized as extensively.

156 Both MAST and Notch-family gene fusions have substantial phenotypic effects in brea

157 reased synergy will catalyze advancements in gene fusion identification, characterization and signifi

158 1 and TP63, the only recurrent somatic novel gene fusion identified in our analysis of transcriptome

159 e rearrangement partners, and the targetable gene fusions identified in TNBC demonstrate the need to

160 work characterizing the molecular biology of gene fusions; (ii) development research on fusion detect

161 pMtNPF6.8:GUS promoter-reporter gene fusion in Agrobacterium rhizogenes-generated transg

162 SFTs identified the presence of a NAB2-STAT6 gene fusion in all tumors.

163 transcription start site (TSS) of a reporter gene fusion in Arabidopsis thaliana The intron increased

164 The predictive value of ERG gene fusion in HGPIN for PCa was interrogated as a post

165 FR-SEPT14 being the most frequent functional gene fusion in human glioblastoma.

166 e also resolve the structure of the EML4-ALK gene fusion in the NCI-H2228 cancer cell line using phas

167 classified rearrangements driving ETS family gene fusions in 133 cases of very low-, low-, intermedia

168 dentify somatic SNVs, small indels, CNVs and gene fusions in 508 tumor-related genes.

169 ptome sequencing to explore the landscape of gene fusions in a panel of breast cancer cell lines and

170 sensitive and specific algorithms to detect gene fusions in cancer do not currently exist.

171 equencing facilitates the discovery of novel gene fusions in cancer.

172 mmary, we identified several novel oncogenic gene fusions in colorectal cancer that may drive maligna

173 tions and unravels the landscape of in-frame gene fusions in glioblastoma.

174 and robust methods for detecting actionable gene fusions in lung cancer and could provide a robust a

175 We identified new gene fusions in patients with lung cancer harboring the

176 lapping cistromes of the two most common ETS gene fusions in PC: overlapping significantly with ETV1

177 scovery of potentially driving and druggable gene fusions in primary tumors.

178 peline, called INTEGRATE-Neo, by identifying gene fusions in prostate cancers that may produce neoant

179 ts further highlight the tumorigenic role of gene fusions in the etiology of pediatric solid tumors a

180 ependymomas are defined by highly recurrent gene fusions in the NF-kappaB subunit gene RELA (ST-EPN-

181 oint mutations, copy number alterations, and gene fusions) in ALK(-) ALCLs.

182 A 3xHA-mCherry-AtCEP2 gene fusion including pro-peptide and KDEL targeting seq

183 me Atlas (TCGA) and found multiple recurrent gene fusions including a subset involving estrogen recep

184 uencing, we identified previously unreported gene fusions, including ACTG1-MITF fusion.

185 n of the 3' genes in tumors and validated 18 gene fusions, including recurrent fusion (2/88) of ABCB1

186 Overexpression of the NAB2-STAT6 gene fusion induced proliferation in cultured cells and

187 ory region-beta-glucuronidase (GUS) reporter gene fusions introduced into Arabidopsis identified one

188 An intra-chromosomal gene fusion involving the estrogen receptor alpha gene E

189 These tumors also frequently displayed ERG gene fusions involving alternative 5'-partners to TMPRSS

190 profiling of PLGGs has also identified rare gene fusions involving another RAF isoform, CRAF/RAF1, i

191 Although recurrent gene fusions involving erythroblastosis virus E26 transf

192 Recurrent gene fusions involving ETS family genes are a distinguis

193 tiple fusion transcripts including recurrent gene fusions involving R-spondin family members RSPO2 an

194 Recently, rare targetable gene fusions involving the anaplastic lymphoma receptor

195 In conclusion, our results indicate that gene fusion is a common class of genomic abnormalities i

196 phoblastic leukaemia in which the ETV6-RUNX1 gene fusion is an early or initiating genetic lesion fol

197 The TMPRSS2:ERG gene fusion is common in androgen receptor (AR) positive

198 se results demonstrated that the FGFR3-TACC3 gene fusion is expressed in human cancer and generates a

199 egmental deletion resulting in DNAJB1-PRKACA gene fusion is now recognized as the signature genetic e

200 ETV6-RUNX1 gene fusion is usually an early, prenatal event in child

201 We show that higher numbers of gene fusions is an independent prognostic factor for poo

202 ges both RNA-seq and WGS data to reconstruct gene fusion junctions and genomic breakpoints by split-r

203 ecimens were defined as harboring a relevant gene fusion (kinase fusions 1.8%).

204 In addressing this question, we assessed gene fusion landscapes by comprehensive RNA sequencing (

205 tion tools to perform large-scale surveys of gene fusion landscapes in specific cancer types.

206 Gene fusions, mainly between TMPRSS2 and ERG, are freque

207 Here we propose a prototype, Gene Fusion Markup Language (GFML) as an initiative to p

208 The Gene Fusion Markup Language (GFML) presented here could

209 rrently lacks a method for identifying which gene fusions may generate neoantigens.

210 f lung cancers, suggesting that similar rare gene fusions may occur in other common epithelial cancer

211 discover and subsequently PCR validate novel gene fusions missed by other algorithms in the ovarian c

212 C is a rhodopsin (Rho)-guanylyl cyclase (GC) gene fusion molecule that is central to zoospore photota

213 le biochemical functions that are not due to gene fusions, multiple RNA splice variants or pleiotropi

214 all malignant PCa cases display a detectable gene fusion mutation between the TMPRSS2 promoter sequen

215 stable overexpression of TMPRSS2-ERG in the gene fusion-negative PC3 cells was associated with the u

216 We demonstrate the application of our gene fusion neoantigen discovery pipeline, called INTEGR

217 mber alterations (CNAs), and a wide range of gene fusions; no current clinically available single ass

218 TMPRSS2-ERG gene fusions occur in over 50% of prostate cancers, but

219 Subsequently, gene fusion occurred between these two horizontally acqu

220 erican patients, including a novel CDC27-OAT gene fusion occurring in 17% of patients.

221 A gene fusion of the transcriptional repressor NAB2 with t

222 We have identified gene fusions of polyamine biosynthetic enzymes S-adenosy

223 Recurrent, gain-of-expression gene fusions of RSPO2 (to EIF3E) and RSPO3 (to PTPRK) oc

224 plants expressing either ProCgNIN::reporter gene fusions or CgNIN RNAi constructs.

225 r example, EGFR and DDR2 gene mutations, ALK gene fusions, or FGFR1 gene amplifications.

226 ent configurations, as independent genes, as gene fusions, or targeted to intracellular membranes, al

227 actory disease (P < 0.0001), presence of ERG gene fusion (P < 0.0001), and nuclear p53 accumulation (

228 -other group revealed the presence of PDGFRB gene fusions, particularly EBF1-PDGFRB, in almost one th

229 Discovery of gene fusions-particularly those expressed with low abund

230 This study demonstrates similar gene fusion partners and mechanisms in human-dog corresp

231 cing complemented DNA sequencing to identify gene fusions, pathway activation, and immune profiling.

232 methods: in-silico two-hybrid, mirror-tree, gene fusion, phylogenetic profiling, gene neighbourhood,

233 ethylation, particularly LINE-1, between ERG gene fusion-positive and -negative cancers, and we confi

234 uncovered the other additional mechanisms in gene fusion-positive lung cancer cells, mouse models, an

235 r subtypes, including mutually exclusive ETS-gene-fusion-positive and SPINK1-overexpressing, CHD1-los

236 cific approach for detecting high-confidence gene fusion predictions.

237 ing this tool to the Fungi, we identified 63 gene fusions present in two or more genomes.

238 number data, we identified 11 novel melanoma gene fusions produced by underlying genomic rearrangemen

239 ative approach, we show that the TMPRSS2-ERG gene fusion product binds to the ERG locus and drives th

240 ically interact with the AR, such as the ERG gene fusion product, FOXA1, MLL2, UTX (also known as KDM

241 made easier by automating the annotation of gene fusion products and generating easily interpretable

242 characteristics of different CRFR2beta-PhoA gene fusion products expressed in bacteria were found to

243 l challenge of visualizing the corresponding gene fusion products to infer their biological consequen

244 prostate cancer, a detailed understanding of gene fusion prostate cancer should help explain the clin

245 usion transcripts on the basis of their tail gene fusion protein product and the roles that these fus

246 st for LNCaP and VCaP cells that express ETS gene fusion proteins.

247 excluding sensitizing EGFR mutations and ALK gene fusions) refractory to more than one prior therapy

248 angements (GRs), which can lead to oncogenic gene fusions, remains poorly characterized in HCC.

249 y deregulated after ETV6-RUNX1 and TCF3-PBX1 gene fusions, respectively.

250 ingle-cell levels with lacZ and gfp reporter-gene fusions, respectively.

251 Novel configurations of BRAF, NTRK3, and RET gene fusions resulting from chromosomal translocations w

252 lines expressing Bn-FAE1.1 promoter:reporter gene fusions revealed a strong expression in the embryo

253 Reporter gene fusions showed that PR has modest activity in an ex

254 Herein, we report a simple and rapid gene fusion strategy which expliots the specificity of D

255 GLDPA promoter reporter gene fusion studies revealed that this promoter is activ

256 ditive activities, consistent with classical gene fusion studies.

257 We also highlight high-confidence gene fusions supported by both genomic and transcriptomi

258 cogene homolog-nuclear factor I/B (MYB-NFIB) gene fusion that activates MYB transcriptional regulator

259 n of its key driver alteration, the EWS-FLI1 gene fusion that encodes this aberrant, chimeric transcr

260 as (PLGGs) are commonly associated with BRAF gene fusions that aberrantly activate the mitogen-activa

261 Nearly 50% of prostate cancers harbor gene fusions that lead to overexpression of the transcri

262 TMPRSS2-ERG gene fusions that occur frequently in human prostate can

263 , the prostatic SFTs demonstrated NAB2-STAT6 gene fusions that were also present in the fibroblast, m

264 Gene fusions therefore are highly labile characters, and

265 Absence of PTEN and presence of ETS gene fusion thus facilitated activation of senescence, w

266 DNA binding sites in the setting of the ETS gene fusion TMPRSS2-ERG, but inversely correlated with t

267 We considered gene fusions to be pathogenically relevant when recurren

268 ans and M. barkeri strains carrying reporter gene fusions to each of the M. acetivorans and M. barker

269 Using reporter gene fusions to QS target genes, we found that fadLSm in

270 spite its decayed status, we found TRIMCypA3 gene fusion transcripts in several primates.

271 ing technology have enabled the discovery of gene fusion transcripts in the transcriptome of cancer c

272 h well-known chromosomal alterations such as gene fusion, translocation, and focal amplification.

273 ective against diseases harboring the common gene fusion transmembrane protease, serine 2 (TMPRSS2):v

274 and characterized seven new cancer-specific gene fusions, two involving the ETS genes ETV1 and ERG,

275 NUP98 gene fusions typically encode a fusion protein that reta

276 that predict structural variations (SV) and gene fusions using whole genome (WGS) and transcriptome

277 ive splicing mechanism as well as novel VAV1 gene fusions (VAV1-THAP4, VAV1-MYO1F, and VAV1-S100A7) i

278 INTEGRATE-Vis is the first comprehensive gene fusion visualization tool to help a user infer the

279 We developed a gene fusion visualization tool, called INTEGRATE-Vis, th

280 The expression of the SS-EC20sp-IgAbeta gene fusion was driven by a modified version of the Baci

281 Using gene fusions we show that Bmh binding to the Adr1 regula

282 Here, using a translational gene fusion, we show that CrsR sequesters and protects s

283 ecome the primary technology for discovering gene fusions, we are still faced with the challenge of e

284 The resulting recombinant gene fusions were analyzed in a high-yielding expression

285 s at sequenced duplication breakpoints; four gene fusions were formed by tandem duplications, one by

286 Gene fusions were formed with the idea of testing the co

287 Two gene fusions were in-frame: MPP5-FAM71D in PC346C and AR

288 TMPRSS2-ERG gene fusions were observed in 44% of cases, and over 90%

289 tic mutations, including point mutations and gene fusions, were commonly found in genes involved in f

290 ion of CsLOB1 and CsSWEET1 promoter reporter gene fusions when coexpressed in citrus or Nicotiana ben

291 Furthermore, we predicted 260 gene fusions which frequently result in aberrant over-ex

292 MtCBS1), using a promoter-beta-glucuronidase gene fusion, which revealed expression in infected root

293 Gene fusions, which result from abnormal chromosome rear

294 ostate cancers are caused by the TMPRSS2-ERG gene-fusion, which enables androgens to drive expression

295 d gene (ERG), which is overexpressed through gene fusion with the androgen-responsive gene transmembr

296 r development, particularly as a result of a gene fusion with the promoter region of the androgen-ind

297 of of principle that MACHETE discovers novel gene fusions with high accuracy in vivo, we mined public

298 s found to be improved when expressed from a gene-fusion with flavodoxin from Desulfovibrio vulgaris

299 identifies substitutions, indels, CNAs, and gene fusions, with similar accuracy to lower-throughput

300 Our approach identified three in-frame gene fusions (YAP1-MAML2, PTPLB-RSRC1, and SP3-PTK2) tha