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 eutic strategy to treat PCa with TMPRSS2-ERG gene fusion.

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

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

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

8 rearrangements, including a large number of gene fusions.

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

10 PCR we validated all the reliable predicted gene fusions.

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

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

13 -number aberrations, structural variants and gene fusions.

14 the expression of therapeutically actionable gene fusions.

15 equent chromosomal translocations leading to gene fusions.

16 al events including alternative splicing and gene fusions.

17 at is specifically tailored for prioritizing gene fusions.

18 hybridization demonstrated evidence of NTRK1 gene fusions.

19 stic interactive exploration and plotting of gene fusions.

20 cluding genetic amplification, deletion, and gene fusions.

21 m long-range MYCN DNA interactions and C19MC gene fusions.

22 We did not find any gene fusions.

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

24 g, we identified a total of 13 (12/13 novel) gene fusions, 231 nonsynonymous single nucleotide varian

25 g overexpression(2), altered splicing(3) and gene fusions(4); however, it is difficult to attribute t

26 or 215 breast tumors catalogued 99 recurrent gene fusions, 57% of which are cryptic adjacent gene rea

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

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

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

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

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

32 Gene fusion analyses found that expression of B. bronchi

33 importance of expanding upon whole gene and gene fusion analyses to include splice variants in basic

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

35 ng and RNA sequencing, we identified a novel gene fusion and demonstrated that it produces a neoantig

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

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

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

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

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

41 Detection of gene fusions and differential expression of known diseas

42 Gene fusions and duplications have further shaped the co

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

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

45 Gene fusions and fusion products were thought to be uniq

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

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

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

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

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

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

52 Gene fusions and somatic genetic variations were identif

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

54 Gene fusions and their encoded products (fusion RNAs and

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

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

57 Finally, we show that the TDDOs create gene fusions and/or truncations and discuss their potent

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

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

60 We find that driver point mutations, gene fusions, and arm-level copy losses typically arise

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

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

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

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

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

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

67 Here, we demonstrate that gene fusions are a source of immunogenic neoantigens tha

68 Gene fusions are being discovered at an increasing rate

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

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

71 Gene fusions are important genomic events in human cance

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

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

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

75 Many gene fusions are reported in tumours and for most their

76 NTRK inhibitors for tumours containing NTRK gene fusions are the most recent targeted agents approve

77 Gene fusions are the result of chromosomal aberrations a

78 ated alterations, such as translocations and gene fusions, are often cancer drivers.

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

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

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

82 Finally, recognition of gene fusions as a driving mechanism in neoplasia has led

83 t TEAD-dependent YAP activity found in these gene fusions as critical for oncogenesis and implicate t

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

85 s of DEEPEST call for increased attention to gene fusions as drivers of cancer and for future researc

86 riptomes and identifies a new way to utilize gene fusions as indicators of regional expression change

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

94 ors were analyzed, identifying depletions of gene fusion breakpoints within coding regions of fused g

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

96 es standardized filtering and annotation for gene fusion calls from STAR-Fusion and Arriba by merging

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

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

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

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

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

102 NUP98 gene fusions co-occur with a set of additional mutations

103 Recurrent gene fusions comprise a class of viable genetic targets

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

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

106 mote cancer, including non-coding mutations, gene fusions, copy-number variants and drug-resistance m

107 d prevalent gene fusions, we also identified gene fusion-derived neoantigens that generate cytotoxic

108 lting in negative selective pressure against gene fusion-derived neoantigens.

109 RNA-seq enhanced gene fusion detection and cancer type classifications.

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

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

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

113 However, current gene fusion detection methodologies are largely dependen

114 ene fusions, their pathogenic mechanism, and gene fusion detection methods in lacrimal gland and prim

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

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

117 and explore biologically-relevant expressed gene fusions, downstream of fusion calling.

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

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

120 Though functional gene fusions encoding oncogenic proteins are the most dr

121 rom mutational frameshifts, splice variants, gene fusions, endogenous retroelements and other process

122 cancers, including copy number alterations, gene fusions, enhancer hijacking events, and chromoplexy

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

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

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

126 Gene fusion events are significant sources of somatic va

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

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

129 antigens and have implications for targeting gene fusion events in cancers that would otherwise be le

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

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

132 hways, and creation of novel transcripts via gene fusion events.

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

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

135 regions, post-horizontal gene transfer (HGT) gene fusions fostering coordinated expression, gene relo

136 inical relevance of fusion events, we detect gene fusions from a cohort of 742 patients from the Mult

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

138 The extent to which gene fusions function as drivers of cancer remains a cri

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

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

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

142 Identification of canonic gene fusions has led to development of sensitive and spe

143 g the essential components of this family of gene fusions has significant therapeutic value.

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

145 Several YAP1 gene fusions have been identified in various human cance

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

147 YAP1 gene fusions have been observed in a subset of paediatri

148 Although gene fusions have been recognized as important drivers o

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

150 Gene fusions have been studied extensively, as frequent

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

152 In addition to diagnostic accuracy, gene fusions have prognostic implications, such as unfav

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

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

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

156 found in AURKA and AURKB expression between gene fusions, immunophenotypic groups, white blood cells

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

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

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

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

161 er, and identify BCL2L14-ETV6 as a recurrent gene fusion in more aggressive form of TNBC tumors.

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

163 We did not identify these gene fusions in 126 control pancreatobiliary lesions.

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

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

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

167 elman Database of Chromosome Aberrations and Gene Fusions in Cancer, we developed an algorithm to par

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

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

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

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

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

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

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

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

176 consequences of chromosomal rearrangement is gene fusions in the cancer genome.

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

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

179 lification and the independent birth of CypA gene fusions in various primate species.

180 The discovery of recurrent gene fusions in various tumors, including those involvin

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

187 chromosomal translocations leading to NUP98 gene fusions involve the intrinsically disordered and N-

188 This new gene fusion involves exons 1-4 from the 5' end of the Tr

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 le more recent advances have uncovered novel gene fusions involving neurotrophic tyrosine receptor ki

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

193 Our studies indicate that Pten-NOLC1 gene fusion is a driver for human cancers.

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

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

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

197 Gene fusion is one of the hallmarks of cancer genome via

198 ERG oncogenic pathway due to the TMPRSS2-ERG gene fusion is the major event that contributes to prost

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

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

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

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

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

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

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

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

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

208 In contrast, four other gene fusions (mTOR-TP53BP1, TMEM135-CCDC67, KDM4-AC01152

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

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

211 actionable targets, n = 132; 4%), as well as gene fusions (n = 51), gene amplifications (n = 35), gen

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

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

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

215 Subsequently, gene fusion occurred between these two horizontally acqu

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

217 TMPRSS2-ERG gene fusion occurs in approximately 50% of cases of pros

218 id tumor from an adolescent revealed a novel gene fusion of MAP3K8, encoding a serine-threonine kinas

219 A gene fusion of the transcriptional repressor NAB2 with t

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

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

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

223 CA1, BRCA2 and TP53) as well as an RNA-based gene fusion panel including ALK, BRAF, FGFR1, FGFR2, FGF

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

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

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

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

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

229 wn to have anti-tumour activity against NTRK gene fusion-positive solid tumours, including CNS activi

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

231 finding that more than 50% of tumors harbor gene fusions predicted to be oncogenic.

232 9,953 gene fusion predictions from 418 primary serious ovarian

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

234 cterization showed that the classical RIN-MC gene fusion, previously believed to be a loss-of-functio

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

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

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

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

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

240 , we report a Pten derived pro-cancer growth gene fusion Pten-NOLC1 originated from a chr10 genome re

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

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

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

244 Gene fusions result from either structural chromosomal r

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

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

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

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

249 ditive activities, consistent with classical gene fusion studies.

250 Recurrent gene fusions, such as ROS1 fusions, are oncogenic driver

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

252 prove the selection of patients eligible for gene fusion testing.See related article by Cocco et al.,

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

254 iptomes occurs within 1 megabase of 78 novel gene fusions that function as central markers of these r

255 tragenic positions, leading to in-frame gene-gene fusions that generate chimeric mRNAs.

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

257 esearchers and clinicians to rapidly discern gene fusions that might be true underlying oncogenic dri

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

259 reveal that cancer transcriptomes select for gene fusions that preserve protein and protein domain co

260 acid pathway, we then created mutations and gene fusions that prevent PlsX's interaction with the me

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

262 A focused review of gene fusions, their pathogenic mechanism, and gene fusio

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

264 We considered gene fusions to be pathogenically relevant when recurren

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

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

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

268 The association of gene fusion transcripts with neighboring gene overexpres

269 e find evidence of many tumour specific gene-gene fusion transcripts, likely due to chromosomal rearr

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

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

272 harbouring oncogenic NTRK1, NTRK2, and NTRK3 gene fusions treated in three ongoing, early-phase trial

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

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

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

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

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

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

279 n, minimal immune infiltration and prevalent gene fusions, we also identified gene fusion-derived neo

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

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

282 In addition, 82% of gene fusions were associated with structural variants, i

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

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

285 mong them, the CCNH-C5orf30 and TRMT11-GRIK2 gene fusions were found in breast cancer, colon cancer,

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

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

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

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

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

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

292 Gene fusions, which result from abnormal chromosome rear

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

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

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

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

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

298 Here, we show that the YAP1 gene fusions YAP1-MAMLD1, YAP1-FAM118B, YAP1-TFE3, and Y

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

300 s have simplified the generation of knock-in gene fusions, yet the prevalent use of gene-specific hom