ライフサイエンスコーパス: synthetic lethal

1 ns are mutually exclusive and experimentally synthetic lethal.

2 was identified as a top candidate, showing a synthetic lethal activity with the PI carfilzomib (CFZ).

3 Here we develop MiSL (Mining Synthetic Lethals), an algorithm that mines pan-cancer h

4 Here we describe SLant (Synthetic Lethal analysis via Network topology), a compu

5 y pooled dual-knockout libraries to identify synthetic lethal and buffering gene pairs across multipl

6 gs establish that Rb1 and Skp2 deletions are synthetic lethal and suggest how this lethal relationshi

7 -selection balance conditions for X-autosome synthetic lethals and steriles.

8 e first clinically implemented examples of a synthetic lethal approach for cancer treatment.

9 Thus, our synthetic lethal approach identified USP11 as a componen

10 e for BRCA-PARP synthetic lethality, how the synthetic lethal approach is being assessed in the clini

11 This provides the basis for a novel synthetic lethal approach to cancer therapy.

12 TR inhibitor response and represents a novel synthetic lethal approach to targeting tumour cells.

13 in triple-negative breast cancers by using a synthetic-lethal approach dependent on cyclin-dependent

14 This provides the basis for a novel "synthetic lethal" approach to cancer therapy.

15 In the laboratory, the success of synthetic lethal approaches suggests another possible di

16 ing chemotherapeutic agents, are amenable to synthetic lethal approaches that exploit defects in DSB/

17 Here, we provide an overview of the synthetic lethal approaches that have been employed to s

18 Synthetic lethal approaches to cancer treatment have the

19 delivers rational combinatorial targets for synthetic lethal approaches with a high potential to pre

20 We provide evidence for why most reported synthetic lethals are not reproducible which is addressa

21 interventional opportunities in relation to synthetic lethal behaviours in arrest-defective tumours.

22 s encoded as protein networks could identify synthetic lethal candidates that are more reproducible t

23 esis, we found that this combination induces synthetic lethal cell death in high xCT-expressing cell

24 Here we develop a synthetic lethal chemical screen in isogenic KRAS-mutant

25 pos5 utr1 is a synthetic lethal combination rescued by plasmid-borne co

26 vivo These findings might pave a way for new synthetic lethal combination therapies.Significance: The

27 ent sporadic tumors to be susceptible to the synthetic lethal combination with PARP inhibitors.

28 a third gene product enhances a pre-existing synthetic lethal combination.

29 pment of JNK inhibitors in DLBCL, ideally in synthetic lethal combinations with inhibitors of chronic

30 Applying the synthetic lethal concept to target non-BRCA-mutant cance

31 Here, using a synthetic lethal CRISPR-Cas9 screen, we identify ferropt

32 tify a distinct biomarker that underlies the synthetic lethal dependence on WRN, and support the deve

33 ng another Z-ring interacting protein, had a synthetic lethal division effect.

34 press both LOF mutations in pha-1 as well as synthetic-lethal double mutants, including lin-35; ubc-1

35 ystem is a practical approach in identifying synthetic lethal drug combinations for cancer treatment.

36 n suppressing chromosomal instability and in synthetic lethal drug combinations inspire optimism that

37 Furthermore, a synthetic lethal drug screen revealed that antagonists o

38 Identifying genetic biomarkers of synthetic lethal drug sensitivity effects provides one a

39 argets in K562 leukemia cells and identified synthetic lethal drug target pairs for which correspondi

40 g, have made possible systematic screens for synthetic lethal drug targets in human cancers.

41 nexpectedly, rec-1; him-5 double mutants are synthetic-lethal due to a defect in meiotic double-stran

42 Clinical ATR inhibitors (ATRi) elicited a synthetic lethal effect in SS tumor cells and impaired g

43 otein interaction network to identify robust synthetic lethal effects associated with passenger gene

44 In contrast to the synthetic lethal effects of hypomorphic ATR suppression,

45 Silencing of FAK or LAMB3 recapitulated the synthetic lethal effects of miR-1298 expression in KRAS-

46 Genetic interactions, including synthetic lethal effects, can now be systematically iden

47 entifies numerous interactions that suppress synthetic lethal effects.

48 enger gene alterations and validated two new synthetic lethal effects.

49 e combined into higher-order strains without synthetic lethal effects.

50 ffects are more robust than oncogene-related synthetic lethal effects; and (ii) robust genetic intera

51 novel and established synthetic enhancers or synthetic lethals for KRAS(MUT) colorectal cancer, inclu

52 We identify BUD31 as a MYC-synthetic lethal gene in human mammary epithelial cells,

53 predictive ability for our reference list of synthetic lethal gene interactions (R = 0.159).

54 rimary gene and over/under-expression in the synthetic lethal gene is evaluated using Kaplan-Meier an

55 similar to those that characterize the known synthetic lethal gene pairs.

56 dhesion kinase (FAK), represents a candidate synthetic lethal gene with GNAQ activation.

57 ntification of Wilms tumor 1 (Wt1) as a Kras synthetic-lethal gene in a mouse model of lung adenocarc

58 de RNA interference screen to search for Myc-synthetic lethal genes and uncovered a role for the SUMO

59 fects of selectively targeting the predicted synthetic lethal genes is tested in silico using shRNA a

60 We identified APEX2 and FEN1 as synthetic lethal genes with both BRCA1 and BRCA2 loss of

61 Among the strongest synthetic lethal genes, polarity defects are more appare

62 Synthetic lethal genetic analysis has identified MAT2A a

63 ary for vegetative Nam8 function in multiple synthetic lethal genetic backgrounds.

64 The yeast synthetic lethal genetic interaction network contains ri

65 When applied to the Saccharomyces cerevisiae synthetic lethal genetic interaction network, we can ach

66 ermore, mutants of P32, Nlp, and Nph exhibit synthetic-lethal genetic interactions.

67 Synthetic lethal hits were validated with specific inhib

68 efficiency of CMG disassembly in vivo and is synthetic lethal in combination with a disassembly-defec

69 ian central nervous system, called SLIC, for synthetic lethal in the central nervous system.

70 Thus, combined loss of Paxx and Xlf is synthetic-lethal in mammals.

71 lymerase (PARP) inhibitors were found to be "synthetic lethal" in cells deficient in BRCA1 and BRCA2

72 We found that only ESCRT-III components are synthetic lethal, indicating that Vps4 and other ESCRT c

73 significant functional interplay and a novel synthetic lethal interaction among the human RecQ helica

74 Our studies show a novel synthetic lethal interaction and identify PPP2R2A as a p

75 xt of a transformed genotype may result in a synthetic lethal interaction and the selective death of

76 aken together, our findings have uncovered a synthetic lethal interaction between AURKB and Haspin, w

77 Here the authors find a synthetic lethal interaction between CDA and the microtu

78 tly required for cell cycle and the reported synthetic lethal interaction between Cdk1 and Myc.

79 Here, we report a novel synthetic lethal interaction between ctf7 and cdc28.

80 We found a synthetic lethal interaction between cytidine deaminase

81 ic of the genotype e(r)(p1) r(hd1-12) or the synthetic lethal interaction between e(r)(p2) and the No

82 Furthermore, we showed that the synthetic lethal interaction between Haspin depletion an

83 of KRAS-mutant cells, suggesting a druggable synthetic lethal interaction between KRAS and p21(WAF1/C

84 Finally, genetic analyses reveal a synthetic lethal interaction between loss of CDC55 and g

85 We identified and validated a synthetic lethal interaction between MTOR and ponatinib

86 orting tumour cell viability and clarify the synthetic lethal interaction between NUAK1 and MYC.

87 CA1- or BRCA2-defective tumors, based on the synthetic lethal interaction between PARP1 and BRCA1/2-m

88 ediatric gliomas such as DIPG, and uncover a synthetic lethal interaction between PPM1D mutations and

89 A synthetic lethal interaction between PPP2R2A deficiency

90 Here, we describe a synthetic lethal interaction between the C. elegans heli

91 These results indicate a synthetic lethal interaction between the two terminal re

92 In addition, the method identified a known synthetic lethal interaction between TP53 and PLK1, othe

93 Using this approach, we identified a synthetic lethal interaction between VHL and the m(6)A R

94 a genome-wide CRISPR/Cas9 screen, we found a synthetic lethal interaction between Wnt pathway activat

95 rast, inhibition of MAPK signaling created a synthetic lethal interaction in the setting of menin los

96 Here we identify a synthetic lethal interaction in which H3K36me3-deficient

97 These data uncover a synthetic lethal interaction involving glutathione produ

98 This synthetic lethal interaction is attributable to inhibiti

99 This synthetic lethal interaction was retained in CREBBP-muta

100 he cohesin complex, STAG2, displays a strong synthetic lethal interaction with its paralog STAG1.

101 non-essential serine-threonine kinase, in a synthetic lethal interaction with MYC.

102 show that Cdk1 inhibition was enough for the synthetic lethal interaction with Myc.

103 quamous cell cancer (HNSCC) cell lines and a synthetic lethal interaction with the extracellular sign

104 c DNA lesion O(6)-methylguanine and caused a synthetic lethal interaction with the PARP-1 inhibitor o

105 ide reductase subunit, is the target of this synthetic lethal interaction.

106 he ATR pathway itself provided the strongest synthetic lethal interaction.

107 53-deficient cancer cells, thus exploiting a synthetic lethal interaction.

108 al, providing mechanistic insights into this synthetic lethal interaction.

109 acy against BRCA1/2-mutant cancers through a synthetic lethal interaction.

110 inoma (ESCC) models, reciprocal to the known synthetic lethal interaction.

111 clinically available drug, revealed a robust synthetic-lethal interaction with native or engineered o

112 Here we demonstrate a "synthetic lethal" interaction between oncogenic BRAF V60

113 by disease-specific and clinically relevant synthetic lethal interactions and experimental validatio

114 this study can identify clinically relevant synthetic lethal interactions and that vitamin D recepto

115 Nineteen of 24 (79%) synthetic lethal interactions are present in at least tw

116 ogram; furthermore, our outcomes uncover new synthetic lethal interactions as potential therapies for

117 tion, we have used this protocol to identify synthetic lethal interactions between genes systematical

118 ombination therapies that are aimed at using synthetic lethal interactions between kinase deficiencie

119 riptional gene regulators, to identify novel synthetic lethal interactions between miRNA inhibition a

120 rating it in therapeutic strategies that use synthetic lethal interactions between SMARCA4-MAX and SM

121 these representations to share knowledge of synthetic lethal interactions between species.

122 anticancer therapies should not only exploit synthetic lethal interactions between two single genes b

123 ies for defining mammalian gene networks and synthetic lethal interactions by exploiting the natural

124 We propose that these synthetic lethal interactions can be explored for target

125 In vivo, synthetic lethal interactions have been identified betwe

126 xperimental procedures, relatively few human synthetic lethal interactions have been identified.

127 roughput RNA interference (RNAi) to identify synthetic lethal interactions in cancer cells harboring

128 To identify synthetic lethal interactions in cancer cells harbouring

129 nal screens can offer a strategy to identify synthetic lethal interactions in cancer cells that might

130 netic screening efforts to gain insight into synthetic lethal interactions of CDK4/6 inhibitors in br

131 p-Rho3p interaction does not account for the synthetic lethal interactions or the exocyst assembly de

132 ti-species approach to develop a resource of synthetic lethal interactions relevant to cancer therapy

133 es for their aberrant growth, thus revealing synthetic lethal interactions that could be exploited fo

134 ational systems approach to predicting human synthetic lethal interactions that works by identifying

135 Exploiting synthetic lethal interactions to target recurrent cohesi

136 interaction networks can be used to predict synthetic lethal interactions with accuracies on par wit

137 ALL therapy and support strategies targeting synthetic lethal interactions with Akt and PIM kinases a

138 e, we report a systematic screen to identify synthetic lethal interactions with ATR pathway-targeted

139 BBDI response and resistance, we identified synthetic lethal interactions with BBDIs and genes that,

140 We elected to identify synthetic lethal interactions with c-MYC overexpression

141 The toutatis gene exhibits strong synthetic lethal interactions with CtBP.

142 on Nug2-associated particles, and both show synthetic lethal interactions with nug2 mutants.

143 n and repair, and has the greatest number of synthetic lethal interactions with Saccharomyces cerevis

144 lular responses to these agents and identify synthetic lethal interactions with specific DNA repair f

145 ertook a genome-wide RNAi screen to identify synthetic lethal interactions with the KRAS oncogene.

146 ing of Synthetic Lethals (MiSL), to identify synthetic lethal interactions with the loss of VHL throu

147 a synthetic genetic array screen to identify synthetic lethal interactions with the yeast CL synthase

148 ction between TP53 and PLK1, other potential synthetic lethal interactions with TP53, and correlation

149 sh the role of acetyltransferase activity on synthetic lethal interactions, and (6) identify new func

150 cting nutrient rescue of essential genes and synthetic lethal interactions, and we provide detailed p

151 ATR inhibitors exhibit synthetic lethal interactions, with deficiencies in the

152 La cells, resulting in networks of conserved synthetic lethal interactions.

153 h expected and uncharacterized buffering and synthetic lethal interactions.

154 cation of genetic suppressors, enhancers and synthetic lethal interactions.

155 apies are being developed that exploit human synthetic lethal interactions.

156 ed to the identification of new, deleterious synthetic lethal interactions.

157 rmacological accessibility of many candidate synthetic-lethal interactions and the swift emergence of

158 Systematic analysis identifies synthetic-lethal interactions as most informative for fu

159 we explore an approach to identify potential synthetic-lethal interactions by screening mutually excl

160 In addition to known synthetic-lethal interactions, this approach uncovered t

161 , sensitize tumors to radiation, and mediate synthetic lethal killing of BRCA2-deficient cancer cells

162 Furthermore, a synthetic lethal kinome shRNA screen with a pan-ERBB inh

163 tion of the EZH2 methyltransferase acts in a synthetic lethal manner in ARID1A-mutated ovarian cancer

164 ma-mediated drug resistance and can act in a synthetic lethal manner in the context of tumor-stroma i

165 cogenic phenotypes caused by mutant p53 in a synthetic lethal manner.

166 , were well tolerated in vivo and acted in a synthetic-lethal manner to induce apoptosis in human gli

167 after CDK inhibition and contributes to this synthetic-lethal mechanism.

168 r functional defects in this pathway through synthetic lethal mechanisms.

169 innovative computational platform, Mining of Synthetic Lethals (MiSL), to identify synthetic lethal i

170 The synthetic lethal mutants have low levels of some lipid s

171 aturating transposon mutagenesis to identify synthetic lethal mutants in a yeast strain lacking ER-PM

172 myces cerevisiae) osmosensor mutants lacking Synthetic Lethal of N-end rule1 and SH3-containing Osmos

173 n-associated proteins, identified unexpected synthetic lethal opportunities and enabled increasingly

174 way in p53-deficient cells can induce such a synthetic lethal outcome.

175 l and cisplatin response beyond those of the synthetic lethal p53 mutant/MK2 combination alone.

176 subtilis MurJ (murJBs; formerly ytgP) are a synthetic lethal pair.

177 ual and biological screening against several synthetic lethal pairs to explore whether two-compound f

178 hen identify over one million putative human synthetic lethal pairs to guide experimental approaches.

179 ilico methods to guide the identification of synthetic lethal pairs.

180 rns that persist across species, to identify synthetic lethal pairs.

181 The synthetic lethal paradigm has provided a framework for t

182 We observe 24 synthetic lethal paralog pairs that have escaped detecti

183 ukemias, and prostate cancer, as a potential synthetic lethal partner of the DNA repair protein polyn

184 MiSL identified FTO as a synthetic lethal partner of VHL because deletions of FTO

185 To identify this factor, we screened for synthetic lethal partners of MOP family members using tr

186 e used systematic RNA interference to detect synthetic lethal partners of oncogenic KRAS and found th

187 Ras-dependent and -independent lines uncover synthetic lethal partners of oncogenic Ras.

188 This supports an alternative paradigm for synthetic lethal partnerships that could be exploited th

189 We also uncover 1024 potential synthetic lethal pharmacogenomic interactions.

190 This synthetic lethal phenotype can be suppressed by disrupti

191 , the absence of all three proteins caused a synthetic lethal phenotype due to extreme Cu sensitivity

192 2Deltalinker constructs exhibited a specific synthetic lethal phenotype in cells lacking CPR7.

193 ATM loss of function can produce a synthetic lethal phenotype in combination with tumor-ass

194 This synthetic lethal phenotype is dependent on A3B catalytic

195 The synthetic lethal phenotype of dgat1 with plip1 indicates

196 uracil DNA glycosylase 2 (UNG) and that this synthetic lethal phenotype requires functional mismatch

197 he major periplasmic protease DegP confers a synthetic lethal phenotype, presumably due to the toxic

198 al rather than technical limitations as most synthetic lethal phenotypes are strongly modulated by ch

199 oss of the cold-sensitive and beta-dependent synthetic lethal phenotypes associated with increased le

200 a CRISPR genetic screen to uncover 140 Polq synthetic lethal (PolqSL) genes, the majority of which w

201 ted published KRAS biology, identified novel synthetic lethal proteins that were experimentally valid

202 to the problems of identifying essential and synthetic lethal reactions and minimal media.

203 /lox);Skp2(-/-) embryos, demonstrating their synthetic lethal relationship at a cell autonomous level

204 tifunctional mediator of HR, and establish a synthetic lethal relationship between DEK loss and NHEJ

205 d on E11.5, establishing an organismal level synthetic lethal relationship between Rb1 and Skp2 On E1

206 Our studies identify a synthetic lethal relationship between SMARCB1-deficient

207 Our results reveal a synthetic lethal relationship between the HR pathway and

208 feration, simultaneous inhibition uncovers a synthetic lethal relationship between these two oncogeni

209 sults of this study indicate that there is a synthetic lethal relationship between UBB and UBC that h

210 It is unclear whether a similar synthetic lethal relationship exists between defects in

211 In response to DNA damage, a synthetic lethal relationship exists between the cell cy

212 the BAF complex, display a well-established synthetic lethal relationship in SMARCA4-deficient cance

213 essary and sufficient for the ABT-737-shDhx9 synthetic lethal relationship.

214 severe loss of cell viability, indicating a synthetic lethal relationship.

215 Our screen was designed to identify synthetic lethal relationships between translation facto

216 These analyses revealed synthetic lethal relationships that may be exploited the

217 other DNA repair defects would give rise to synthetic lethal relationships, we queried dependencies

218 Here, we use a genome-wide RNAi-synthetic lethal screen and transcriptomic profiling to

219 line, was employed in a paclitaxel-dependent synthetic lethal screen designed to identify gene target

220 e of these drugs, we conducted a genome-wide synthetic lethal screen for candidate olaparib sensitivi

221 the case of KRAS, we identify that published synthetic lethal screen hits significantly overlap at th

222 Using a synthetic lethal screen in human PDAC cells, we identifi

223 Using a synthetic lethal screen of a RNAi library of nuclear enz

224 e we report the results of a small molecule, synthetic lethal screen using mouse embryonic fibroblast

225 Here, we report a synthetic lethal screen with a library of deubiquitinase

226 hese three components, we have carried out a synthetic lethal screen with cdc9-p, a DNA ligase mutati

227 lin 1, we performed an unbiased, genome-wide synthetic lethal screen with yeast cells lacking profili

228 In a synthetic lethal screen, pan-PI3K inhibition synergized

229 From a high throughput synthetic lethal screen, we identified a small molecule,

230 Using a synthetic lethal screen, we identified residues of YidC

231 Using data from a genome-wide shRNA synthetic lethal screen, we show that BRCA1 and members

232 n redundantly in cytokinesis, we conducted a synthetic-lethal screen in a septin-deficient strain and

233 T301) by using a small interfering RNA-based synthetic lethal screening method.

234 er of correlative studies, here we develop a synthetic lethal screening methodology for the mammalian

235 We demonstrate the usefulness of synthetic lethal screening of a conditionally BCL6-defic

236 Synthetic lethal screens have the potential to identify

237 We used synthetic lethal screens in budding yeast to identify mu

238 to whole-genome forward-genetic analysis and synthetic-lethal screens.

239 o these drugs, we performed a PARP-inhibitor synthetic lethal short interfering RNA (siRNA) screen.

240 Similarly, a synthetic lethal siRNA screen conducted in a broad panel

241 A PARP1/2 inhibitor-synthetic lethal siRNA screen revealed that ERCC1 defici

242 elop novel drug combinations, we conducted a synthetic lethal siRNA screen using a library that targe

243 Using a genome-wide synthetic lethal siRNA screen, we identified the folate

244 These results highlight the potential of synthetic lethal siRNA screens with chemical inhibitors

245 genes in a given cancer and targeting their synthetic lethal (SL) partners.

246 ild-type or mutant PIK3CA to search for PI3K synthetic-lethal (SL) genes.

247 Synthetic sick or synthetic lethal (SS/L) screens are a powerful way to id

248 irect targeting of MYC has remained elusive, synthetic lethal strategies are attractive.

249 We found that the synthetic lethal strategy employing dinaciclib and nirap

250 erges from drug-tolerant cells and unveils a synthetic lethal strategy for enhancing responses to EGF

251 x vivo and in vivo, representing a promising synthetic lethal strategy for treating the disease.

252 cell cytotoxicity can be achieved through a synthetic lethal strategy using poly(ADP)-ribose polymer

253 otoxic agents or PARP inhibitors following a synthetic lethal strategy.

254 Our data therefore identify a new synthetic-lethal strategy to selectively target cancer c

255 The RecQ DNA helicase WRN is a synthetic lethal target for cancer cells with microsatel

256 h cisplatin, suggesting ITPKB as a promising synthetic lethal target for cancer therapeutic intervent

257 Werner syndrome ATP-dependent helicase, as a synthetic lethal target in tumours from multiple cancer

258 n kinases for growth and survival as well as synthetic lethal targets for combined inhibition with EG

259 results identify viral transformation-driven synthetic lethal targets for therapeutic intervention.

260 DNA repair processes represent attractive synthetic lethal targets, because many cancers exhibit a

261 In a search for potential synthetic-lethal targets for FLCN using a phosphatase si

262 pient miRNA technology to the aforementioned synthetic lethal therapeutic strategies.

263 te that cellular context will be critical to synthetic-lethal therapies.

264 s olaparib, have been proposed to serve as a synthetic lethal therapy for cancers that harbor BRCA1 o

265 ifying small molecule compounds that (1) are synthetic lethal to mutant KRAS, (2) block KRAS/GEF inte

266 nce (RNAi) screen to identify genes that are synthetic lethal to the IDH1(R132H) mutation in AML and

267 stance and myelosuppression attributed to a 'synthetic lethal toxicity' arising from simultaneous inh

268 in a new era of research on biomarker-driven synthetic lethal treatment strategies for different canc

269 These findings show that WRN is a synthetic lethal vulnerability and promising drug target

270 represents a promising approach for inducing synthetic lethal vulnerability in cells harboring otherw

271 Using a random screen for synthetic lethals we found a ppGpp-dependent functional

272 In Escherichia coli, the synthetic lethal with a defective Min system (SlmA) prot

273 addressing the molecular mechanism of SlmA (synthetic lethal with a defective Min system)-mediated N

274 , we demonstrated that RNASEH2 deficiency is synthetic lethal with ATR inhibition both in vitro and i

275 e-specific endonuclease ERCC1-XPF (ERCC4) is synthetic lethal with ATR pathway inhibitors.

276 utation rate at the yeast CAN1 locus, and is synthetic lethal with both proofreading deficiency and m

277 Furthermore, SMARCA4 loss is synthetic lethal with CDK4/6 inhibition both in vitro an

278 rd with these data, 1 and 3 were found to be synthetic lethal with certain mutations in DNA DSB repai

279 We also show that loss of DBP2 is synthetic lethal with deletion of the nuclear RNA decay

280 ied MTBP as the metazoan orthologue of yeast synthetic lethal with Dpb11 7 (Sld7).

281 Synthetic lethal with Dpb11-1 (Sld2) is required for the

282 Here we report that ATM loss-of-function is synthetic lethal with drugs inhibiting the central growt

283 ile removal of uracil catabolism alleles was synthetic lethal with eogt knock-down.

284 ATM (ataxia telangiectasia mutated) as being synthetic lethal with FLT3 inhibitor therapy.

285 ISPR screens, we establish that ALC1 loss is synthetic lethal with homologous recombination deficienc

286 PARG inhibition is synthetic lethal with inhibition of DNA replication fact

287 gues report that oncogenic MYC activation is synthetic lethal with inhibition of the core spliceosome

288 sistent with this observation, ldb18Delta is synthetic lethal with mutations affecting the Kar9 spind

289 ective, we discover that EXD2's depletion is synthetic lethal with mutations in BRCA1/2, implying a n

290 o mediate single-stranded DNA (ssDNA) and is synthetic lethal with mutations in other key recombinati

291 e F-BAR protein Cdc15, and for3 deletion was synthetic lethal with mutations that cause defects in co

292 athway reduction to 16% of normal levels was synthetic lethal with oncogenic Ras expression in cultur

293 Defining processes that are synthetic lethal with p53 mutations in cancer cells may

294 genes, including pbp1Delta, were found to be synthetic lethal with pfy1Delta.

295 two snr7 alleles, U5A and U6A, are dominant synthetic lethal with prp18 alleles.

296 targeting the Na(+)/K(+)-ATPase (ATP1A1) is synthetic lethal with STK11 mutations in lung cancer.

297 lymerase and aurora kinase inhibitors may be synthetic lethal with the common aberrations in DNA dama

298 Consequently, BRAF or MEK1/2 inhibitors are synthetic lethal with the MCL1 inhibitor AZD5991, drivin

299 that fail to synthesize enterobactin are not synthetic lethal with these C. elegans mitochondrial mut

300 In BY4741, rrp44-exo was synthetic-lethal with loss of the cytoplasmic 5'-exonucl