ライフサイエンスコーパス: growth advantage

1 nd FBN2 resulted in an anchorage-independent growth advantage.

2 nary phase and the presence of Rsr confers a growth advantage.

3 death, but in cycling cells, the result is a growth advantage.

4 beta phosphorylation and rescued the EC cell growth advantage.

5 y require genomic re-stabilization to gain a growth advantage.

6 d mTOR signaling provides tumors a selective growth advantage.

7 when the transgene might impart an intrinsic growth advantage.

8 selection, suggesting that it may provide a growth advantage.

9 o mutations in a subset of genes that confer growth advantage.

10 inhibition ameliorates the Nf1-/- astrocyte growth advantage.

11 red unless a mutation provides a survival or growth advantage.

12 onment, p53 mutant cells exhibit a selective growth advantage.

13 while simultaneously using this cytokine for growth advantage.

14 dampen the p53 response to gain a selective growth advantage.

15 apable of conferring upon the cell an actual growth advantage.

16 s some of the mutant clones with a selective growth advantage.

17 eurofibromin-deficient SCs had a substantial growth advantage.

18 xidant carcinogens, that provide a selective growth advantage.

19 with excess expression may have a selective growth advantage.

20 e deregulated with microvascular invasion or growth advantage.

21 forming growth factor-beta, thus providing a growth advantage.

22 spontaneous somatic mutations that provide a growth advantage.

23 in human liver cancer cells that may offer a growth advantage.

24 ed editing event does not confer a selective growth advantage.

25 es two distinct metabolic strategies to gain growth advantage.

26 s how FH inactivation can endow cells with a growth advantage.

27 s and NKTL cell lines leads to a significant growth advantage.

28 ions are passengers that confer no selective growth advantage.

29 ssage, suggesting it conferred a significant growth advantage.

30 rred an approximately 3.0-fold intracellular growth advantage.

31 corresponding to cancer drivers with strong growth advantages.

32 netic mechanisms confer equivalent selective growth advantages.

33 tion-defective counterpart, fully mimics the growth advantages afforded by EGF to these cancer cells.

34 stem cells (KSC), which confers a selective growth advantage allowing clonal expansion during tumor

35 cyte cultures did not show a cell-autonomous growth advantage, anchorage-independent growth, increase

36 on related; they have mutations conferring a growth advantage and are enriched during the propagation

37 s, termed driver mutations, confer selective growth advantage and are implicated in cancer developmen

38 model, repaired hepatocytes have a selective growth advantage and are thus able to proliferate to eff

39 ronment where the glycolytic phenotype has a growth advantage and consequently is most likely to appe

40 Primary Runx2-null osteoblasts have a growth advantage and exhibit loss of p21(WAF1/CIP1) and

41 he growth factor/receptor family that confer growth advantage and metastasis.

42 kinase), H-Ras-transformed cells lose their growth advantage and no longer form colonies.

43 dow of opportunity for PFI to bind provide a growth advantage and possibly a predisposition to resist

44 ltransferase activity is also able to confer growth advantage and rescue growth inhibition on endogen

45 ned expression of CBX7 in EC cells confers a growth advantage and resistance to retinoic acid-induced

46 iver, up-regulation of MAT2A also provides a growth advantage and SAMe and MTA can block mitogenic si

47 ty of latent pathways consistently offers no growth advantage and tends, in fact, to inhibit growth a

48 creatic ductal epithelial cells had a slight growth advantage and were resistant to premature senesce

49 onfer producing organisms with a competitive growth advantage, and also are thought to be virulence f

50 nce to apoptotic stimuli, enhanced survival, growth advantage, and differentiation arrest of CD34+ pr

51 ancer genes, where they can confer selective growth advantage, and over fragile sites, where they are

52 ed an increase in MIPS activity, conferred a growth advantage, and partially rescued sensitivity to v

53 at developmental pathways giving a selective growth advantage are often recapitulated in tumors, we i

54 that have been provided with a survival and growth advantage as a consequence of overexpression of t

55 hat loss of caveolin-1 confers a significant growth advantage, as measured via cellular proliferation

56 on for alterations that promote survival and growth advantage, as well as by the particular dysfuncti

57 Nf1+/- astrocytes) exhibit a cell autonomous growth advantage associated with increased RAS pathway a

58 lls in vivo and demonstrate that a selective growth advantage at a level distal to HSC can result in

59 n the other hand, RUNX1 conferred no obvious growth advantage at low cell density and actually delaye

60 Alternative models of upward growth advantage based on redox/resource gradients fail,

61 expression confers thyroid cells with little growth advantage because of concomitant activation of DN

62 these genes serve dual functions, providing growth advantages both in the primary tumour and in the

63 o provide the mutant clone with an extrinsic growth advantage, but some features of PNH argue that th

64 regulatory pathways and provide a selective growth advantage by activation of transforming oncogenes

65 ells harboring activated ras could provide a growth advantage by conferring resistance to apoptosis.

66 erexpressing GIT tumors may gain a selective growth advantage by escaping from TRAIL-induced apoptosi

67 Cancer cells often gains a growth advantage by taking up glucose at a high rate and

68 Hematologic maligancies exhibit a growth advantage by up-regulation of components within t

69 , in addition to the mutations that confer a growth advantage, cancer genomes accumulate a large numb

70 elevation provided human cancer cells with a growth advantage, caused chromosomal instability in vitr

71 mutation providing AML cells with a greater growth advantage compared with cells having the FLT3(WT/

72 n to bone marrow stromal cells; overcome the growth advantage conferred by antiapoptotic protein Bcl-

73 y, expression of miR-9 antagonizes the tumor growth advantage conferred by DeltaEGFR.

74 ageous mutations rather than from an initial growth advantage conferred by the polymerase variant its

75 ot rapamycin alone, was able to overcome the growth advantage conferred on MM cells by interleukin-6

76 nase (ERK) activation and also overcomes the growth advantages conferred by interleukin-6, insulin-li

77 defined regions during clonal selection for growth advantage define the minimally lost regions as th

78 ation of mutations that conveyed a selective growth advantage during adaptation to a glycerol-based g

79 beta-Catenin overexpression offers growth advantage during liver regeneration.

80 a) initiated, pre-malignant cells can have a growth advantage during repopulation, not just during th

81 n or class of mutations that confers a large growth advantage during the respiratory phase of yeast c

82 ikely responsible for conferring a selective growth advantage during tumour evolution and outgrowth.

83 in a solid tumor, Mtss1 does not confer any growth advantage, either in basal conditions or followin

84 ty modalities give P. aeruginosa a selective growth advantage, enabling it to self-segregate from oth

85 controlling properties that confer selective growth advantages even in the presence of a high backgro

86 hese larger placentas did not confer a fetal growth advantage; fetal size was normal in Ipl nulls wit

87 elial cells confers them with a survival and growth advantage, following exposure to DNA-damaging age

88 cative advantage for mutated mtDNA copies, a growth advantage for a cell containing certain mtDNA mut

89 Mutations in the AR likely confer a growth advantage for a subset of progressive prostate ca

90 rozygosity may provide a non-cell-autonomous growth advantage for astrocytes that may involve p27-Kip

91 of Tsc1 in mice provides a context-dependent growth advantage for astrocytes that results in abnormal

92 tein (neurofibromin) expression may confer a growth advantage for astrocytes, such that inactivation

93 of the bacterial food source, resulting in a growth advantage for both organisms, similar to that ach

94 e of the deleted gene; in two cases, a clear growth advantage for cells acquiring the extra chromosom

95 e microenvironment would provide a selective growth advantage for cells that have lost wild type p53

96 ve no abnormalities and offer a considerable growth advantage for future exploitation.

97 e also observe a significant and competitive growth advantage for KITD816V in Tet2-nullizygous compar

98 tion of the JmjC domain of dUTX results in a growth advantage for mutant cells over adjacent wild-typ

99 hese results suggest that Melk may provide a growth advantage for neoplastic cells and, therefore, in

100 rathionate as an electron acceptor produce a growth advantage for S. Typhimurium over the competing m

101 rdinated surface modifications may provide a growth advantage for Salmonella in host tissues by limit

102 plication, and that human STAT2 can confer a growth advantage for SV5 in the murine host.

103 These increases are not caused by a growth advantage for the revertants and are restricted t

104 e mutation confers a host factor-independent growth advantage for the survival of HBV variants in gra

105 These trade-offs add up to a significant growth advantage for the two natural isoforms.

106 L. pneumophila feoB gene conferred a modest growth advantage for the wild type over the mutant in a

107 his metabolic phenotype provides a selective growth advantage for tumour cells in vivo.

108 ort a novel function of PCGEM1 that provides growth advantages for cancer cells by regulating tumor m

109 overexpression of putative oncogenes confer growth advantages for tumor development.

110 monacha-lucida likewise obtains an intrinsic growth advantage from reduced investment in male gametes

111 also show that it detects growth-defect and growth-advantage genes previously shown to impair or enh

112 resource-poor, bacteria may gain significant growth advantages if they can exploit the ephemeral nutr

113 o the wild-type parent strain and also had a growth advantage in a continuous flow biofilm system.

114 y event in liver carcinogenesis, providing a growth advantage in a subset of hepatic tumors with a mo

115 Evidence is provided that S. Typhimurium's growth advantage in an inflamed gut is because of its ab

116 rgeted role in hTERT regulation leading to a growth advantage in cells expressing HPV16 E6.

117 ht to endow P. aeruginosa with a competitive growth advantage in colonized tissue and is also thought

118 oma formation, but can provide a cooperative growth advantage in concert with genetic alterations in

119 tem l transport, and these cells displayed a growth advantage in conditions of limited arginine.

120 gnaling in Nf1-/- astrocytes abrogated their growth advantage in culture, restoring normal proliferat

121 r variants that provide mutated cells with a growth advantage in culture.

122 cells from the transgenic tumors exhibited a growth advantage in culture.

123 One of these genes, Bcl11a, confers a growth advantage in cultured Nf1 mutant hematopoietic ce

124 n conventionally raised mice, but provide no growth advantage in germ-free mice.

125 gnificant proliferative stimulation and/or a growth advantage in hepatocarcinogenesis of woodchucks w

126 with high glutamate release have a distinct growth advantage in host brain that is not present in vi

127 mutant GNAO1(R243D) conferred a significant growth advantage in human mammary epithelial cells, conf

128 A mechanism for clonal growth advantage in isolated del(5q) disease remains elu

129 ement by CCL22 in ATLL cells and conferred a growth advantage in long-term in vitro cultures.

130 Y705 (Y705F/S727E) resulted in a remarkable growth advantage in low-serum, enhanced anchorage-indepe

131 at increased STAT5A/B copy numbers conferred growth advantage in PCa cells in vitro and as xenograft

132 LA-deficient DC subsets displayed a specific growth advantage in repopulating the spleen in competiti

133 t interact cooperatively to gain a selective growth advantage in some cases.

134 Despite having no growth advantage in standard laboratory conditions, near

135 Mutants of increased fitness express a growth advantage in stationary phase (GASP) phenotype, e

136 These mutants express the growth advantage in stationary phase (GASP) phenotype.

137 evolved under prolonged stress often have a growth advantage in stationary phase (GASP); we expect G

138 These mutants also fail to express the "growth advantage in stationary phase" phenotype as do wi

139 tead expressing two additional new types of "growth advantage in stationary phase" phenotype.

140 play an increased fitness referred to as the growth advantage in stationary phase, or GASP, phenotype

141 The quadruple mutant displayed a growth advantage in the amoebal host Dictyostelium disco

142 r emerging neoplastic cells with a selective growth advantage in the hostile tumor microenvironment.

143 umor/host estrogen production and acquired a growth advantage in the presence of host bone marrow cel

144 and selecting for transformants exhibiting a growth advantage in the presence of the anti-microbial a

145 in one gene, ponA1, demonstrated an in vitro growth advantage in the presence of the drug rifampicin.

146 ETC-impaired cells display a marked growth advantage in the presence or absence of oncogenic

147 suggests that d-serine catabolism provides a growth advantage in the urinary tract.

148 these systems provide B. pseudomallei with a growth advantage in vitro and in vivo, but relatively li

149 -MMP, confers tumor cells with a distinct 3D growth advantage in vitro and in vivo.

150 We report that p12 conferred a selective growth advantage in vitro and increased the colony forma

151 se mice do not demonstrate a cell-autonomous growth advantage in vitro and lack properties of transfo

152 NOS2(-/-) and wild-type C57BL/6 mice, and a growth advantage in vitro in liquid culture.

153 r cdk4 overexpression provides a cooperative growth advantage in vitro, CDK4-overexpressing C6 glioma

154 ugh TWEAK-overexpressing cells do not have a growth advantage in vitro, they form larger and more hig

155 ve mutant, in a glioma cell line conferred a growth advantage in vitro.

156 deleterious mutation and showed a selective growth advantage in vivo.

157 ing to external stimuli are likely to gain a growth advantage in vivo.

158 es, greater maximum culture densities, and a growth advantages in pairwise competition relative to th

159 roperties in PDA cells by enabling them with growth advantages in stressful tumor microenvironment ni

160 MAOA provides tumor cell growth advantages in the bone microenvironment by stimul

161 Cancer cells gain growth advantages in the microenvironment by shifting ce

162 ins, losses, and mutations, some providing a growth advantage, including alterations in MLL2, EPHA7,

163 The IL-15-mediated growth advantage is abolished by mitogen-activated prote

164 This growth advantage is diminished if cells with only oncoge

165 using IL-15-responsive SD-1 cells shows this growth advantage is maximal under low-serum conditions,

166 by which these LMW forms give tumor cells a growth advantage is not known and is the subject of this

167 lysis and is suggested to bestow a selective growth advantage, is a promising target.

168 for in oncogenesis because it confers clonal growth advantage, may also provide an important mechanis

169 ll cell population experiences a significant growth advantage, much greater than with cooperation or

170 such strains endow host cells with a general growth advantage, not only on cefotaxime but also on sev

171 n of PRL-3 confers cytokine independence and growth advantage of AML cells.

172 es and the EBV LMP-1 gene, which mediate the growth advantage of B cells infected with type 1 EBV.

173 The growth advantage of dUTX mutant tissue is caused, at lea

174 stoma (Rbf in Drosophila) contributes to the growth advantage of dUTX mutant tissue.

175 These results demonstrate that the growth advantage of G207 in FUdR-treated cells is primar

176 The selective growth advantage of gene-modified cells in patients with

177 ecause of a second mutation or a conditional growth advantage of GPI(-) cells in the presence of an i

178 hus by functional loss may contribute to the growth advantage of neoplasia.

179 s and could be dictated by either selection (growth advantage of one phase) or signaling (preferentia

180 death, whereas its overexpression leads to a growth advantage of prostate cancer cells.

181 e in SI growth rate results in a significant growth advantage of SI over NSI when the immune system i

182 rgely normalizes oxygen consumption, and the growth advantage of these cells can be suppressed by inh

183 with eGFP-transposons revealed no selective growth advantage of transposon-harboring cells.

184 Rapamycin also reverts a growth advantage of Tsc2(-/-)TP53(-/-) cells.

185 tumor progression by allowing for selective growth advantage of tumor cells.

186 w the PPP is regulated to confer a selective growth advantage on cancer cells is not well understood.

187 hate pathway, thereby conferring a selective growth advantage on cancer cells.

188 c pathway is predicted to confer a selective growth advantage on cells.

189 ens and identified genes conferring a clonal growth advantage on normal and neoplastic (cutaneous squ

190 The circadian clock confers a growth advantage on plants and uses environmental inform

191 fic nutrient (ethanolamine) confers a marked growth advantage on Salmonella enterica serovar Typhimur

192 sabotage the mouse immune system to confer a growth advantage on T. cruzi and transgenic L. major.

193 mutation nor the grvA(+) plasmid conferred a growth advantage or disadvantage in laboratory media.

194 od for ascertaining whether a gene confers a growth advantage or disadvantage in skin tumorigenesis.

195 of epigenetic marks that confer a selective growth advantage or through a specific pathway initiated

196 tor system, the wild-type strain exhibited a growth advantage over 042PicS258A in a culture of cecal

197 that a pyelonephritis clinical isolate had a growth advantage over a laboratory strain of E. faecalis

198 death upon growth factor deprivation, and a growth advantage over control cells under suboptimal gro

199 ssion of Wnt3a in H929 MM cells conferred no growth advantage over empty vector-transfected cells in

200 However, P18 had a growth advantage over ISP794 at all temperatures, sugges

201 ed hepatocytes (Fah(-/-)/Hpd(-/-)) display a growth advantage over non-edited hepatocytes (Fah(-/-)/H

202 toward malignancy, including (1) providing a growth advantage over normal cells, (2) maintaining the

203 G1 arrest, which may account for a selective growth advantage over normal cells.

204 chanism whereby malignant cells can obtain a growth advantage over normal cells.

205 he Philadelphia chromosome (Ph+) clone has a growth advantage over normal hematopoiesis.

206 Each phenotype was designed to confer a growth advantage over the other phenotype in a certain e

207 38 Ile) virus had a slight, but reproducible growth advantage over the wild-type s55 (nsP1 538 Thr) v

208 pression may provide the transformed cells a growth advantage over their normal counterpart.

209 Here we show that trr mutant cells have a growth advantage over their wild-type neighbors and disp

210 onal lymphoid cells that possess a selective growth advantage over those carrying disruptive IL2RG mu

211 ahymena, the Stx-encoding bacteria display a growth advantage over those that do not produce Stx.

212 cells with larger CTG repeat expansion had a growth advantage over those with smaller expansions in c

213 fective mutant killer virus with a selective growth advantage over those with WT killer virus.

214 hl(2B/2B) teratomas additionally displayed a growth advantage over Vhl(-/-)-derived teratomas, sugges

215 ne, overexpression of EGFR-T790M displayed a growth advantage over wild-type (WT) EGFR.

216 DeltaHmga2-derived BM cells had a growth advantage over wild-type cells in competitive rep

217 degradation-resistant HOXB4 that conferred a growth advantage over wild-type HOXB4 in myeloid progeni

218 virus growth kinetics and conferred a robust growth advantage over wild-type rVSV-MAK-GP on Vero E6 c

219 defining viral characteristics that confer a growth advantage, pathogenicity, or cell adaptability in

220 owing for the detection of growth-defect and growth-advantage regions.

221 pressed GAL gene expression and had a robust growth advantage relative to S. bayanus; transgenesis of

222 lar signaling, if and how fumarate confers a growth advantage remain unclear.

223 sistant to herbicides, providing them with a growth advantage so that they can outcompete weeds.

224 t defects in AR corepressor function yield a growth advantage specifically in AR-dependent cells.

225 age-encoded "anti-sRNA" provided EHEC with a growth advantage specifically in bovine rectal mucus rec

226 PIGA(-) cells had no growth advantage, suggesting that other factors are need

227 te fold representation is more predictive of growth advantage than a host of other potential growth-l

228 ence is observed for subpopulations with any growth advantage that comprise even 0.1% of the prolifer

229 taneous immortalization and confers an early growth advantage that is resistant to stress-induced gro

230 Nf1 mutant stem cells demonstrated a growth advantage that was greatest in myeloid lineage ce

231 associated with this QTL confer competitive growth advantages that depend on ascaroside secretion, i

232 show that IRAK1 overexpression confers TNBC growth advantage through NF-kappaB-related cytokine secr

233 Cancer cells gain a growth advantage through the so-called Warburg effect by

234 s suggest that TGFBR1*6A confers a selective growth advantage to both normal appearing and cancerous

235 at a major hTERT splice variant can confer a growth advantage to cancer cells independent of telomere

236 hermore, enforced TFRC1 expression confers a growth advantage to cells and significantly enhances the

237 of the TSC2 tumor suppressor gene confers a growth advantage to cells by repressing hypoxic mTOR inh

238 xpressed by other tumors and could provide a growth advantage to cells that express it.

239 ion of GAL1 transcripts provides a transient growth advantage to cells upon addition of glucose.

240 Genes that provide growth advantage to cells via loss-of-function mutations

241 the contribution of a number of genes giving growth advantage to cells when transformed.

242 ed by IFN plus retinoic acid and conferred a growth advantage to cells.

243 timulatory loops and is believed to convey a growth advantage to cells.

244 tive impairment of normal LTHSC growth and a growth advantage to CML LTHSC.

245 owth to energy storage could have provided a growth advantage to early cells, once the membrane compo

246 of estrogen receptor activity and provides a growth advantage to estrogen-dependent cells.

247 is a promising agent capable of providing a growth advantage to genetically modified hematopoietic s

248 reased levels of C18-ceramide might impart a growth advantage to HNSCC cells and that increased gener

249 Furthermore, GPR84 conferred a growth advantage to Hoxa9/Meis1a-transduced stem cells.

250 /-) mice, indicating that TdmhMtb provides a growth advantage to intracellular Mtb in an immunocompro

251 ld inhibit growth, PhtC and PhtD conferred a growth advantage to L. pneumophila thyA(+) strains.

252 wth of normal CD34+ cells, thus conferring a growth advantage to normal hematopoietic cells over leuk

253 FR-DNR approach suggests that EGFR confers a growth advantage to NuTu-19 cells in vivo.

254 allosteric stimulation of Sos and confers a growth advantage to oncogenic K-Ras harbouring cancer ce

255 nstream of Smad7 in a pathway that confers a growth advantage to pancreatic cancer cells and that inc

256 uiding modification on H69 provided a slight growth advantage to PCF parasites at 30 degrees C.

257 lung carcinogenesis may provide a selective growth advantage to premalignant cells.

258 epatocellular proliferative lesions with the growth advantage to progress to hepatoblastoma.

259 es the AR pathway and confers a survival and growth advantage to prostate cancer cells in an androgen

260 f a gene(s) located in this region confers a growth advantage to some primary human lymphomas.

261 burgdorferi mouse infectivity and provide a growth advantage to spirochetes in the tick.

262 e cotraveling stromal cells provide an early growth advantage to the accompanying metastatic cancer c

263 The enzyme confers a growth advantage to the bacterium, providing essential a

264 down-regulation of either molecule confers a growth advantage to the cells.

265 uct of the inflammatory response conferred a growth advantage to the commensal bacterium Escherichia

266 tion, they steadily proliferate and confer a growth advantage to the entire population.

267 ls, suggesting that this mutation provides a growth advantage to this subset of MSI colon tumors.

268 with increased phosphorylated protein and a growth advantage to transduced cell lines or normal NK c

269 Oncogene amplification confers a growth advantage to tumor cells for clonal expansion.

270 lation of STRAP in human cancers may provide growth advantage to tumor cells via TGF-beta-dependent a

271 that although Gab2 overexpression may confer growth advantage to tumor cells, the functional requirem

272 poptotic sensitization by Pfn1 and confers a growth advantage to tumors.

273 sary for aerobic glycolysis and to provide a growth advantage to tumors.

274 ctly regulates the PPP to confer a selective growth advantage to tumours.

275 -regulated pilus) that confers a significant growth advantage to V. cholerae on a chitin surface; (ii

276 ses transcription of these genes, conferring growth advantages to cancer cells.

277 conjunction with cofactors, confers several growth advantages to cancer cells.

278 ion that ectopically expressed hTERT conveys growth advantages to cells, without having to postulate

279 on, some haplotypes confer proliferative and growth advantages to cells.

280 ges that lead to filopodia formation, confer growth advantages to fibroblasts under low serum conditi

281 mitochondrial biogenesis, affording distinct growth advantages to the prostate cancer cells.

282 an lead to alterations that confer selective growth advantages to the tumor, some of which play a rol

283 identify clonal genetic hits associated with growth advantage, tracking the evolution of bladder canc

284 bearing a functional EfeUOB displays a major growth advantage under aerobic, low-pH, low-iron conditi

285 ells suppress this signaling pathway to gain growth advantage under conditions of energy stress is la

286 h and that Atg1 mutant cells have a relative growth advantage under conditions of reduced TOR signali

287 ls are initiated cells that have a selective growth advantage under conditions that inhibit the growt

288 hift to glycolytic metabolism and provides a growth advantage under hypoxic conditions, and HIF-1 kno

289 of YlxM conferred a significant competitive growth advantage under nonstress and acid stress conditi

290 t cells lacking MLH1 may possess a selective growth advantage under oxidatively stressed conditions v

291 sitive LNCaP cells with RGS2 silencing had a growth advantage under steroid-reduced conditions.

292 rmal and malignant cells, thereby conferring growth advantages under stress as well as resistance to

293 with an EBV miRNA mutant conveyed a cellular growth advantage upon IFN treatment, and relevant miRNAs

294 a perineural location acquire a survival and growth advantage using a NFkappaB survival pathway.

295 This growth advantage was attributable to increased cell prol

296 n growth, and a defined lasR mutant showed a growth advantage when cocultured with the parent strain.

297 in IKKalpha expression provided a selective growth advantage, which cooperated with H-Ras mutations

298 ction mutations in these strains conferred a growth advantage with particular carbon and nitrogen sou

299 ve stress, MtbFHb-expressing cells exhibited growth advantage with reduced levels of lipid peroxidati

300 ay provide select prostate phenotypes with a growth advantage within the bone microenvironment.