ライフサイエンスコーパス: negative cell

1 ed in saliva is derived from an HLA class II-negative cell.

2 ased in frequency mainly consisted of Helios-negative cells.

3 or-encoding gene are required only for nanos-negative cells.

4 ally around the cell just as they do in Gram-negative cells.

5 IM, but not dasatinib, while sparing bcr-abl-negative cells.

6 an adaGb(3) without incorporating into Gb(3)-negative cells.

7 re shown to be antagonists of entry into CD4-negative cells.

8 ; there was a minimal effect on phospho-JAK2-negative cells.

9 ween ANG and p53 was also observed in LANA-1-negative cells.

10 in in CR3-positive cells but only 25% in CR3-negative cells.

11 b/CD18 (CR3), ACT is more potent than in CR3-negative cells.

12 form detectable A3G complexes by 24 h or A3G-negative cells.

13 2A) receptor-positive but not A(2A) receptor-negative cells.

14 nhibitor of HIV-1 replication in herpesvirus-negative cells.

15 acts on dendrites of both TH-positive and TH-negative cells.

16 l-x(L) and cell death in the sensitive Bcl-2 negative cells.

17 ells would have a higher redox ratio than ER-negative cells.

18 leads to the reduced sumoylation of Z in EBV-negative cells.

19 so enhanced cell motility and invasion of ER-negative cells.

20 mutation frequencies when compared with HPV-negative cells.

21 neous population of SSEA3 positive and SSEA3 negative cells.

22 es and PML bodies in immortalized telomerase-negative cells.

23 th sfRON-T47D and other ERalpha-, E-cadherin-negative cells.

24 re maintained in total marrow and in lineage-negative cells.

25 totactic migration compared to those of LMP1-negative cells.

26 ion is radioresistant relative to the marker-negative cells.

27 nd A, in centrosome amplification in the p53-negative cells.

28 g memory B cells, to the frequencies of CD21-negative cells.

29 ive and luminal epithelial estrogen receptor negative cells.

30 E2F1 coimmunoprecipitate from extracts of RB-negative cells.

31 fferentiation of CD34 positive cells but not negative cells.

32 expression compared with stem cell antigen 1-negative cells.

33 ls in Tie2-expressing cells, but not in Tie2-negative cells.

34 of ER resident MHC I is decreased in tapasin-negative cells.

35 S)) expression in HBxAg positive compared to negative cells.

36 y 8-1 in HBV-producing cells, but not in HBV-negative cells.

37 FA, and no activity was detected against FR-negative cells.

38 tly higher in EBV-positive cells than in EBV-negative cells.

39 itive cells but also the neighboring antigen-negative cells.

40 optosis in NeuroD-positive cells than NeuroD-negative cells.

41 th class II major histocompatibility complex-negative cells.

42 ound to have chromosomal abnormalities in Ph-negative cells.

43 ic nuclear fragmentation compared to Id3-GFP-negative cells.

44 containing both antigen-positive and antigen-negative cells.

45 moderate Src activation was seen in dominant-negative cells.

46 s sensitized by reintroduction of AR into AR-negative cells.

47 ion, although this was not the case in N-Ras-negative cells.

48 bnormalities in Philadelphia chromosome (Ph)-negative cells.

49 s excluded propidium iodide as well as gp350-negative cells.

50 f spontaneous NO production compared with SE-negative cells.

51 FR-alpha expression in a variety of receptor-negative cells.

52 transfection to re-express MART-1 in MART-1-negative cells.

53 lcholine in CEL-expressing cells than in CEL-negative cells.

54 BPalpha does not promote proliferation in Rb-negative cells.

55 BCR-ABL+ cells induced apoptosis in BCR-ABL negative cells.

56 g leukocytes than did infection with laccase-negative cells.

57 ive ovarian cancer cells but not to integrin-negative cells.

58 e one-day-differentiated cells than in Nanog-negative cells.

59 and adenovirus receptor (CAR)-positive and -negative cells.

60 51 fold enrichment of PPI-positive over PPI-negative cells.

61 9L is potently active, however, against ASNS-negative cells.

62 n species (ROS) in both HPV-positive and HPV-negative cells.

63 on with wild-type or OS-untransduced lineage-negative cells.

64 e cells gave rise to additional positive and negative cells.

65 whereas PLX4720 selectively targeted JARID1B-negative cells.

66 rs that expressed IL-15, eliminating antigen-negative cells.

67 er of peptidoglycan in similarly shaped Gram-negative cells.

68 Tph2(+) neurons, also with some Tph2(low or negative) cells.

69 ells relative to Jurkat and K562 (both NKG2A negative) cells.

70 gly, restoration of wild-type AR in PC-3 (AR negative) cells abrogated both Par-4 induction and apopt

71 ells even in a 1,000-fold excess of ephrinB2-negative cells, all without any loss of specificity, as

72 CD28-negative cells also arise in cell cultures of CD8(+)CD28

73 Activation of BMP signaling in SMAD4-negative cells altered protein and messenger RNA levels

74 Similar results were also observed in ATM-negative cells, although comparable levels of viral DNA

75 of 123 proteins from both KSHV-positive and -negative cells, among which most were identified exclusi

76 fferentiation experiments with human lineage-negative cells and CD34(+) progenitors suggest that ther

77 loss boosts Akt phosphorylation only in PTEN-negative cells and cooperates with PTEN loss for tumor g

78 coding DNA polymerase B (polB-c)] and intein-negative cells and examining the dispersal efficiency of

79 cally expressed in luminal estrogen receptor negative cells and functional assays confirmed that it m

80 tivity against both telomerase-positive and -negative cells and induces robust apoptosis within 16 h

81 oepithelial cells, luminal estrogen receptor negative cells and luminal estrogen receptor positive ce

82 ient calreticulin constructs in calreticulin-negative cells and monitored the effects on the biogenes

83 acquire them during uptake of dead class II-negative cells and present them via a process called ind

84 nfers xenograft tumor formation upon t(4;14)-negative cells and promotes oncogenic transformation of

85 to induce CREB phosphorylation, rescued ATM negative cells and restored differentiation.

86 ted the expression of endogenous p21 in KSHV-negative cells and strongly attenuated the cell cycle ar

87 tory concentration of vancomycin enters Gram-negative cells and that this concentration is potentiate

88 act between aggregate-positive and aggregate-negative cells and transfer of Sup35GPI from aggregate-p

89 91-20 cells was 20% higher than that in core-negative cells and was enhanced 3-fold in CYP2E1-express

90 ient in generating neurospheres than are GFP-negative cells and, despite their small number, give ris

91 -positive and -negative (PAF-R-positive and -negative) cells and PAF-R-deficient mice to demonstrate

92 ; corneal epithelium: cK12-positive and MUC1-negative cells), and cell morphologic features (corneal

93 tron 2, was primarily hypersensitive in EPCR-negative cells, and capable of initiating antisense tran

94 lation occurred in both GFP-positive and GFP-negative cells, and the resilencing correlated with a gr

95 inhibited etoposide-induced apoptosis in p53-negative cells, apoptosis was enhanced by Trim39 knockdo

96 UJ-1-positive cells were generated from A2B5-negative cells ( approximately 70%) than from A2B5-posit

97 f cAMP accumulation inside CR3-positive and -negative cells are comparable.

98 Yet, the extent to which individual Nanog-negative cells are differentiated, both from ESCs and fr

99 In contrast to DETCs, these Vgamma5-negative cells are IL-7R(hi)CCR6(hi) retinoic acid-relat

100 Furthermore, CD9-negative cells are less dependent on FDCs for their surv

101 PI in normal cells, whereas PIG-A mutant GPI-negative cells are spared.

102 eversal of the anti-CD3 stop-signal on FoxP3-negative cells at concentrations that had no effect on F

103 tissues exhibiting EMAST contained more MSH3-negative cells (average, 31.5%) than did the tissues not

104 important roles these compounds play in Gram-negative cell biology.

105 eptor alpha (PDGFRalpha)-positive and VEGFR2-negative cells by enabling indirect activation of PDGFRa

106 Moreover, the CLDN4-negative cells can be induced to express CLDN4 through t

107 hical cancer stem cell model because JARID1B-negative cells can become positive and even single melan

108 -1R, externally induced DNA damage in IGF-1R-negative cells caused G1 cell cycle arrest and S phase f

109 ive T cells (CEM and H9), but not in A3G/A3F-negative cells (CEM-SS).

110 reatment with carboplatin enriches for CA125-negative cells, co-treatment with carboplatin and birina

111 terized by the expansion of immature lineage-negative cells, common myeloid progenitors, and granuloc

112 emonstrated enhanced selectivity in receptor-negative cells compared to SAPs and 4-thiazolidinone ami

113 Surprisingly, both Ag-positive and Ag-negative cells continued to divide; because of this cont

114 Here, we show that the negative cell cycle regulator p21(WAF1) gene is up-regul

115 LIN B expression, and an accumulation of the negative cell cycle regulator WEE1 RNA.

116 er a novel role and mechanism for FOXD3 as a negative cell cycle regulator, and have implications for

117 e we report a novel function of ALDH3A1 as a negative cell cycle regulator.

118 Thus, the paradigm that RBR genes are negative cell cycle regulators cannot be considered univ

119 by maintaining limited transcription of the negative cell cycle regulators p16Ink4a and p19Arf from

120 cle and suppresses the expression of several negative cell cycle regulators that are associated with

121 GF-1 that tightly controls both positive and negative cell cycle regulators, and indicate that the PI

122 tion of genes encoding tumor suppressors and negative cell cycle regulators.

123 near complete silencing of Cdkn1c, encoding negative cell-cycle regulator p57-Kip2.

124 protein is a eukaryotic tumor suppressor and negative cell-cycle regulator.

125 protein (betaGBP) molecule, a cytokine and a negative cell-cycle regulator.

126 (ssTNI, betaMHC) mRNA was increased whereas negative cell-cycle regulators (p21, Meis1) were decreas

127 g of PANE1 alleles in mHAg-positive and mHAg-negative cells demonstrates that differential T-cell rec

128 R-positive cells with no activity against FR-negative cells, demonstrating the specificity of redirec

129 both VEGF receptor 2 (VEGFR2)-positive and -negative cells depended on VEGF to endure hypoxia.

130 election of imatinib-resistant DOG1- and KIT-negative cells derived from parental DOG1 and KIT-positi

131 ssing cells, but overexpressing YAP1 in MSLN-negative cells did not induce MSLN expression.

132 cells readily formed spheres, whereas c-Met-negative cells did not.

133 Single cell analysis showed that Nanog-negative cells display substantial and coherent heteroge

134 increase excitation efficacy onto calbindin-negative cells during dopamine inhibition, suggesting th

135 ta-cells as well as in proliferating hormone-negative cells during pancreatogenesis.

136 e model of HIV-1 infection, these coreceptor negative cells engraft and traffic normally, and are pro

137 n after DNA packaging and implicated in Gram-negative cell envelope penetration.

138 key to the mechanical integrity of the Gram-negative cell envelope.

139 cell envelope compared to those with a Gram-negative cell envelope.

140 xidative stress conditions; conversely, Fhit-negative cells escape apoptosis, carrying serious oxidat

141 ths, 21 (9%) patients developed 23 CAs in Ph-negative cells; excluding -Y, this incidence was 5%.

142 tive UM171-treated cells, as opposed to EPCR-negative cells, exhibit robust multilineage repopulation

143 Here, we show the transcriptome of Nanog-negative cells exhibits expression of classes of genes a

144 ed that, for both fusion-positive and fusion-negative cells, exosome miRNA clustered well together an

145 Furthermore, ATM-negative cells failed to differentiate into neuronal-lik

146 In addition, ZAP 70-negative cells failed to exhibit normal protein kinase C

147 All of the independently immortalized K-Ras-negative cells failed to migrate upon the addition of PD

148 uction of hyaluronan receptor CD44 into CD44-negative cells followed by transduction in the presence

149 ually phosphorylated in EBV-positive and EBV-negative cells following interferon treatment.

150 vironment involving both NFATc1 positive and negative cells for prostate tumorigenesis.

151 Lineage-negative cells from mice with OS were transduced with an

152 Cultured CD4 and CD8 double-negative cells from NOD mice exhibited major defects in

153 of SP-Tatm3x in heparan sulfate proteoglycan-negative cells further improves its transduction activit

154 eurons expressing TH and Pitx3, whilst FolR1 negative cells generate non-dopaminergic neurons and gli

155 The resultant CD9-negative cells grow faster than CD9-positive cells due t

156 castration-recurrent PC cells but not for AR-negative cell growth.

157 GFP-negative cells had histone modifications and promoter nu

158 utants in telomerase-positive and telomerase-negative cells have also led us to speculate that the te

159 In Bcl-2-negative cells, high concentrations of anti-CD3 antibody

160 In primary glioma-derived CD133 negative cells, hypoxia was able to induce neurospheres

161 ifying the CD25 mRNA content of positive and negative cells identified by anti-chicken CD25 Ab.

162 CAs occur in Ph-negative cells in a small percentage of patients with ne

163 lations formed from CanAg-positive and CanAg-negative cells in culture and in xenograft tumors in mic

164 r genetic alterations restricted to the HER2-negative cells in each case.

165 ts were found in both ChAT-positive and ChAT-negative cells in MHbV.

166 nt cell-cell fusion but could not infect CD4-negative cells in single-round infections.

167 g proteins are absorbed and degraded by FcRn-negative cells in the distal small intestine (ileum).

168 es in total numbers of NeuN-positive or NeuN-negative cells in the P21 caudate-putamen or frontal cor

169 ucleus is formed by radially migrating Nr4a2-negative cells in the ventral pallium; it is therefore d

170 f functional P-gp from P-gp-positive to P-gp-negative cells in vitro and in vivo.

171 es and enhanced transduction efficacy in CAR-negative cells in vitro.

172 e blocking differentiation of lineage marker-negative cells in vitro.

173 S), with expansion to infection of truly CD4-negative cells in vivo.

174 S GnTI(-) (N-acetylglucosaminyltransferase I-negative) cells in suspension culture and overexpress th

175 addition, expression of hTERT in telomerase-negative cells (including primary and ALT cancer cell li

176 rsely, experimental expression of Brk in Brk-negative cells increased cell survival whereas kinase-in

177 Expression of p210(BCR-ABL) in BCR-ABL negative cells induced transcription of the proximal Hsp

178 ER transgene expression in ER-negative cells inhibited NO-induced upregulation of the

179 Reconstitution of LPA(4) converted LPA(4)-negative cells into a less motile phenotype.

180 hat HMBPP transforms MHC-class II(+) but not negative cells into Vdelta2 expanders.

181 ready discrimination of positive cells from negative cells is achieved.

182 age-specific marker gene expression in Nanog-negative cells is associated with spontaneous differenti

183 Conversely, MDA-MB-231 (estrogen receptor-negative) cells lack detectable miR-200c and E-cadherin

184 nstructs were characterized using an antigen-negative cell line (HT-1080), cell lines positive for ea

185 new estrogen signaling network in an ERalpha-negative cell line and in an original patient-derived xe

186 had no significant effect on the herpesvirus-negative cell line CA46.

187 enerated MCV-infected cell lines and one MCV-negative cell line from MCC tumors.

188 and H838 (higher EpoR expression), the EpoR-negative cell line H2030, and EpoR/EGFP-overexpressing H

189 whereas Adora1 over-expression in an ERalpha-negative cell line induced proliferation.

190 ed retinal cells and an L1-expressing, ALCAM-negative cell line, consistent with an ALCAM-L1 heteroph

191 L) cells, as well as in a cotransfected KSHV-negative cell line.

192 he p53-positive cell line but not in the p53-negative cell line.

193 cancer cell line but not in an isogenic DLC1-negative cell line.

194 ot be reversed by expression of DLC1 in DLC1-negative cell line.

195 estoration in vitro, endogenous Wwox protein-negative cell lines (A549, H460, and H1299) underwent ap

196 ivated human PBMCs and A3G/A3F-positive and -negative cell lines (CEM and CEM-SS, respectively) with

197 CA IX negative cell lines (HCT-116 and MDA-MB-231), as well as

198 MCF-7, HCT-116, and HEK293T) and telomerase-negative cell lines (U2OS and GM847).

199 ophages and its ectopic expression in CD300a-negative cell lines also decreased the engulfment of dea

200 effects were mediated through Vav1, as Vav1-negative cell lines and tumors were largely resistant to

201 dditionally, our cellular data show that HPV-negative cell lines are more dependent on TMEM16A for su

202 amined HCMV entry into two EGFR-positive or -negative cell lines but observed no increase in entry wh

203 urthermore, gene transfer of IL-13Ralpha2 in negative cell lines enhanced invasion, whereas its silen

204 HDAC9 were greatly overexpressed only in BRM-negative cell lines indicating that HDAC9 may be a good

205 introduction of ELF3 expression in claudin7-negative cell lines induced mRNA expression of the claud

206 cted EBV-positive 293 cells, and in some EBV-negative cell lines it can activate the Z promoter in re

207 315I), with minimal toxicity against Bcr-Abl-negative cell lines or normal bone marrow.

208 knockdown, whereas the proliferation of MCV-negative cell lines remained unaffected.

209 uptake of these particles in folate-receptor-negative cell lines such as A549.

210 In contrast, PTEN-negative cell lines tended to be less responsive (4-fold

211 novo FR synthesis in any of a variety of FR-negative cell lines tested.

212 here mRNA from PGE2-G response-positive and -negative cell lines was subjected to transcriptome-wide

213 In both ER alpha-positive and -negative cell lines, both proteasome and Src inhibitors

214 In triple-negative cell lines, RNAi-mediated PLK1 depletion or inh

215 However, EGFR-negative cell lines, such as hematopoietic cells, are kn

216 When overexpressed in CLCA2-negative cell lines, their tumorigenicity and metastasis

217 ncer cell lines, with minimal toxicity in AR-negative cell lines.

218 ration of EBV-positive cells relative to EBV-negative cell lines.

219 ic cancer cell lines but not in IL-13Ralpha2-negative cell lines.

220 ve cancer cell lines but not in IL-13Ralpha2-negative cell lines.

221 -PP Gln was unable to inhibit invasion by ER-negative cell lines.

222 B and CatL in integrin-positive and integrin-negative cell lines.

223 ER alpha t(1/2) was reduced in ER alpha-negative cell lines.

224 s more than 100-fold selective against FGFR2-negative cell lines.

225 an cancer cell line, OVCAR3, but not in apoE-negative cell lines.

226 ion and adhering equally to NRP positive and negative cell lines.

227 ity and this phenotype is enriched in triple-negative cell lines.

228 No effects were seen in HTLV-1-negative cell lines.

229 However, in telomerase-negative cells, low-frequency recombination mechanisms c

230 Since the decreased entry in RhoA dominant-negative cells may be due to inefficient signaling downs

231 data indicate that alpha(5)beta(1)-integrin-negative cells may be refractory to infection by GP pseu

232 hat therapeutic strategies that target CA125-negative cells may be useful in the treatment of HGSC.

233 s are consistent with the concept that Nanog-negative cells may contain subpopulations of both lineag

234 Of the elevated miRNAs in ERalpha-negative cells, miR-221 and miR-222 directly interact wi

235 xpression of CathepsinK was detected in TRAP-negative cells of the inner periosteal layer also expres

236 x, and was subsequently covered by the Nr4a2-negative cells of the insular cortex.

237 In most double-negative cells, one Tcrb allele was recruited to pericen

238 ive human breast cancer arises from an ER/PR-negative cell or from an ER/PR-positive cell that later

239 cells but show little or no activity in CD4-negative cells or against vesicular stomatitis virus-G p

240 sion in AR-positive PCa cells, but not in AR-negative cells or tested AR-positive cells of other line

241 GF receptor alpha-positive, and beta-tubulin-negative cells originating in the SVZ migrated into corp

242 ymal tumor cell invasion, whereas in MT1-MMP-negative cells, palladin overexpression was insufficient

243 wever, recent evidence points towards a Gram-negative cell plan for Planctomycetes, although in-depth

244 d proteomic analyses support an altered Gram-negative cell plan for Planctomycetes, including a defin

245 n, hyper-activation, and modification of CD4-negative cell populations.

246 In contrast, COX-negative cells predominantly harbored mutations in the M

247 Furthermore, in DHF, cytokine-high CD107a-negative cells predominated.

248 ising hormone receptor-positive and receptor-negative cells, presumably ductal and alveolar progenito

249 , in ADAM23-heterotypic environments, ADAM23-negative cells promote tumor growth and metastasis by en

250 Knockdown of the BMP receptor in SMAD4-negative cells reduced their invasive activity in vitro.

251 E7 or E6 oncogenes into human papillomavirus-negative cells rescues the BRCA1 repression of ER-alpha

252 king TSP1 in the medium conditioned by MCT-1-negative cells restored its angiogenic potential to that

253 genous saposins were added to the prosaposin-negative cells, saposin B was the most efficient in rest

254 ntargeted nanoprobe, whereas alpha(v)beta(3)-negative cells showed no enhancement of cell uptake over

255 Ablation of LGI4 and NO in A23-negative cells significantly attenuates A23-positive cel

256 When Syk was transfected into Syk-negative cells (SIHN-011A), chemomigration was enhanced

257 reen fluorescent protein, whereas in ERalpha-negative cells, Smad4 did not reduce the tumor size.

258 Overexpression of SREC-I in SREC-I-negative cells specifically reduces cell-surface levels

259 ngly, the frequency of YOYO-1-positive, CD71-negative cells strongly correlated with parasitemia, def

260 ent in bacterial species that exhibit a Gram-negative cell structure.

261 n in resident CD4(low) cells, as well as CD4-negative cells, such as astrocytes, proposed as a major

262 2a does not affect p53 protein levels in HPV-negative cells, such as HCT116, U2OS, and C33A cells.

263 s of catecholaminergic cells as fluorescence-negative cells, suggesting inappropriate transcription f

264 to coexpress annexin V than equivalent, Fas-negative cells, suggesting that Fas mediates early eryth

265 almost sixfold higher MCT4 levels than CD133-negative cells, suggesting that the stem-like population

266 ntous growth under embedded conditions, less negative cell surface charges and diminished adherence t

267 ZAP 70-negative cells that were reconstituted with active ZAP 7

268 nd, hence, the restriction of Doc to the Tin-negative cells that will form ostia.

269 In telomerase-negative cells, the loss of Rad51 or Brh2 caused acceler

270 ith the reduced virus entry in RhoA dominant-negative cells, these results suggest that activated Rho

271 Birinapant sensitizes CA125-negative cells to carboplatin by mediating degradation o

272 ory group, higher ratios of CD25(high) FoxP3-negative cells to CD25(high) FoxP3-positive cells correl

273 at express MEK1 stimulate adjacent transgene-negative cells to divide and become incorporated into th

274 king of both normal and malignant L-selectin-negative cells to the draining lymph nodes.

275 ddition, we studied the contribution of KLF2-negative cells to the formation and subsequent different

276 blastoma LN18 (PTEN-positive) and A172 (PTEN-negative) cells to Taxol for induction of apoptosis.

277 anges in gene expression in p53-positive or -negative cells treated with WR1065 were examined using c

278 gainst ASNS-positive cell types but not ASNS-negative cell types.

279 in V-positive, 7-amino-actinomycin D (7-AAD)-negative cells upon TA knockdown, activation of caspases

280 by targeting cell wall growth to regions of negative cell wall curvature.

281 TDAG8 was expressed in double-negative cells, was downregulated at the double-positive

282 ring DAC-treated sorted GFP-positive and GFP-negative cells, we found that their methylation levels w

283 s of Trim39 function in p53-positive and p53-negative cells, we have found, surprisingly, that p53-po

284 Whereas HBV-positive and -negative cells were indistinguishable with respect to ce

285 Rare EBV-negative cells were isolated alongside EBV-positive cell

286 ve oligodendrocyte progenitor cells and A2B5-negative cells were isolated and cocultured with resting

287 ecombination when intein-positive and intein-negative cells were mated.

288 , AR-positive yet androgen-independent or AR-negative cells were refractory to androgen influence on

289 Approximately 0.02% of the infected GFP-negative cells were stably converted to GFP positive cel

290 EGFP-negative cells were transduced with rAAV vectors carryin

291 RB1-positive cells but had no effect in RB1-negative cells, which continued to proliferate and expre

292 inc finger nucleases (ZFNs) to generate CCR5-negative cells, which could then give rise to HIV-resist

293 e results show a viability of almost 80% for negative cells while only 50% of the target cells remain

294 a subpopulation of luminal estrogen receptor negative cells with a novel potential role as non-profes

295 s were decreased after infection of APOBEC3G-negative cells with APOBEC3G-containing virions relative

296 ubclones from a single tumor, to compare EBV-negative cells with EBV-positive cells displaying either

297 We also show that treatment of EBV-negative cells with LMP1-exosomes increases migration an

298 The fraction of GPI-negative cells within the CD56(dim) NK cells was markedl

299 criminating between the cancer-positive and -negative cells, without any amplification step, in less

300 nsity in positive cells versus background in negative cells yields a quantitative metric (positive-to