ライフサイエンスコーパス: doubling time

1 oli under moderate growth conditions (67 min doubling time).

2 te blood cell counts, and shorter lymphocyte doubling time.

3 ss than 10 microM retarded growth within one doubling time.

4 , 11q22/17p13 deletion, and short lymphocyte doubling time.

5 py, continued PSA progression, and rapid PSA doubling time.

6 cells for time periods greater than the cell doubling time.

7 ical recurrence as prostate-specific antigen doubling time.

8 mor cell proliferation as determined by cell doubling time.

9 vels in E. coli are constant irrespective of doubling time.

10 ion of FtsZ remains constant irrespective of doubling time.

11 ng structures divided and grew with a normal doubling time.

12 orporated thymidine-3H within one population-doubling time.

13 resulted in cells with a drastically reduced doubling time.

14 ore rapid growth rate with a 5-h decrease in doubling time.

15 nes showing approximately a 50% reduction in doubling time.

16 of metastatic disease, PSA velocity, or PSA doubling time.

17 8 years, similar to the all-cause mortality doubling time.

18 strains, which corresponds with the cellular doubling time.

19 1944 cell lines significantly decreased cell doubling time.

20 -induced DSB and greatly improved population-doubling times.

21 ng six cytokeratins, and inhibited cell line doubling times.

22 d was suppressed for cell types with shorter doubling times.

23 n oscillator in the suprachiasmatic nucleus (doubling time = 0.5-1.3 h).

24 with mice without Treg-cell ablation (tumor doubling time, 16.7 vs 4.9 days, respectively; P = .02).

25 jected compared with untreated tumors (tumor doubling time 3.1 and 10.6 d, respectively; p < 0.01), w

26 gnificant association could be found for PSA doubling time (82.7%, 96.2%, and 90.7% in >6, 4-6, and <

27 th slow rates of disease progression (median doubling time: 84 days, 95% uncertainty range 62-104) an

28 t of control was achieved without population doubling time acceleration.

29 NC cells exhibited a nearly fourfold faster doubling time after populating the branchial arches.

30 display a higher growth fraction and shorter doubling time, along with a shorter interval to generati

31 Differences in endpoint survival and tumor doubling time among the groups were highly significant (

32 We performed volumetric and doubling time analysis on 63 non-small cell lung cancers

33 pproximately 1.5-fold increase in population doubling time and a 2-fold reduction in mitotic index co

34 se in S-phase fraction, a 10-15% decrease in doubling time and a 20% increase in colony formation com

35 cycle defects, including reduced population-doubling time and a delay in cell cycle reentry from qui

36 AR-beta-transfected TE-3 cells had a shorter doubling time and became resistant to RA.

37 rence, there was a tendency toward increased doubling time and decreased percentage of MCM2 in the ce

38 aHP1(Hsbeta) showed a decrease in population doubling time and decreased sensitivity to IR compared t

39 An increase in the cell population doubling time and higher sensitivity to cell killing by

40 s pT58 levels, leading to an increase in the doubling time and impairment of cell cycle progression.

41 s and cell-cycle arrest, elevating the tumor doubling time and increasing mouse survival.

42 s individual-level dynamics-including a long doubling time and low probability of immune recovery-tha

43 nes correlated with functional phenotypes of doubling time and oxidative stress.

44 rage-independent growth, shortens population-doubling time and reduces contact inhibition.

45 herapy is associated with postrecurrence PSA doubling time and with preradiation PSA level only.

46 Between doubling times and (18)F-DOPA PET positivity, no signifi

47 antisense approaches, resulted in prolonged doubling times and decreased anchorage-independent growt

48 osomal HR HPV genomes had shorter population doubling times and formed dysplastic stratified epitheli

49 Additionally, we provide measurements of doubling times and in-vivo metabolic fluxes through the

50 Doubling times and radial growth rates were examined und

51 GF-C expression and COX2 expression, shorter doubling times and reduced expression of angiopoietin 2

52 ty increased for cell types with the longest doubling times and was suppressed for cell types with sh

53 ility to grow in Fe(III) citrate medium with doubling times and yields that were ca. 145% and 70% of

54 ation of simulated aggressive (2-month tumor doubling time) and nonaggressive (18-month tumor doublin

55 ase progression, defined in terms of the PSA doubling time, and "upgrading" at repeat biopsy.

56 imated cell energy consumption by population doubling time, and cell survival and growth by succinate

57 The telomere-telomerase axis, population-doubling time, and insulin-like growth factor-1 receptor

58 ific antigen (PSA) level, postrecurrence PSA doubling time, and positive digital rectal examination (

59 on the DNA copy number, gene location, cell doubling time, and the rates of transcription and degrad

60 tomatic presentation of tumors, tumor volume doubling time, and time between screenings were examined

61 r cell cycle time ( approximately 13 h) than doubling time ( approximately 35 h), suggesting that the

62 n, absolute pre-RT PSA level, and pre-RT PSA doubling time are emerging as important determinants of

63 to 1.51) for Sierra Leone; the corresponding doubling times are 15.7 days (95% CI, 12.9 to 20.3) for

64 alcitonin and carcinoembryonic antigen (CEA) doubling times are currently the most reliable markers f

65 , fraction of proliferating cells, and tumor doubling times are of critical importance for the dynami

66 antigen (PSA) dynamics (PSA velocity and PSA doubling time) are widely advocated as useful prognostic

67 Labeled cells showed normal morphology and doubling time as control cells.

68 The results from doubling time assay suggested that PTPgamma is capable o

69 passaging ability, cycling quiescence, long doubling time, asymmetric division, high metastatic and

70 Population doubling time averaged 27 hours in mCSCs and vCSCs; 5x10

71 The doubling time based on a Poisson regression was 5.5 year

72 Our model makes accurate estimates of doubling times based on an optimized compartment shell p

73 ells renew and proliferate in culture with a doubling time between 3 and 4 days.

74 There was considerable overlap in doubling time between histologic subtypes.

75 showed significantly increasing trends with doubling times between 5.5 and 13 years.

76 ous and endogenous apoE increased population doubling times by 30-50% over a period of 14 days by pro

77 were evaluated using an Alamar Blue reagent, doubling time calculations and quantitative TEM, respect

78 Volume-doubling time can only indicate overdiagnosis and was es

79 ns on population-level characteristics, like doubling time, carrying capacity, and growth rate.

80 degrees C), individual cell lines displayed doubling times consistent with endothelial cells possess

81 tients (n = 26) in whom the on-treatment PSA doubling time could be calculated, the median PSA doubli

82 We determined whether the BCR-ABL1 doubling time could distinguish nonadherence from resist

83 bor null mutations in MELK exhibit wild-type doubling times, cytokinesis, and anchorage-independent g

84 nificantly with WBMTB on (18)F-DOPA PET, but doubling times did not.

85 ind excellent agreement between the observed doubling-time distribution and the predicted universal d

86 a combination of data representing cellular doubling time, DNA content, chromosome number, metacentr

87 MCT-1 has been shown to decrease cell-doubling time, dramatically shortening the duration of G

88 ST PSA nadir (pCox < .0001), the pre-AST PSA doubling time (DT) (pCox = .002), PSA level (P = .0001),

89 Reciprocal of doubling time (DT) (RDT) was calculated.

90 eoperative predictors of a postoperative PSA doubling time (DT) of less than 3 months and more than 1

91 Median PSA doubling time (DT) was 2.5 years for those who underwent

92 Doubling time (DT) was calculated by using the volume an

93 e time to PSA failure, the posttreatment PSA doubling time (DT), and the timing of salvage hormonal t

94 the first and last study to calculate tumor doubling time (DT).

95 The population doubling times (DT) of sham-irradiated cells varied from

96 Doubling times (DT) were divided into three groups: rapi

97 alcitonin and carcinoembryonic antigen (CEA) doubling times (DTs).

98 New data show that prostate-specific antigen doubling time during prostate-specific antigen recurrenc

99 rom Cdk4(R24C/R24C) mice displayed decreased doubling times, escape from replicative senescence, and

100 ession total serum prostate-specific antigen doubling times, failure to respond to salvage local radi

101 led MTHF depended upon a combination of cell doubling time, folate receptor status, S phase percentag

102 A short doubling time for a patient in CP should raise the suspi

103 Median tumor doubling time for controls was 5.5 d (interquartile rang

104 l wall 14000 times in the course of a single doubling time for E. coli.

105 The mitotic index and doubling time for LLCPK-1alpha were not significantly di

106 The corresponding doubling times for BTBPE are about 5 and 7 years in Lake

107 Mean endpoint survival and tumor doubling times for the three RF levels (0, 70 degrees C,

108 in tumor weight, and the extension of tumor-doubling time from 8.5 +/- 1.38 to 12 +/- 1.07 days as c

109 k-transfected cells) included an increase in doubling time (from 36 to 175 h) in the clone in which b

110 2/25) of (18)F-FDG PET-negative patients had doubling times greater than 24 mo (P < 0.001).

111 Winning clones exhibited shorter doubling times, greater maximum culture densities, and a

112 The initial viral doubling time had a median of 0.65 days with an interqua

113 The study of tumor marker doubling times has guided the extent of surgery and lymp

114 illion peptidoglycan strands within a single doubling time (i.e., generation) of E. coli.

115 for in vitro growth correlated directly with doubling time in blood, in the case of B-CLL with Ig H c

116 variable but significant average increase in doubling time in lymphoblastoid cell lines derived from

117 2 STI arms had a significantly longer median doubling time in the period of the initial rise of viral

118 Differences in endpoint survival and tumor doubling time in the six groups were highly significant

119 evidence that calculation of PSA velocity or doubling time in untreated patients provides predictive

120 ET or (18)F-DOPA PET with calcitonin and CEA doubling times in 47 MTC patients.

121 nt/nearly identical increase in the ratio of doubling times in DMDM medium in the presence/absence of

122 st recent literature on volumetry and volume doubling times in lung nodule management, outlining thei

123 Cancer cell doubling times in patient tumors are longer than in cult

124 Despite very different doubling times in vitro, all three establish similar lev

125 The doubling time (in hours) of HCECs from the central area

126 onin and carcinoembryonic antigen (and their doubling times), in addition to comprehensive imaging to

127 Tumor-doubling time increased from 3.5 +/- 0.5 d to 5.2 +/- 1.

128 ing time could be calculated, the median PSA doubling time increased from 8.4 months to 15 months (P

129 t, with a lower-dose inoculum, the bacterial doubling time increased to 56 min and the S. pneumoniae

130 a number of oncogenic properties: decreased doubling times, increased clonogenicity and viability, f

131 The population doubling time is approximately 4 days.

132 lure exceeds 3 years, and post-treatment PSA doubling time is at least 12 months, and who did not hav

133 The sharp change in doubling time is followed by a sharp change in phenotypi

134 Optimal doubling time is obtained by maintaining a sufficiently

135 stage disease or a prostate-specific antigen doubling time less than 12 months) may also receive bene

136 aHR], 1.72; 95% CI, 1.17-2.52; P = .01), PSA doubling time less than 9 months (aHR, 2.06; 95% CI, 1.2

137 d, and tumor number, diameter, growth rates (doubling time), location, presence of metastatic disease

138 lating efficiency, elongated cell population doubling time, lower clonogenic fraction in soft agar, a

139 A failure < 3 years and a post-treatment PSA doubling time < 3 months place a man at increased risk f

140 e-specific antigen [PSA] >/=8.0 mug/L or PSA doubling time </=10.0 months, or both) were enrolled at

141 gen [PSA] failure, PSA nadir >0.5 ng/mL, PSA doubling time <9 months, and interval to PSA failure <30

142 dynamically on the basis of two factors: PSA doubling time (</= 3 v > 3 months) and nodal versus non-

143 aller (<3.0 cm) tumors displayed longer mean doubling times (mean, 927 vs 351 days) than did larger (

144 les, preradiation PSA and postrecurrence PSA doubling time measured before radiation were the only st

145 ize clones using whole-genome sequencing and doubling time measurements.

146 pes examined include ODC enzymatic activity, doubling time, morphological change, anchorage dependent

147 Long doubling times observed with mutations in CP allow time

148 Longer doubling times occurred for patients with mutations who

149 Short doubling times occurred with blast crisis (median, 9.0 d

150 rate of any known organism, with a reported doubling time of <10 min.

151 the sole terminal electron acceptor, with a doubling time of 1 day.

152 from which biosulfur showed fastest growth (doubling time of 1.9 days), followed by colloidal, chemi

153 41% (95% CI, 31% to 51%) who also had a PSA doubling time of 10 months or less or poorly differentia

154 replication, with an estimated S. pneumoniae doubling time of 16 min.

155 hase fraction by flow cytometry and a faster doubling time of 24-36 h compared with 72 h for parental

156 rred over a median of 7 weeks, with a median doubling time of 3 days.

157 , have a high self-renewal capability with a doubling time of 46 h.

158 as characterised by fast exponential growth (doubling time of 5-7 days) and fast spatial expansion (4

159 n receptor, and an unusually rapid growth (a doubling time of 6.5 days) for prostate cancer xenograft

160 Treated animals gave a tumor-doubling time of 9 +/- 4 days, which is a 300% increase

161 d a maximum growth rate of 0.078 h(-1) and a doubling time of 9 h, and the DeltaG of the reaction ran

162 g thymic glucose metabolism, with a mean SUV doubling time of 9.0 wk (range, 6.0-17.5 wk).

163 f pharmaceuticals in sediment cores showed a doubling time of 9.2 years.

164 Amplification occurs with a doubling time of about 1 hour and can be continued indef

165 cking 46 N-terminal amino acids, which had a doubling time of about 3 h.

166 ion for Biomedical Research, we estimate the doubling time of adult mortality rate as 4.8 years.

167 replicates rapidly in its human host with a doubling time of approximately 1 day.

168 nd from 10 degrees C to 35 degrees C, with a doubling time of approximately 15 h at pH 6.3 and 22 deg

169 ll line, ID6, had a normal karyotype, a cell doubling time of approximately 17 h, and has been mainta

170 ared similar morphology and had a population doubling time of approximately 2 days.

171 of genome sequencing was established, with a doubling time of approximately 20 months for bacteria an

172 ties (approximately 1 x 10(8) per ml) with a doubling time of approximately 24 h.

173 s in a serum-free, defined medium and with a doubling time of approximately 36 h.

174 ly under photoautotrophic conditions, with a doubling time of approximately 40 h, and had severely re

175 cells divide very rapidly with an estimated doubling time of approximately 6 h.

176 cells can be expanded without feeders with a doubling time of around 24 h.

177 The doubling time of CD3-activated PBTs was 1 day, while tha

178 also inhibits colony formation and increases doubling time of colon tumor cells.

179 For T > 30 degrees C, the doubling time of E. coli increases exponentially with pr

180 The doubling time of ENF-resistant viruses was highly correl

181 study was a prostate-specific antigen (PSA) doubling time of less than 12 mo after initial treatment

182 ffered for a prostate-specific antigen (PSA) doubling time of less than 3 years, Gleason score progre

183 ave grown, and 8.3% (66 of 794) had a volume doubling time of less than 400 days.

184 ited to men with a prostate-specific antigen doubling time of less than 6 months and remained after a

185 l among men with a prostate-specific antigen doubling time of less than 6 months, independent of othe

186 We have observed retarded growth and longer doubling time of MBP-1 knockdown PC3 cells as compared w

187 The doubling time of non-small lung cell cancer lines, which

188 cells that divide less than once every year (doubling time of over 450 days).

189 cage readily infect each other, and that the doubling time of P. carinii in vivo is approximately 3 d

190 The doubling time of the menB26 mutant cells, but not the me

191 Although the doubling time of the mutant was identical to that of the

192 dependence of the solutions is scaled to the doubling time of the prostate specific antigen (PSADT) b

193 The doubling time of the slowly cycling population was estim

194 The doubling time of this strain with increasing doxycycline

195 The doubling time of tumours in mice treated with MLN0518 wa

196 y the low transformation efficiency and long doubling time of yeast relative to bacteria.

197 h is the case for this system and provides a doubling time of ~20 min.

198 slow-cycling melanoma cells that cycle with doubling times of >4 weeks within the rapidly proliferat

199 tic growth coalescent models reveal epidemic doubling times of 0.86 and 1.12 years for the US and Car

200 over time at the rural and remote sites with doubling times of 2.2 and 3.7 years, respectively.

201 y colloidal, chemical and sublimated sulfur (doubling times of 2.2, 2.5, and 3.6 days, respectively).

202 populations in Tanzania and in Kenya showed doubling times of 3.5 and 3.8 years, respectively.

203 Eleven (22%) of 50 tumors had doubling times of 465 days or more.

204 or phase concentrations were increasing with doubling times of 5-10 years at Sturgeon Point, Sleeping

205 rapidly over the first 4 h of infection with doubling times of approximately 15-28 min.

206 Doubling times of cells from each area were compared.

207 of cell cycle progression revealed shortened doubling times of Hyal1-expressing cells.

208 We calculate the distribution of doubling times of such optimally scheduled self-replicat

209 first few hours of growth and lengthened the doubling times of the populations in strains with an ind

210 n were rapidly increasing at most sites with doubling times of ~2 years.

211 lues are equivalent to average intermitotic (doubling) times of 15 and 48 d, respectively.

212 hP) showed an apparent temporal trend with a doubling-time of 11 months (p = 0.044).

213 d correlation of specific microRNAs with the doubling-time of cells or their radiation sensitivity.

214 st, including an approximately 12 h delay in doubling time on exposure to 25 mg/L CdTe QD ( approxima

215 t active mutant ribosomes are robust, with a doubling time only 14% longer than wild-type.

216 of alpha (32)P-dTTP relative to either cell doubling time or alpha (32)P-dCTP incorporation was incr

217 tic disease (rapid prostate-specific antigen doubling time or velocity) but otherwise is not suggeste

218 g exponential growth with a decreased volume doubling time, or 2) Gompertz-repopulation using the gra

219 sm and not simply to increased cell density, doubling time, or other nonspecific effects.

220 aging, such as progressive changes in size, doubling time, or sibling health.

221 prostatectomy Gleason grade (P < .001), PSA doubling time (P < .001), surgical margins (P < .001), a

222 with stage of disease (P < .001), lymphocyte doubling time (P = .01), V(H) gene mutation status (P <

223 fossa, prebiopsy PSA, and postrecurrence PSA doubling time predict which patients will have biopsy-pr

224 erum deprivation after which cell population doubling time, proliferation fraction, and cell cycle pe

225 te-specific antigen (PSA), PSA velocity, PSA doubling time, proPSA, PCA3, TMPRSS2-ERG.

226 to metastasis, including post-treatment PSA doubling time (PSA-DT), Gleason score, and interval to P

227 In a multivariate analysis, PSA doubling time (PSA-DT; P < .001), the clinical T stage (

228 fore the BS (trigger PSA), PSA kinetics (PSA doubling time, PSA slope, and PSA velocity), and time fr

229 cific antigen (PSA) >/= 8.0 ng/mL and/or PSA doubling time (PSADT) </= 10.0 months.

230 gins (HR, 1.9; 95% CI, 1.4-2.5; P<.001), PSA doubling time (PSADT) of 10 months or less (HR, 1.7; 95%

231 whether pretreatment PSA velocity (PSAV) or doubling time (PSADT) predicted outcome in men undergoin

232 that postoperative prostate-specific antigen doubling time (PSADT) was associated with risk of prosta

233 At multivariate analysis, PSA, PSA doubling time (PSAdt), and ongoing ADT were significant

234 apse and 75% (P < 0.001) cases for short PSA doubling time (PSADT, <4 months).

235 tivity correlated positively with population doubling time (R(2) = 0.91 for PAC, 0.76 for QTH, 0.68 f

236 on influences telomere stability, population doubling time, radioresistance, and tumorigenicity in a

237 ither grown under a variety of conditions at doubling times ranging from 0.1 to 2.2 doublings per hou

238 th varying depleted levels of YlqF, yielding doubling times ranging from 38 min to 150 min, all displ

239 rom metabolically synchronized cultures with doubling times ranging from 5 to 14 h.

240 ) size control is effected by changes in the doubling time, rather than in the single-cell elongation

241 These cell lines showed elongated cell doubling time, reduced anchorage-independent growth in s

242 /- 4 days, which is a 300% increase in tumor-doubling time relative to the 3 +/- 2 days for untreated

243 ecreased EGFR expression and increased tumor doubling time, relative to controls receiving EGFR siRNA

244 The doubling time revealed major differences in kinetics acc

245 nkov) telescopes, revealing variability with doubling time scales faster than 4.8 min.

246 MCT-1), that has been shown to decrease cell-doubling time, shorten the duration of G(1) transit time

247 ith glucose under low light conditions, with doubling times similar to that of the wild type, but the

248 pecific cell type used and on its population-doubling times so that the required numbers of cells are

249 and may be associated with an increased PSA doubling time suggests that a multi-institutional phase

250 in a chemically defined medium at fast mass doubling time (t(d) = 1.8 h) and slow (t(d) = 11 h) grow

251 higher numbers when cultured at a cell mass doubling time (t(d)) of 1.8 h than at a slower t(d) of 1

252 erotype, grown in a chemostat at a cell mass-doubling time (t(d)) of 1.8 h with oxygen invaded human

253 ing permits the calculation of the potential doubling time (T(pot)) of the population, plus the durat

254 of a biphasic increase, a rapid slope (mean doubling time [t(2)] = 0.5 days) followed by a slower sl

255 When the doubling time (Td) is shorter than the duration of chrom

256 ment the growth kinetics of CSCs, population-doubling time, telomere length, telomerase activity, and

257 gly, the J-lo1.3 cells had a 1.2-fold faster doubling time than did the Jn.9 cells.

258 cells at the old pole attractor had a longer doubling time than ones at the new pole attractor; and (

259 PM II and PM IV/I disruptions have longer doubling times than the 3D7 parental line in rich RPMI m

260 wth from glucose is feasible up to a minimum doubling time that is proportional to the OxPhos burden

261 o changes in growth, cell-cycle phasing, and doubling times that were elicited by overexpression.

262 iscA mutants grew photoautotrophically with doubling times that were similar to the wild type under

263 emi-automatically measured volume and volume-doubling time; that national quality assurance boards sh

264 stage of disease at presentation, lymphocyte doubling time, time to first treatment, or progression-f

265 erefore exists for prostate-specific antigen doubling time to be accepted as a trial endpoint, which

266 re-generated a similar strain and found the doubling time to be twice that of normal cells.

267 sters transmit most of the response of yeast doubling time to galactose; one contains mainly galactos

268 This mutant had comparable doubling times to wild type (WT) in continuous-light-gro

269 is (and other pathogens with relatively long doubling times) to maintain continuous inhibition of ant

270 ate is too slow to account for some observed doubling-time-to-incubation-time ratios inferred from da

271 en varying severity of cirrhosis, age, tumor doubling time, tumor growth pattern, blood type, regiona

272 ling time) and nonaggressive (18-month tumor doubling time) tumors as early as 7.2 months and 8.9 yea

273 ecreased colony formation 75%, increased the doubling time twofold, and arrested H1299 cells in G1.

274 graphy (LDCT) screening, expressed as volume-doubling time (VDT), may help to distinguish aggressive

275 e assessed for morphologic change and volume doubling time (VDT), which was calculated by using a mod

276 With the perimeter method, median doubling time was 181 days, with a very wide range.

277 Cell-doubling time was 48 to 72 hours, and cells have been ex

278 APFV doubling time was 6.31 weeks.

279 The mean doubling time was 856 days for diameter and 285 days for

280 By using these volumes, tumor doubling time was determined for each patient.

281 When the doubling time was increased by growing cells at a lower

282 ded on the measurement interval, whereas the doubling time was independent of the interval.

283 Overall, the prostate-specific antigen (PSA) doubling time was observed to increase from a median 6.5

284 rch 2007 in which a PSA dynamic (velocity or doubling time) was calculated in patients before definit

285 of treatments on endpoint survival and tumor doubling time were analyzed by means of the Kaplan-Meier

286 Changes in cell number and doubling time were insignificant, but cultures exhibited

287 ree MMAE, mutation of cancer genes, and cell doubling time were poorly correlated with in vitro activ

288 In vitro doubling times were also dramatically reduced, as was th

289 Doubling times were available for 38 of 40 patients unde

290 Whereas these doubling times were consistently short and indicated rap

291 Cell population doubling times were determined and correlated with antio

292 earance half-lives and bacterial replication doubling times were estimated using a mathematical model

293 Doubling times were less than 24 mo in 77% (n = 10/13) o

294 The effects on cell doubling times were paralleled by effects on tumorigenic

295 Predicted short and long doubling times were validated on an independent cohort m

296 bstitutions had the same effect on bacterial doubling time when measured at 20 degrees .

297 tcompeted the wild type and exhibited faster doubling times when grown in mucus and on individual com

298 nt recovery of ATPB P:M, ATPase activity and doubling time, whereas Zn and desferrioxamine extended t

299 These cells also exhibited longer population doubling times which did not arise through reduced proli

300 lated into a 2-3-fold increase in tumor cell doubling time without increased apoptosis.