ライフサイエンスコーパス: hyperproliferative

1 tes and lymphoma cells from MTA1-TG mice are hyperproliferative.

2 llicular proliferation, the epidermis became hyperproliferative.

3 AR+/+ cells, uPAR-/- kidney fibroblasts were hyperproliferative.

4 mmary epithelial cells were disregulated and hyperproliferative.

5 Hyperproliferative ACF had significantly increased mRNA

6 In hyperproliferative ACF, 44% possessed significant increa

7 COX-2 mRNA, the protein was not increased in hyperproliferative ACF.

8 Keratin 6 is a marker of hyperproliferative, activated keratinocytes, found in wo

9 that T(reg) from NIK-deficient mice display hyperproliferative activities upon GITR stimulation thro

10 These data suggest that epidermal hyperproliferative activity is accompanied by the upregu

11 This CD62(low) subset is responsible for the hyperproliferative activity upon GITR stimulation.

12 me a critical role of NF-kappaB in mediating hyperproliferative affects of PG on colonic crypts of Fa

13 However, the reentry of hyperproliferative alphaB-/- cells into S phase and mito

14 of chromosomes 1 and 9 demonstrated that the hyperproliferative alphaB-/- cells were 30% diploid and

15 of genomic instability was obtained when the hyperproliferative alphaB-/- cells were labeled with ant

16 ack of mutations in the p53 coding region of hyperproliferative alphaB-/- cells.

17 We now demonstrate that the hyperproliferative alphaB-/- lens epithelial cells under

18 Examination of the hyperproliferative alphaB-/- mitotic profiles revealed t

19 Hyperproliferative alphaB-crystallin-/- cells were shown

20 ted a critical role of NFkappaB in mediating hyperproliferative and anti-apoptotic effects of progast

21 muscle cells (PASMCs) from PAH patients are hyperproliferative and apoptosis-resistant and demonstra

22 monary arterial hypertension (IPAH) involves hyperproliferative and apoptosis-resistant pulmonary art

23 AnxA2 might therefore mediate the hyperproliferative and cocarcinogenic effects of progast

24 SMCs in elastin mutants, and these SMCs are hyperproliferative and dedifferentiated.

25 Similarly, formation of hyperproliferative and disorganized mammary acini induce

26 PASMCs from monocrotaline rats are hyperproliferative and display normoxic activation of hy

27 In aging men, the prostate gland becomes hyperproliferative and displays a propensity toward carc

28 ) keratinocytes expressing oncogenic RAS are hyperproliferative and fail to up-regulate proinflammato

29 neonatal megakaryocyte (MK) progenitors are hyperproliferative and give rise to MKs smaller and of l

30 ed therapy is feasible and may be useful for hyperproliferative and inflamed skin diseases.

31 cinomas is largely through the creation of a hyperproliferative and inflammatory niche that facilitat

32 Psoriasis is a chronic hyperproliferative and inflammatory skin disease caused

33 s strongly upregulated in human psoriasis, a hyperproliferative and inflammatory skin disease.

34 We show that these hyperproliferative and invasive Drosophila phenotypes ar

35 milar in Zbtb7b mutant mice, these cells are hyperproliferative and most lack CD4 and instead express

36 Null epidermis is hyperproliferative and overexpresses keratins 6 and 16,

37 the recovery period the progenitor cells are hyperproliferative and potentially more radiosensitive)

38 T cells from untreated Sphk2(-/-) mice were hyperproliferative and produced more IFN-gamma than did

39 Instead, their T cells were hyperproliferative and relatively, but not completely, r

40 and ASM cells from patients with asthma are hyperproliferative and release more IL-6 and CXCL8.

41 signaling, Smad2/3-deficient podocytes were hyperproliferative and resistant to TGF-beta-induced gro

42 Thus, ST14 hypomorphic mice developed hyperproliferative and retention ichthyosis with impaire

43 Golli-deficient T cells were hyperproliferative and showed enhanced calcium entry upo

44 (-/-) mammary lesions contain cells that are hyperproliferative and stain positively with nucleolar (

45 CD43(-/-) T cells are hyperproliferative and the cytoplasmic tail of CD43 has

46 fic deletion of Pten in mice causes multiple hyperproliferative and tumor lesions that strikingly res

47 Ikkalpha(-/-) mice present with a hyperproliferative and undifferentiated epidermis charac

48 elective antibody rendered endothelial cells hyperproliferative, and caused defective cell fate speci

49 res derived from LMP2A-expressing cells were hyperproliferative, and epithelial differentiation was i

50 ultured from PRKO mouse aortae were markedly hyperproliferative, and their growth was not affected by

51 Hyperproliferative apoptosis-resistant cells were also g

52 ave previously demonstrated the existence of hyperproliferative, apoptosis-resistant, proinflammatory

53 Because all lesions are hyperproliferative, are associated with inflammation, an

54 gamma-secretase inhibitor (GSI) rescued the hyperproliferative baseline phenotype in the Mtgr1(-/-)

55 Additionally, loss of Dab2 protein occurs in hyperproliferative, but histological benign ovarian epit

56 Px44-TRAIL caused apoptosis of the hyperproliferative, but not differentiating, cultured ke

57 This contributes to the hyperproliferative capacity of T cells from c-FLIP(L)-tr

58 fect of reconstituting CD43 mutants into the hyperproliferative CD43(-/-) T cells.

59 35 samples revealed the presence of foci of hyperproliferative cells in the bronchiolar epithelium,

60 become activated: they turn into migratory, hyperproliferative cells that produce and secrete extrac

61 hway and that the dead cells are replaced by hyperproliferative cells, leading to epidermal hyperplas

62 few stratified foci/microadenomas containing hyperproliferative cells, resembling precursors of papil

63 l tumor suppressor mechanism for eliminating hyperproliferative cells.

64 hether inflammatory events occur pre or post hyperproliferative changes.

65 ived from alphaB-crystallin-/- mice produced hyperproliferative clones at a frequency of 7.6 x 10(-2)

66 d with cytomegalovirus (CMV) infection and a hyperproliferative CMV-specific T-cell response.

67 ollicular epidermis and sebaceous glands are hyperproliferative, coincident with expanded nuclear Yap

68 d only in keratinocytes and the keratinocyte hyperproliferative component of the TGFbeta1 -/- phenoty

69 t targets of Nrf2, which are activated under hyperproliferative conditions in the liver.

70 However, many squamous hyperproliferative conditions, including HPV-induced war

71 proliferation by triggering cell death under hyperproliferative conditions.

72 e ARF tumor suppressor is a potent sensor of hyperproliferative cues emanating from oncogenic signali

73 Notably, the hyperproliferative Cxcr4(-/-) HSCs are able to maintain

74 CYP4F expression is up-regulated in situ in hyperproliferative dermatoses-an innate mechanism to rep

75 ch as anemia, patients have elevated risk of hyperproliferative disease (cancer) by midlife.

76 and low-risk HPVs (e.g., HPV-6) cause benign hyperproliferative disease.

77 S100A7 is highly expressed in epidermal hyperproliferative disease; however, its function is not

78 d as important drug targets for treatment of hyperproliferative diseases and inflammation.

79 tor (EGFR) has frequently been implicated in hyperproliferative diseases of renal tubule epithelia.

80 unt for their beneficial effects in treating hyperproliferative diseases such as psoriasis, actinic k

81 o mTOR activation that plays a major role in hyperproliferative diseases, in some cases rapamycin doe

82 TIG3 level is reduced in hyperproliferative diseases, including psoriasis and ski

83 anism of retinoid action in the treatment of hyperproliferative diseases, we used a long-range differ

84 (ROS) and may underlie certain therapies for hyperproliferative diseases.

85 e successful treatment of a variety of human hyperproliferative diseases.

86 Surprisingly, rather than a hyperproliferative disorder expected from the loss of a

87 used to diagnose lymphangioleiomyomatosis, a hyperproliferative disorder of lung smooth muscle cells

88 However, in epidermal hyperproliferative disorders and tumors, integrins are a

89 or 1alpha,25-dihydroxyvitamin D(3)) to treat hyperproliferative disorders is hampered by calcemic eff

90 However, in certain hyperproliferative disorders of the skin, including psor

91 gastrointestinal stromal tumors (GISTs) are hyperproliferative disorders of the stomach caused by dy

92 porine also is associated with a spectrum of hyperproliferative disorders ranging from reactive lymph

93 oint that can be therapeutically targeted in hyperproliferative disorders such as PAH.

94 ue new approach for the topical treatment of hyperproliferative disorders such as psoriasis and skin

95 ribozymes have potential as therapeutics for hyperproliferative disorders such as restenosis and canc

96 ation of MEF cultures in vitro and, in vivo, hyperproliferative disorders that progress to cancer.

97 eful for developmental studies, for treating hyperproliferative disorders, and for developing animal

98 eases their susceptibility to autoimmune and hyperproliferative disorders, including cancer.

99 In contrast, in other hyperproliferative disorders, such as basal cell carcino

100 S100A7 is markedly increased in epidermal hyperproliferative disorders.

101 ed antitumor drug, also for the treatment of hyperproliferative disorders.

102 oth RB(-/-) and RB(+/+) tumors as well as in hyperproliferative disorders.

103 lymph node T cells from PKR:(-/-) mice were hyperproliferative during Con A-mediated stimulation.

104 mors present without an obvious premalignant hyperproliferative dysplastic lesion.

105 The hyperproliferative ECs of human pulmonary arterial hyper

106 both necessary and sufficient to mediate the hyperproliferative effect of a gain-of-function mutation

107 eta/NFkappaB pathway, may be integral to the hyperproliferative effects of progastrin on proximal col

108 d formation of plexiform lesions composed of hyperproliferative endothelial and vascular smooth-muscl

109 lar growth in keratinocytes, carcinomas, and hyperproliferative epidermal disorders, including psoria

110 der psoriasis vulgaris is characterized by a hyperproliferative epidermis and aberrant immune activit

111 K5 Myc transgenic mice have hyperplastic and hyperproliferative epidermis and develop spontaneous tum

112 liferating epidermis, we produced a model of hyperproliferative epidermis by topical application of d

113 The hyperproliferative epidermis from the affected regions e

114 e and Wy-14,643, activators of PPARalpha, on hyperproliferative epidermis in hairless mice, induced e

115 ome and popliteal pterygium syndrome, have a hyperproliferative epidermis that fails to undergo termi

116 In hyperproliferative epidermis there was decreased express

117 The hyperproliferative epidermis was characterized by an inc

118 Finally, treatment of hyperproliferative epidermis with oxysterols restored ep

119 ealing, prolonged secretion of chemokines, a hyperproliferative epidermis, and neutrophil infiltratio

120 with wild-type littermates consistent with a hyperproliferative epidermis.

121 with a lentiviral miR vector, resulted in a hyperproliferative epidermis.

122 and are lined by abnormally functioning and hyperproliferative epithelial cells.

123 rapy was associated with a more well defined hyperproliferative epithelial region, higher cell densit

124 e as a consequence of persistent exposure of hyperproliferative epithelial stem cells to an inflammat

125 Similarly, in the hyperproliferative epithelium of regenerating murine ski

126 DeltaK5-M2SMO mouse epidermis is hyperproliferative, ex presses BCC protein markers and g

127 types: dysplastic sessile ear papillomas and hyperproliferative follicular/interfollicular chest dysp

128 Development of these hyperproliferative gammadelta T cells was not dependent

129 These data point to hyperproliferative glial progenitors as the source of th

130 cation mutants from these patients transduce hyperproliferative growth responses.

131 t often transition from hypoproliferative to hyperproliferative growth.

132 kening of skin after treatment, illustrating hyperproliferative growth.

133 associated with pigmented melanocytes in the hyperproliferative hair follicles in the Tyr-MIP-2 trans

134 72 show enhanced Ca(2+) mobilization and are hyperproliferative in response to BCR ligation.

135 Unexpectedly, cells expressing Y559F were hyperproliferative in response to CSF-1.

136 s expressing mutant human (h)IL-4Ralpha were hyperproliferative in response to IL-4 compared with cel

137 verexpressing wild type SHIP are found to be hyperproliferative in response to IL-4 in comparison to

138 PTEN-deficient B cells were hyperproliferative in response to mitogenic stimuli, and

139 f B cell activation, as CD72-/- B cells were hyperproliferative in response to various stimuli and sh

140 keratinocytes grown without TGF-beta 1 were hyperproliferative in response to wounding, and re-epith

141 tudy that murine Treg are prone to death but hyperproliferative in vitro and in vivo, which is differ

142 ferentiated with interleukin-12 present, are hyperproliferative in vitro, compared with CTLA-4(+/+)Tc

143 Cav-1-/- mammary epithelia were hyperproliferative in vivo, with dramatic increases in t

144 not CD44(low) T cells, are hyperreactive and hyperproliferative in vivo.

145 role of alpha(E)beta(7) in a murine model of hyperproliferative inflammatory skin disorders that is i

146 res in common with human psoriasis and other hyperproliferative inflammatory skin disorders.

147 al role for SRF as the master regulator of a hyperproliferative, inflammatory phenotype accompanied b

148 at has been shown to play a role in numerous hyperproliferative/inflammatory diseases.

149 kin epidermis systematically transforms to a hyperproliferative, invasive tissue replete with inflamm

150 nic inflammatory dermatosis characterized by hyperproliferative keratinocytes (KC).

151 lays an epidermal phenotype characterized by hyperproliferative keratinocytes and undifferentiated ep

152 ctivated lymphocytes and causes apoptosis of hyperproliferative keratinocytes, features of various sk

153 To determine whether a hyperproliferative (Koebner) reaction could be induced,

154 These hyperproliferative lesions appeared to progress through

155 ta-catenin led to the formation of localized hyperproliferative lesions by 3 months, which did not pr

156 All SRF-VP16iHep mice develop hyperproliferative liver nodules that progresses to leth

157 nd in epithelial layers of dilated ducts and hyperproliferative lobular regions in the mammary glands

158 Hyperproliferative mammary epithelia contained increased

159 y stem cells resulted in the regeneration of hyperproliferative mammary glands in vivo.

160 reepithelialization of skin wounds to become hyperproliferative, migratory, and invasive.

161 espond to injury by becoming activated, i.e. hyperproliferative, migratory, and proinflammatory.

162 or no difference in JNK and ERK activity in hyperproliferative mucosa from DMH-treated animals compa

163 ic factors, consistent with the inflammatory hyperproliferative nature of KS lesions.

164 therapeutic strategy has been to target the hyperproliferative nature of the disease.

165 let cell carcinomas develop from multifocal, hyperproliferative nodules that show the histological ha

166 ed from these mice became hypermigratory and hyperproliferative on overexpression of CTGF.

167 ent checkpoint that safeguards cells against hyperproliferative, oncogenic signals.

168 actor-related protein-8 (MRP-8), a marker of hyperproliferative or abnormal keratinocyte differentiat

169 se subunits could be beneficial for treating hyperproliferative or fibrogenic diseases of the skin.

170 enzoic acid) porphyrin (MnTBAP) reverses the hyperproliferative PAH phenotype.

171 ulmonary hypertension through suppression of hyperproliferative pathways, including STAT3-mediated si

172 ol cells) whereas the surviving cells became hyperproliferative (PCNA positive).

173 At the protein level, 46% of ACF were hyperproliferative (PCNA, 3.2 +/- 1.2-fold).

174 tutive activation of oncoprotein Stat3 and a hyperproliferative phenotype characterized by increased

175 Resolution of the hyperproliferative phenotype correlated with reduced Fyn

176 This ACA11-driven hyperproliferative phenotype depended on increased ROS l

177 een documented, the molecular basis for this hyperproliferative phenotype has not been fully characte

178 asthma that contributes to its secretory and hyperproliferative phenotype in asthma, and which may pl

179 Here, the mechanism underlying the hyperproliferative phenotype in RPE was investigated.

180 BrdU labeling similarly failed to identify a hyperproliferative phenotype in T cells lacking IL-16.

181 l mononuclear cells recapitulated the B-cell hyperproliferative phenotype in vitro.

182 the TGFbeta1 transgene, suggesting that the hyperproliferative phenotype may result in part from dev

183 ession increased apoptosis and abrogated the hyperproliferative phenotype of blood-outgrowth ECs from

184 E cells, providing a molecular basis for the hyperproliferative phenotype of Hfe(-/-) and Hjv(-/-) RP

185 ologic activation of Trpv4 might reverse the hyperproliferative phenotype of PCK cholangiocytes.

186 NAs are consistent with the inflammatory and hyperproliferative phenotype of psoriatic lesions.

187 ed with mCTLA4Ig reverses the activation and hyperproliferative phenotype of the CTLA-4-deficient T c

188 ing mutants of Rac1, RhoA, or Cdc42 caused a hyperproliferative phenotype of the p19Arf(-/-) and p53(

189 The hyperproliferative phenotype of these transgenic mice wa

190 ll-differentiated epidermal layer, exhibit a hyperproliferative phenotype similar to wounded native s

191 expression of keratin 6 associated with the hyperproliferative phenotype was observed in transgenic

192 CR-stimulated Abcg1(-/-) T cells rescues the hyperproliferative phenotype.

193 ion by the d715 G-CSFR may contribute to its hyperproliferative phenotype.

194 /Srcasm transgenic mice did not manifest the hyperproliferative phenotype.

195 osphorylatable Srcasm mutant, maintained the hyperproliferative phenotype.

196 t outflow tract explant cultures rescued the hyperproliferative phenotype.

197 d PCNA overexpression, consistent with their hyperproliferative phenotype.

198 valves, providing a molecular basis for the hyperproliferative phenotype.

199 orescein isothiocyanate-albumin; and (iii) a hyperproliferative phenotype.

200 testis, pancreas, kidney, and adrenal gland, hyperproliferative phenotypes associated with p18 loss w

201 e retinoblastoma-dependent pathway, yielding hyperproliferative phenotypes in pupae and adult flies.

202 ll proliferation, it is not required for the hyperproliferative pituitary phenotype caused by p19 los

203 istrafficked EREG form significantly larger, hyperproliferative, poorly differentiated, and locally i

204 ependent elevation of Mmp1 expression, and a hyperproliferative population lacking elevated JNK signa

205 CD4 T cells from Apc(Min/+) mice showed hyperproliferative potential in vitro and in vivo and in

206 Although this hyperproliferative process has been proposed to represen

207 ased chimeras to recipient nude mice produce hyperproliferative psoriasiform epidermal keratinocytes

208 Hyperproliferative pulmonary vascular fibroblasts isolat

209 formation, starting with rapid but transient hyperproliferative reactivation, followed by a long peri

210 flammatory responses and ultraviolet-induced hyperproliferative rebound.

211 tate tissue that was less differentiated and hyperproliferative relative to WT littermates.

212 The hyperproliferative response can be reversed by reintrodu

213 Mice deficient for the VDR display a hyperproliferative response in the hair follicle and epi

214 reversed the potentially tumor-predisposing hyperproliferative response of BLNK(-/-) pre-B cells to

215 or deficiency of SHP-1 activity results in a hyperproliferative response of myelomonocytic cell popul

216 autoreactive B cells lacking CD11b exhibit a hyperproliferative response to B cell receptor (BCR) cro

217 Despite this evidence for a hyperproliferative response to G-CSF, no cases of AML ha

218 GF-I stimulation of VSMC proliferation and a hyperproliferative response to vascular injury.

219 This hyperproliferative response was due, at least in part, t

220 to the stratum corneum elicits an epidermal hyperproliferative response, a pathogenic feature in man

221 ry low minimal erythemal dose and a dramatic hyperproliferative response.

222 tained matrix adhesion and provoked a strong hyperproliferative response.

223 atin 14, which reflect the antimicrobial and hyperproliferative responses of keratinocytes.

224 attenuated induction of Klf5 expression, and hyperproliferative responses to C rodentium were reduced

225 se mutations affect one allele and result in hyperproliferative responses to G-CSF, presumably throug

226 on of the endogenous phosphatase and induces hyperproliferative responses to interleukin-3 (IL-3) and

227 and seborrheic dermatitis (D/SD) are common hyperproliferative scalp disorders with a similar etiolo

228 Palpha(-/-) fetal liver (FL) progenitors are hyperproliferative, show decreased differentiation poten

229 t excessive telomerase activity may act as a hyperproliferative signal in cells and induce a senescen

230 DNA damage and/or hyperproliferative signals activate the wild-type p53 tu

231 induced in response to potentially oncogenic hyperproliferative signals and activates p53 by interfer

232 ropose that nucleolin, like ARF, responds to hyperproliferative signals by upregulation of p53 throug

233 m of nucleophosmin induction and showed that hyperproliferative signals emanating from oncogenic H-Ra

234 r limits ribosome biogenesis and responds to hyperproliferative signals to activate the p53 checkpoin

235 In response to hyperproliferative signals, ARF is upregulated, resultin

236 rucial component of the cellular response to hyperproliferative signals, including oncogene activatio

237 In response to hyperproliferative signals, p14(Arf) stabilizes p53 by b

238 ut is induced by high thresholds of aberrant hyperproliferative signals, thereby activating p53 in in

239 limits cell cycle progression in response to hyperproliferative signals.

240 Most of these hyperproliferative skin changes improve when a MEK inhib

241 a, with the main toxicity being a variety of hyperproliferative skin conditions due to paradoxical ac

242 elafin and SLPI, has been related to several hyperproliferative skin conditions.

243 ye discrete epidermal hyperplasia (WEH) is a hyperproliferative skin disease that is prevalent on adu

244 Psoriasis is a common inflammatory and hyperproliferative skin disease with a multifactorial ge

245 vulgaris (PsV) is a common inflammatory and hyperproliferative skin disease.

246 epidermis, the importance of amphiregulin in hyperproliferative skin diseases has been further suppor

247 LML3 localization in normal epidermis and in hyperproliferative skin diseases including actinic kerat

248 ytes has been implicated in inflammatory and hyperproliferative skin diseases.

249 be an effective strategy in the treatment of hyperproliferative skin diseases.

250 epithelial malignancies and in psoriasis, a hyperproliferative skin disorder.

251 regulating the expression of ErbB ligands in hyperproliferative skin disorders and wound healing.

252 y play a role in the pathogenesis of certain hyperproliferative skin disorders via modulation of gene

253 d tissue sections from normal human skin and hyperproliferative skin disorders were examined by immun

254 ound effects on epidermal gene expression in hyperproliferative skin disorders.

255 The hyperproliferative skin inflammation in this novel murin

256 itions, such as the psoriasis, a nonallergic hyperproliferative skin inflammatory disorder with a neu

257 d WEHV2, respectively) are associated with a hyperproliferative skin lesion on walleyes that appears

258 native skin, including genes associated with hyperproliferative skin or activated keratinocytes.

259 and S100A8/A9, were also up-regulated in the hyperproliferative skin.

260 culturing C/EBPalpha(-/-) FL cells in vitro Hyperproliferative spleen colonies and myelodysplastic s

261 We previously proposed that the keratinocyte hyperproliferative state in psoriatic skin results from

262 , and establishment of a TGF-beta-resistant, hyperproliferative state in the colonic epithelium.

263 minution of p21 and p27 levels resulted in a hyperproliferative state in VHL-negative cells, leading

264 This hyperproliferative state is thought to represent the pre

265 an essential process that helps maintain the hyperproliferative state of most cancer cells.

266 ose obtained from healthy volunteers and the hyperproliferative state of the lesions was characterize

267 s from untreated HIV(+) individuals are in a hyperproliferative state that is modulated by type I int

268 Cx26 expression kept wounded epidermis in a hyperproliferative state, blocked the transition to remo

269 It can be induced in hyperproliferative states such as wound healing, inflamm

270 ich Connexin 26 is up-regulated in epidermal hyperproliferative states).

271 times (T2) in magnetic resonance imaging of hyperproliferative states, for example, malignancy.

272 ein ARF provides a defence mechanism against hyperproliferative stresses that can result from the abe

273 two distinct types of 3D structures: large, hyperproliferative structures and small, growth-arrested

274 opels disease by nourishing the inflamed and hyperproliferative synovium.

275 d show that loss of TIGIT in mice results in hyperproliferative T cell responses and increased suscep

276 rker, CD151 in humans thus marks and enables hyperproliferative T cells.

277 intrahepatic Treg numbers were increased and hyperproliferative, the intrahepatic CD4/CD8 ratio was d

278 n ureteric morphogenesis, including dilated, hyperproliferative tips and decreased branching.

279 indicative of spontaneous activation and are hyperproliferative upon in vitro stimulation.

280 ink in the emergence of apoptosis-resistant, hyperproliferative vascular cells after EC apoptosis.

281 Pulmonary arterial hypertension (PAH) is a hyperproliferative vascular disorder observed predominan

282 Obese ZSF1 rats developed hyperproliferative vascular foci in the subendocardium,

283 ll adult vascular beds produced CNS-specific hyperproliferative vascular malformations.

284 dvancement with lesions at early stage being hyperproliferative, whereas lesions at late stage are cl

285 At the RNA level, 38% of ACF were hyperproliferative, with proliferating cell nuclear anti