ライフサイエンスコーパス: hyperproliferation

1 contribute to enhanced inflammation and cell hyperproliferation.

2 search for novel agents against keratinocyte hyperproliferation.

3 xposure but are dispensable for premalignant hyperproliferation.

4 ositive cells, but there was no evidence for hyperproliferation.

5 om binding to the kinetochore does not cause hyperproliferation.

6 estored microabscess formation and epidermal hyperproliferation.

7 oxide synthase expression, and keratinocyte hyperproliferation.

8 uses cutaneous inflammation and keratinocyte hyperproliferation.

9 ced paradoxical ERK activation, resulting in hyperproliferation.

10 catenin, which maintain Hras(G12V)-dependent hyperproliferation.

11 at signaling in the regulation of intestinal hyperproliferation.

12 stion revolves around the nature of cellular hyperproliferation.

13 preting studies of both normal and malignant hyperproliferation.

14 of activated BRAFV600E resulted in astrocyte hyperproliferation.

15 and retinal degeneration associated with RPE hyperproliferation.

16 geing intestines required Wg and Myc for ISC hyperproliferation.

17 crease in basal cell number and luminal cell hyperproliferation.

18 , over time, could not prevent CD4(+) T cell hyperproliferation.

19 Egfr signaling suppresses Apc1-dependent ISC hyperproliferation.

20 ssociated with diminished p21 expression and hyperproliferation.

21 liminated cilia, and many (not Kif3a) caused hyperproliferation.

22 ions, which ultimately promote transition to hyperproliferation.

23 activation and cell-cycle arrest to prevent hyperproliferation.

24 2+)](i) in cholangiocytes is associated with hyperproliferation.

25 ar senescence, whereas in others it produces hyperproliferation.

26 eases, cyst formation involves cholangiocyte hyperproliferation.

27 in the surface pit epithelium, resulting in hyperproliferation.

28 ns junction component alphaE-catenin lead to hyperproliferation.

29 ory subsets); and 3) CD4(+) and CD8(+) T(EM) hyperproliferation.

30 CDK4-induced, but not myc-induced epidermal hyperproliferation.

31 dent of their ability to prevent unwarranted hyperproliferation.

32 bined Mek1/2 loss also abolished Raf-induced hyperproliferation.

33 rmalizes KITD814V-induced ligand-independent hyperproliferation.

34 entified as potent instigators of epithelial hyperproliferation.

35 mpartment were not protected from epithelial hyperproliferation.

36 oplasmic reticulum stress, inflammation, and hyperproliferation.

37 cts may be avoided through control of B-cell hyperproliferation.

38 signaling, resulting in SMC misalignment and hyperproliferation.

39 in tumors or in Rasopathies correlates with hyperproliferation.

40 nd by p53-dependent parietal epithelial cell hyperproliferation.

41 metabolism, higher rates of glycolysis, and hyperproliferation.

42 l role of the gut microbiota in heme-induced hyperproliferation.

43 -secreting capacity, suggesting compensatory hyperproliferation.

44 tion of VEGF-R2 tyrosine, thus preventing EC hyperproliferation.

45 in expression and resulted in ex vivo B-cell hyperproliferation, a phenotype similar to that of the P

46 PP1 in mouse epidermis resulted in epidermal hyperproliferation, a reduced adherence of basal keratin

47 Prior studies showed that Hmga1 drives hyperproliferation, aberrant crypt formation and polypos

48 ence is thought to be invariably preceded by hyperproliferation, aberrant replication, and activation

49 n an abundance of abnormal vesicles and show hyperproliferation, abnormal epidermal differentiation,

50 We did not identify signs of hyperproliferation, abnormal growth, or immune mediated

51 henotype characterized by basal keratinocyte hyperproliferation, acanthosis, hyperkeratosis, intraepi

52 tic ablation of N-cadherin (N-cad KO) caused hyperproliferation, accelerated mPanIN progression, and

53 of CDK2 is sufficient to induce keratinocyte hyperproliferation, activation of CDK2 alone does not in

54 Kidneys from these mice demonstrated marked hyperproliferation and a concomitant increase in label-r

55 y skin disease characterized by keratinocyte hyperproliferation and a disease-related infiltration of

56 s is a common skin disorder characterized by hyperproliferation and aberrant differentiation of epide

57 scular injury, they display a marked intimal hyperproliferation and abnormal activation of mitogen-ac

58 K14cre;Dlx3(Kin/f) mice exhibited epidermal hyperproliferation and abnormal differentiation of kerat

59 , inflammatory skin disease characterized by hyperproliferation and abnormal differentiation of kerat

60 Knockdown of RUNX1 causes hyperproliferation and abnormal morphogenesis, both of w

61 itors, which also attenuated IPAH-associated hyperproliferation and apoptosis-resistance ex vivo, and

62 The T cell hyperproliferation and autoimmune phenotypes that manife

63 ay is constitutively active, reversed T-cell hyperproliferation and autoimmunity.

64 n-of-function phenotype, characterized by EC hyperproliferation and blood vessel enlargement.

65 mediated mTORC1 induction, resulting in cell hyperproliferation and cancer growth.

66 A in maximizing MYC expression, resulting in hyperproliferation and cellular transformation into canc

67 decanoylphorbol-13-acetate-induced epidermal hyperproliferation and closure rates of full-thickness s

68 gen-induced airway smooth muscle cell (ASMC) hyperproliferation and cyclin D1 (an important cell prol

69 homozygous PRKCD mutation results in B-cell hyperproliferation and defective apoptosis with conseque

70 silencing of Abi1 or Wasf2 induced cellular hyperproliferation and defects in architecture of the in

71 , embryo arrest is associated with endosperm hyperproliferation and delayed development similar to pa

72 strong hyperactivation of ERK1/2, promoting hyperproliferation and depletion of HSCs and expansion o

73 N signaling by Irgm1 is necessary to prevent hyperproliferation and depletion of the stem cell compar

74 nse (DDR), which may follow oncogene-induced hyperproliferation and ensuing DNA replication stress.

75 is responsible for costimulation independent hyperproliferation and excess cytokine production in TRA

76 TG16-knockout intestines had increased crypt hyperproliferation and expansion of ISCs, but enterocyte

77 on or localization could contribute to tumor hyperproliferation and explain how polarity disruption c

78 and expands the Axin2(+) cell pool to cause hyperproliferation and gland hyperplasia.

79 iota is required for heme-induced epithelial hyperproliferation and hyperplasia because of the capaci

80 arget for epidermal diseases associated with hyperproliferation and impaired differentiation.

81 e are hyperactivated and that they displayed hyperproliferation and increased production of interleuk

82 an skin condition characterized by epidermal hyperproliferation and infiltration of multiple leukocyt

83 Epidermal hyperproliferation and inflammation are hallmarks of the

84 nsic mechanism to limit injury-induced crypt hyperproliferation and inflammation-associated colon can

85 coid receptor knockout lung, suggesting that hyperproliferation and lack of maturation of the alveola

86 oriasis-like phenotypes including epithelial hyperproliferation and leukocyte infiltration.

87 Blockade of any of these steps causes hyperproliferation and loss of arterial specification.

88 an oncogenic signaling program that leads to hyperproliferation and loss of polarity in three-dimensi

89 ic microabscess formation and contributes to hyperproliferation and markedly attenuated differentiati

90 ures of human AMKL, including megakaryoblast hyperproliferation and maturation block, thrombocytopeni

91 mmation, mdb3 deficiency resulted in colonic hyperproliferation and mbd3(DeltaG/DeltaG) mice showed m

92 gamma(null) mice, resulted in both thymocyte hyperproliferation and multiple pre- and post-beta-selec

93 ring early development resulted in transient hyperproliferation and overproduction of OPCs but genera

94 mice lacking neutrophils, NK cells displayed hyperproliferation and poor survival and were blocked at

95 short-term hematopoietic stem cells exhibit hyperproliferation and preferential susceptibility to mi

96 strin gene, has been shown to induce colonic hyperproliferation and promote colorectal cancer in mice

97 creased PDK4 is associated with PAH pericyte hyperproliferation and reduced endothelial-pericyte inte

98 This causes hyperproliferation and reduced sensitivity to chemothera

99 n mutants lacking functional Pten suppressed hyperproliferation and released the differentiation arre

100 This in turn leads to hyperproliferation and replication stress.

101 ETS2-overactivation in epidermal-SCs induces hyperproliferation and SCC super-enhancer-associated gen

102 ers (InvEE transgenics) results in epidermal hyperproliferation and skin inflammation.

103 ylphorbol-13-acetate (TPA)-induced epidermal hyperproliferation and skin tumor development.

104 d mice lacking these genes display epidermal hyperproliferation and soft-tissue fusions that result i

105 T cells in primary infection resulting from hyperproliferation and stress induced signals, demonstra

106 intestine (Usp28(DeltaIEC)) ameliorated the hyperproliferation and the impaired goblet and Paneth ce

107 nvironment is closely related to BPH stromal hyperproliferation and tissue remodeling with a local hy

108 to c-Myc protein and inhibits c-Myc-induced hyperproliferation and transformation with a concomitant

109 eracts with c-Myc and controls c-Myc-induced hyperproliferation and transformation.

110 ed NPM dramatically stimulates c-Myc-induced hyperproliferation and transformation.

111 dent proliferation signaling to prevent cell hyperproliferation and tumor initiation.

112 some cancers, most notably immortalization, hyperproliferation, and dissemination.

113 resulting in commensal dysbiosis, stem cell hyperproliferation, and epithelial dysplasia.

114 promoting cholangiocarcinoma cell anaplasia, hyperproliferation, and higher malignant grading in this

115 te-derived inflammatory mediators, epidermal hyperproliferation, and increased neutrophil infiltratio

116 ating hallmarks of ICD such as angiogenesis, hyperproliferation, and inflammation.

117 cant leukocytosis with neutrophilia, myeloid hyperproliferation, and myeloid cell infiltration into d

118 phosphorylation, supports ligand-independent hyperproliferation, and promotes promiscuous cooperation

119 signaling in a feedback mechanism to prevent hyperproliferation, and that this regulation can be lost

120 stinal stem cell (ISC) signature, progenitor hyperproliferation, and transformation.

121 eads to constitutively active WNT signaling, hyperproliferation, and tumorigenesis.

122 mouse skin led to severe alopecia, epidermal hyperproliferation, and ulceration, without obvious effe

123 ce of this pathway, the role of NF-kappaB in hyperproliferation appears rooted in its impact on epide

124 that augmented Smad signaling and fibroblast hyperproliferation are contributing factors in the patho

125 lation, mTOR-Stat3 signaling, and epithelial hyperproliferation are integrated and simultaneously lin

126 We show that epidermal hyperproliferation arising from p120 loss can be abrogat

127 -jun reverted physiological and pathological hyperproliferation, as well as the increased tumorigenes

128 xide was confirmed in the keratinocyte-based hyperproliferation assay.

129 ) from E47-deficient mice exhibit a striking hyperproliferation associated with a loss of cell cycle

130 n Lyn-deficient BMMCs not only represses the hyperproliferation associated with the loss of Lyn but a

131 stitution models, depletion of STRA6 induced hyperproliferation-associated differentiation, resulting

132 By its influence on hyperproliferation-associated differentiation, STRA6 cou

133 f inflammatory cells and a reduced epidermal hyperproliferation at lesional skin sites.

134 T cell hyperproliferation, but not other autoimmune symptoms, w

135 mouse head and neck epithelia gives rise to hyperproliferation, but only a few lesions progress to H

136 pable of simultaneous hypertranscription and hyperproliferation by activating topoisomerases.

137 entiating MYC to promote G1-S transition and hyperproliferation by downregulating cyclin-dependent ki

138 In contrast, inhibition of intestinal hyperproliferation by statins in an Apc/KrasG12D-mutant

139 etween scrib(-) and wild-type cells prevents hyperproliferation by suppressing Yki activity in scrib(

140 uced apoptosis and it decreased TPA-mediated hyperproliferation, coinciding with reduced epidermal th

141 architectural irregularities and epithelial hyperproliferation compared with wild-type mice.

142 cy of miR-31 in keratinocytes inhibits their hyperproliferation, decreases acanthosis and reduces the

143 TEC hyperproliferation development is accelerated in mice gi

144 have marked megakaryocytic progenitor (MkP) hyperproliferation during early fetal liver (FL) hematop

145 utophagy was also critical to maintain early hyperproliferation during metabolic stress.

146 iasis include keratinocyte dysregulation and hyperproliferation, elongated rete ridges, and inflammat

147 In contrast, PTPRF silencing led to cell hyperproliferation, enhanced tumor colony formation in s

148 Psoriasis is characterized by keratinocyte hyperproliferation, erythema, as well as a form of pruri

149 Exogenous IFN-alpha markedly reduced the hyperproliferation FL-derived MkPs of GATA1s mice in vit

150 nd maintenance of intestinal stem cell (ISC) hyperproliferation following Apc1 loss.

151 nificant increase in epidermal thickness and hyperproliferation following exposure to the tumor promo

152 c-Cbl(-/-) mice exhibit augmented pool size, hyperproliferation, greater competence, and enhanced lon

153 ty of vitamin D analogs in causing epidermal hyperproliferation has been distinguished from that resu

154 e, including in intestinal epithelium, where hyperproliferation has been reported, and in skin epithe

155 Both exhibit epidermal hyperproliferation, immature desmosomes lacking a dense

156 mmunoblot analyses of these regions revealed hyperproliferation, impaired terminal differentiation, a

157 ate inflammation, lysosomal dysfunction, and hyperproliferation in a cell-autonomous manner.

158 s(G12D) in the colonic epithelium stimulated hyperproliferation in a Mek-dependent manner.

159 dation were significantly reduced and caused hyperproliferation in cell lines expressing these mutate

160 h the loss of polarity genes associated with hyperproliferation in Drosophila melanogaster.

161 to abnormal keratinocyte differentiation and hyperproliferation in EKV patient skin.

162 ng that the up-regulation of EGFR stimulates hyperproliferation in epithelia of mice with genetic red

163 While the virus induces hyperproliferation in infected cells, it downregulates e

164 y reported that loss of Cbl functions caused hyperproliferation in lymphoid and hematopoietic systems

165 in adult mice as well as naturally occurring hyperproliferation in neonatal mouse epidermis.

166 ing factor as a protein that promoted B-cell hyperproliferation in Nlrc5(mo-KO) mice.

167 ute to excessive Epo signaling and erythroid hyperproliferation in PFCP.

168 ow activated NF-kappaB promotes keratinocyte hyperproliferation in psoriasis is largely unknown.

169 is a possible pathomechanism of keratinocyte hyperproliferation in psoriasis.

170 and wound healing and may be a mechanism for hyperproliferation in skin disorders such as psoriasis.

171 ive epidermal acanthosis and inflammatory KC hyperproliferation in the effector phase of CHS.

172 nt response in the absence of FRK-1 leads to hyperproliferation in the endoderm, as is also seen when

173 years of chronic inflammation, fibrosis, and hyperproliferation in the host liver.

174 e absence of ABCG1 in CD4 T cells results in hyperproliferation in vitro, but only when cells are sti

175 EGF) receptor blockade, which resulted in EC hyperproliferation, increased IL-32 three-fold.

176 Cell hyperproliferation, inflammation, and angiogenesis are b

177 vivo model to study the pathogenesis of cell hyperproliferation, inflammation, and angiogenesis.

178 results in the rescue of the epithelial cell hyperproliferation, inflammation, and neovascularization

179 No difference in TPA-induced hyperproliferation, inflammation, or Erk activation was

180 ssociated with inflammation, carcinogenesis, hyperproliferation, invasion, and angiogenesis, we hypot

181 Hyperproliferation is a major contributor to cyst growth

182 curs at an age (11 weeks) at which epidermal hyperproliferation is most visible and is spatially cont

183 se cells in vitro, suggesting that epidermis hyperproliferation is not epidermal cell-autonomous but

184 Yet at the same time, cellular hyperproliferation is the fundamental pathological condi

185 We propose that RPE hyperproliferation is the primary cause for the observed

186 cient increased mTOR signaling and astrocyte hyperproliferation is unaffected by Rheb shRNA silencing

187 d elicits epithelial damage and compensatory hyperproliferation, leading to hyperplasia.

188 tant mice restores OCD but does not decrease hyperproliferation, leading to non-cystic harmonious hyp

189 kin wounds, the K5.CtBP1 epidermis displayed hyperproliferation, loss of E-cadherin, and failed termi

190 oth craniofacial and skin defects, including hyperproliferation, loss of spinous and granular keratin

191 3 cKO mice were infertile due to endometrial hyperproliferation observed as early as 6 weeks of postn

192 ystemic toxicity of IL-15 SA was mediated by hyperproliferation of activated NK cells.

193 Notably, hyperproliferation of ALPS DNT cells is associated with

194 demonstrate a key role of LMP2A in promoting hyperproliferation of B cells by enhancing MYC expressio

195 sence of PTEN, p110beta is important for the hyperproliferation of basal cells in PHTS.

196 lor, a polarized distribution of melanin and hyperproliferation of basal keratinocytes.

197 Hyperproliferation of bile duct epithelial cells due to

198 at the genetic ablation of the Casr leads to hyperproliferation of colonic epithelial cells, expansio

199 Hyperproliferation of cystic cholangiocytes is linked to

200 lel to natural T1D development, potentiating hyperproliferation of diabetogenic T cells.

201 somatic deletion of Foxo1 is associated with hyperproliferation of ECs.

202 haracterized by abnormal differentiation and hyperproliferation of epidermal keratinocytes.

203 s target, ppp6c, as critical factors for the hyperproliferation of epidermis in psoriasis.

204 lomavirus (HPV) infection frequently induces hyperproliferation of epithelial cells, leading to both

205 in any core PRC1 component cause pronounced hyperproliferation of eye imaginal tissue, accompanied b

206 pamycin complex 1 (mTORC1), which results in hyperproliferation of hepatocytes.

207 c T cell progenitors results in compensatory hyperproliferation of immature thymocytes and developmen

208 Deletion of MED1 also caused hyperproliferation of interfollicular epidermal KCs, and

209 tion, but a dermal inflammatory response and hyperproliferation of interfollicular epidermis accompan

210 in reversed the excessive mTOR signaling and hyperproliferation of Itpkb(-/-) HSC without rescuing co

211 egulated in psoriasis and contributes to the hyperproliferation of keratinocytes by maintaining centr

212 ization in wound healing and is critical for hyperproliferation of keratinocytes in atopic dermatitis

213 Blocking MED1/MED21 expression caused hyperproliferation of keratinocytes, accompanied by incr

214 n induced by imiquimod treatment and inhibit hyperproliferation of keratinocytes.

215 while deletion of GRP94 in the liver led to hyperproliferation of liver progenitor cells, deletion o

216 These benign tumors represent clonal hyperproliferation of melanocytes that are in a senescen

217 xpression is induced in association with the hyperproliferation of mitochondria.

218 ve compounds that could effectively suppress hyperproliferation of mouse brain primary astrocytes def

219 rived metabolites such as butyrate that fuel hyperproliferation of MSH2(-/-) colon epithelial cells.

220 rant activation of Notch signaling underlies hyperproliferation of mutant cardiomyocytes, and forced

221 opoietic stem cell disorders associated with hyperproliferation of myeloid cells.

222 GSK-3 deletion resulted in massive hyperproliferation of neural progenitors along the entir

223 Our results provide a mechanism linking hyperproliferation of NPCs with the pathogenesis of ASD

224 revealed that SOX5/6/21 prevent detrimental hyperproliferation of oncogene expressing SVZ cells by f

225 Hyperproliferation of PCK cholangiocytes in response to

226 we report here that loss of CARM1 results in hyperproliferation of pulmonary epithelial cells during

227 Finally, depletion of DCAF1 inhibits the hyperproliferation of Schwannoma cells from NF2 patients

228 blast number that was likely to be driven by hyperproliferation of Sp7(+) preosteoblasts.

229 tiated cells resulted in non-cell-autonomous hyperproliferation of stem cells and prevented their com

230 ased expression of Indian Hedgehog (Ihh) and hyperproliferation of surface mucous cells.

231 signal-regulated kinase 1/2 is required for hyperproliferation of SVAS iPSC-SMCs.

232 suppressed synovial recruitment of EPCs and hyperproliferation of synovial cells.

233 molecules and matrix metalloproteinases, and hyperproliferation of synovial fibroblasts.

234 es characterized by clonal hematopoiesis and hyperproliferation of terminally differentiated myeloid

235 inocyte differentiation in AD skin result in hyperproliferation of the basal layer of epidermis, inhi

236 Hyperproliferation of the colonic epithelium, leading to

237 The hyperproliferation of the endometrium affected both impl

238 more, the homozygous affected mice exhibited hyperproliferation of the epidermis, disturbed cornifica

239 Interestingly, hyperproliferation of the external granule layer (EGL) w

240 Mice exposed to desiccating stress showed hyperproliferation of the meibomian gland and ductal dil

241 nding of the molecular mechanisms underlying hyperproliferation of the palmoplantar epidermis in both

242 genesis without affecting TPA- or E7-induced hyperproliferation of the skin.

243 Mice lacking Crebbp in GC B cells exhibited hyperproliferation of their GC compartment upon immuniza

244 mor stem cells can paradoxically promote the hyperproliferation of their wild-type counterparts.

245 y and EZH1 mutations cooperate to induce the hyperproliferation of thyroid cells.

246 e-specific deletion of VHL led to dysplastic hyperproliferation of tubular epithelial cells, confirmi

247 ice lacking TSC2 in developing SCs displayed hyperproliferation of undifferentiated SCs incompatible

248 These findings are accompanied by hyperproliferation of WASp-deficient follicular and germ

249 activation of Notch signaling recapitulates hyperproliferation of working myocytes but not the condu

250 Increased stratification and hyperproliferation only happened in the limbal, but not

251 hanisms, as IL-4 deficiency does not prevent hyperproliferation or elevated mTORC1 signalling in Ndfi

252 , however, does the distal RPE show signs of hyperproliferation or respecification, likely due to loc

253 radic cases, AR-DLBCL demonstrated increased hyperproliferation (P < .001) and c-Myc rearrangements,

254 We further show that the hyperproliferation phenotype of NHERF-2-silenced EC is b

255 This transition from hypo- to hyperproliferation presents an intriguing paradox in the

256 TGFbeta signaling in epithelial cells causes hyperproliferation, reduced apoptosis and increased geno

257 and growth associated with hypermutation and hyperproliferation, respectively, in conjunction with at

258 a contrived compensatory non-cell-autonomous hyperproliferation response when cell-autonomous apoptos

259 ification, it is not apparently required for hyperproliferation resulting from excessive Wnt signalin

260 Epidermal hyperproliferation resulting in acanthosis is an importa

261 ts polarity and tight junctions and promotes hyperproliferation, resulting in large, filled structure

262 for phosphorylation of Smad1/5/8 reduced the hyperproliferation seen in c.474delA fibroblasts.

263 Strikingly, hyperproliferation, self-renewal, and autophagy defects

264 FVB mice developed epithelial cell hyperproliferation, severe inflammation with erosions an

265 ties in the cornea including epithelial cell hyperproliferation, stromal inflammation, and neovascula

266 expression was induced only during epidermal hyperproliferation, such as in psoriasis and in murine w

267 by reduced BMPR2 expression and endothelial hyperproliferation, supporting the relevance of this mec

268 ting that in spite of extensive keratinocyte hyperproliferation, susceptibility to carcinogen-depende

269 oimmune thyroid disease characterized by TEC hyperproliferation that develops spontaneously in IFN-ga

270 infection, EBV induces a transient period of hyperproliferation that is suppressed by the activation

271 malities, as well as growth factor-dependent hyperproliferation that underlies PH.

272 s includes host predisposition to epithelial hyperproliferation; therefore, a possible association of

273 arization-scrambling RPE layer, ranging from hyperproliferation to focal atrophy.

274 d IL-17(+) gammadelta T cells, and epidermal hyperproliferation to levels similar to a Rag1-/- backgr

275 sed apoptosis, increased p21 expression, and hyperproliferation to reinstate intestinal integrity.

276 Expansion, in part, involved E1 cell hyperproliferation together with rapid E2 conversion plu

277 he hESC-derived RPE cells showed no signs of hyperproliferation, tumorigenicity, ectopic tissue forma

278 T lymphocytes showed normal development but hyperproliferation upon stimulation, which correlates wi

279 role of CXCR4 in IL-23-induced keratinocyte hyperproliferation using an epidermal-specific knockout

280 d for their ability to suppress keratinocyte hyperproliferation using HaCaT cells as the primary test

281 sis, we found that Myc-mediated keratinocyte hyperproliferation was abolished by the loss of Skp2.

282 We observed that the severity of epithelial hyperproliferation was accentuated by lymphocytes, where

283 the presence of the gut microbiota, because hyperproliferation was completely eliminated by antibiot

284 Hyperproliferation was explored using Ki67 and cell cycl

285 vidence of canonical hedgehog signaling, and hyperproliferation was not blocked by smoothened (SMO) i

286 Heme-induced hyperproliferation was shown to depend on the presence o

287 he most potent analogue against keratinocyte hyperproliferation was the 1,2,4-oxadiazole 18, the pote

288 oxide synthase expression, and keratinocyte hyperproliferation were suppressed.

289 a by Helicobacter pylori leads to epithelial hyperproliferation, which increases the risk for gastric

290 n and organization, express RANK and undergo hyperproliferation, which is abrogated by RANKL neutrali

291 el1L in hematopoietic tissues drives HSCs to hyperproliferation, which leads to complete loss of HSC

292 heir potency for suppression of keratinocyte hyperproliferation, which was evaluated using HaCaT cell

293 tatic intraepithelial neoplasia (HG-PIN) and hyperproliferation, while Pten single-knockouts develope

294 They undergo moderate hyperproliferation with increased self-renewal.

295 nism that coordinates oncogenic HRAS-induced hyperproliferation with loss of progenitor self-renewal

296 We speculate that B cell hyperproliferation within parotid glands of pSS patients

297 Immunohistochemistry showed hyperproliferation within the punctate lesions.

298 trophic myopathy was caused by cardiomyocyte hyperproliferation without hypertrophy and was associate

299 haviours such as differentiation defects and hyperproliferation, yet fail to produce macroscopically

300 IL-15 administration, followed by influx and hyperproliferation yielding 10-fold expansions of NK cel