ライフサイエンスコーパス: neoplasia

1 ial neoplasias (eg, cervical intraepithelial neoplasia).

2 metaplasia was detected in two cases, but no neoplasia.

3 (AGR2) in the earliest stages of pancreatic neoplasia.

4 h a screening colonoscopy with no identified neoplasia.

5 ce of the potential threat from pathogens or neoplasia.

6 ooperate with mutant APC in driving invasive neoplasia.

7 oducts were thought to be unique features of neoplasia.

8 of various immune disorders and plasma cell neoplasia.

9 po pathway leads to aberrant cell growth and neoplasia.

10 n use of lithium and increased risk of renal neoplasia.

11 e II, hijack this essential enzyme and drive neoplasia.

12 idemia is associated with risk of colorectal neoplasia.

13 ation associated with oncogenic Kras-induced neoplasia.

14 ailed to develop CML-like myeloproliferative neoplasia.

15 mple contributes to understanding of colonic neoplasia.

16 RTKs) play important roles in EBV-associated neoplasia.

17 ing hyperplasia or prostatic intraepithelial neoplasia.

18 al states, including diabetes, epilepsy, and neoplasia.

19 of B cells and has a critical role in B-cell neoplasia.

20 ty to detect cellular atypia associated with neoplasia.

21 WS disease pathogenesis or the high risk of neoplasia.

22 10 wk after dosing, well before evidence of neoplasia.

23 urbs differentiation and ultimately leads to neoplasia.

24 ysplastic lesions/pancreatic intraepithelial neoplasia.

25 ce hyperplasia and prostatic intraepithelial neoplasia.

26 touch dome keratinocytes but no Merkel cell neoplasia.

27 onally reprograms cell metabolism to promote neoplasia.

28 facilitating the progression of established neoplasia.

29 to modulate gene expression in early colonic neoplasia.

30 cell survival, and other hallmarks of early neoplasia.

31 mediates associated with type II endometrial neoplasia.

32 in patients treated for high-grade cervical neoplasia.

33 for refractory proctitis, and 20% for rectal neoplasia.

34 cally refractory disease or to treat colonic neoplasia.

35 e genetic models of clonal hematopoiesis and neoplasia.

36 or initiation in a mouse model of intestinal neoplasia.

37 is sufficient for the development of T cell neoplasia.

38 otective immunity and limit autoimmunity and neoplasia.

39 ticular, the development of parasite-induced neoplasia.

40 a mechanism by which its deficiency promotes neoplasia.

41 n, suggesting these mutations play a role in neoplasia.

42 biomarkers for early detection of pancreatic neoplasia.

43 significantly associated with progression to neoplasia.

44 probiotic-mediated suppression of colorectal neoplasia.

45 tors (DNMTis) for treatment of hematological neoplasias.

46 s, referred to as pancreatic intraepithelial neoplasias.

47 tic targets for these frequent hematological neoplasias.

48 t alter growth of pancreatic intraepithelial neoplasias.

49 re a very complex and heterogeneous group of neoplasias.

50 ositive CS/CSL patients and sporadic thyroid neoplasias.

51 ed with the ability of a retrovirus to cause neoplasias.

52 y, resulting in growth inhibition of several neoplasias.

53 r treating usual-type vulvar intraepithelial neoplasia?

54 RAS, premalignant pancreatic intraepithelial neoplasia 1 (PanIN1) lesions rarely become fully maligna

55 of ADM as well as pancreatic intraepithelial neoplasia-1 (PanIN-1), PanIN-2, and PanIN-3 and delayed

56 eatic lesion: intraductal papillary mucinous neoplasia (14 patients, 35%) and pancreatic ductal adeno

57 found more disease (cervical intraepithelial neoplasia 3 or worse [CIN3+]) and also found it earlier

58 omas, 2 grade 2 conjunctival intraepithelial neoplasias, 7 in situ squamous carcinomas) and 5 as nons

59 their role in the earliest stages of colonic neoplasia, 75% of the loci harboring methylation changes

60 ntraepithelial neoplasia (PanIN) lesions and neoplasia accompanied by prominent acute and chronic inf

61 Large polyps, advanced neoplasia (advanced adenomas and cancer), and invasive c

62 (referred to herein as multilocus inherited neoplasia alleles syndrome [MINAS]) in patients with unu

63 quent endoscopy, the odds for progression to neoplasia also increased greatly (odds ratio, 9.28; 95%

64 like mucosal inflammation, preneoplasia, and neoplasia, although suggested by several studies, remain

65 This index stratifies risk for advanced neoplasia among average-risk persons by identifying lowe

66 previously published risk index for advanced neoplasia (AN) in a large, well-characterized cohort.

67 and later development of colorectal advanced neoplasia (AN).

68 with an estimated low prevalence of advanced neoplasia and colonoscopy screening in high prevalence p

69 omparisons were 0.91 (0.85-0.96) between all neoplasia and controls, 0.79 (0.70-0.88) between colorec

70 to progress beyond prostatic intraepithelial neoplasia and did not harbor genomic CNAs.

71 ative treatment for cervical intraepithelial neoplasia and early invasive cervical cancer adversely a

72 ate the entire spectrum of human plasma cell neoplasia and illustrate the utility of humanized models

73 to detect early cases of advanced colorectal neoplasia and improve survival of colorectal cancer pati

74 ice shows hepatobiliary cysts, early hepatic neoplasia and increase in serum alpha-fetoprotein.

75 hemoattraction to pancreatic intraepithelial neoplasia and increased abdominal hypersensitivity cause

76 subsequent diagnosis of myeloid or lymphoid neoplasia and increased all-cause mortality.

77 , driven by genetic alterations that lead to neoplasia and inflammation, and an extrinsic pathway, dr

78 es significantly in cervical intraepithelial neoplasia and invasive squamous cervical cancer.

79 involvement of RTKs in EBV-regulated B-cell neoplasia and malignancies remain largely unclear.

80 uidelines effectively stratified the risk of neoplasia and malignancy.

81 ontrols, 0.79 (0.70-0.88) between colorectal neoplasia and other cancers, and 0.98 (0.96-1.0) between

82 a synchronous intraductal papillary mucinous neoplasia and pancreatic ductal adenocarcinoma.

83 c alterations across the spectrum of thyroid neoplasia and present the resulting model of thyroid can

84 out mice developed prostatic intraepithelial neoplasia and prostatic adenocarcinoma.

85 rly onset of mouse prostatic intraepithelial neoplasia and the progression of prostate lesions to inv

86 etected in up to 90% of anal intraepithelial neoplasias and anal cancers.

87 ic mice regenerated prostate intraepithelial neoplasias and prostatic adenocarcinoma lesions.

88 omas, 1 low-grade intraepithelial pancreatic neoplasia, and 1 case of polycystic kidney disease.

89 6% of classic lesions were unassociated with neoplasia, and 71% of lesions arose in papillomas.

90 ation of kidney cysts, renal intraepithelial neoplasia, and invasive papillary renal carcinoma.

91 ic pancreatitis, pancreatic intra-epithelial neoplasia, and PDAC tissues from patients expressed high

92 ic pancreatitis, pancreatic intra-epithelial neoplasia, and PDAC tissues from patients.

93 itotic activity, axonal disruption, vascular neoplasia, and with several brain metabolites including

94 ion of high-grade pancreatic intraepithelial neoplasias, and accelerated development of PDAC with sho

95 ormation of IPMN, pancreatic intraepithelial neoplasias, and PDAC, in addition to proliferation and p

96 etion, hypofertility, intratubular germ cell neoplasias, and seminoma development.

97 o the pathogenesis of particular hematologic neoplasia are also discussed.

98 e show that many patients with hematological neoplasia are markedly vitamin C deficient.

99 Among neoplasia-associated epigenetic alterations, changes in

100 ogical features of prostatic intraepithelial neoplasia at 7 months of age; these features were associ

101 aplasia-associated prostatic intraepithelial neoplasia at a low frequency.

102 RB loss occurs commonly in neoplasia but its contributions to advanced cancer have

103 iseases like retinitis pigmentosa or myeloid neoplasia, but its genome-wide effects on constitutive a

104 the progression of prostate intraepithelial neoplasia, by promoting cell proliferation, micro-invasi

105 T in asthma, autoimmune disorders, malignant neoplasias, cardiovascular diseases, acquired immunodefi

106 The biology of neoplasia caused by germline mutations has led to paradi

107 relationship between blastic plasmacytoid DC neoplasia cells and healthy DCs; and circulating progeni

108 L) is a hematopoietic stem cell (HSC)-driven neoplasia characterized by expression of the constitutiv

109 stiocytosis (LCH) is an inflammatory myeloid neoplasia characterized by granulomatous lesions contain

110 fied an intermediate category of melanocytic neoplasia, characterized by the presence of more than on

111 yield of high-grade cervical intraepithelial neoplasia (CIN) and the influence on biopsy and treatmen

112 logically confirmed cervical intraepithelial neoplasia (CIN) in 2.5 years after the baseline testing

113 lomaviruses (HPVs), cervical intraepithelial neoplasia (CIN) is common, and current treatments are ab

114 onal treatment for cervical intra-epithelial neoplasia (CIN) is linked to significant adverse sequela

115 ial lesion (SIL) or cervical intraepithelial neoplasia (CIN) prevalence, incidence, progression, or r

116 he population-based cervical intraepithelial neoplasia (CIN) trends when adjusting for changes in cer

117 Comparison of conjunctival intraepithelial neoplasia (CIN) vs SCC revealed SCC with greater diffuse

118 ibed in women with cervical intra-epithelial neoplasia (CIN).

119 h disease severity (cervical intraepithelial neoplasia [CIN] 3, 17.9% [+/-7.2] vs CIN2, 11.6% [+/-6.5

120 ased from low-grade cervical intraepithelial neoplasia (CIN1) to precancerous CIN3 lesions.

121 ction of high-grade cervical intraepithelial neoplasia (CIN2+) in a total of 8,610 cervical cytology

122 g in 16 cases of UDH, nine unassociated with neoplasia (classic) and seven arising within papillomas.

123 s with CRC and 10 persons without colorectal neoplasia (control samples) and a second series of 81 pa

124 as, as well as 24 persons without colorectal neoplasia (control samples).

125 s, as well as 129 persons without colorectal neoplasia (control samples); 72 FIT samples from a third

126 datasets from REpository for Molecular BRAin Neoplasia DaTa (REMBRANDT), caArray studies of lung and

127 Mice with pancreatic intra-epithelial neoplasia-derived systemic increases in TIMP1 developed

128 rizes current evidence for FIT in colorectal neoplasia detection and the comparative effectiveness of

129 -based screening, (2) the potential gains in neoplasia detection probabilities if screening occurred

130 en-group differences in adenoma and advanced neoplasia detection rates were higher for both outreach

131 In contrast, small intestinal neoplasia development significantly correlated with age

132 ng oncoprotein critical for the evolution of neoplasia driven by Apc mutation.

133 Together, these data suggest that myeloid neoplasia driven by PTEN loss is dependent on p110beta v

134 I undergoes significant deformation in early neoplasia due to focal epithelial expansion and proteoly

135 ity of current screening protocols to detect neoplasia (dysplasia and early preclinical EAC) in the e

136 n-associated premalignant and malignant skin neoplasia, E-cadherin is downregulated in association wi

137 , oral warts, and anogenital intraepithelial neoplasias (eg, cervical intraepithelial neoplasia).

138 esearch in high-germline risk for pancreatic neoplasia, elucidating early ontogeny in BRCA1-mutation

139 The bft gene is associated with colorectal neoplasia, especially in late-stage CRC.

140 nguished: a low-grade triple-negative breast neoplasia family, which includes nonobligate precursors

141 prostatic susceptibility to hormone-induced neoplasia from early-life exposure to low-dose bisphenol

142 nd prediction model differentiate colorectal neoplasia from patients with other neoplasms and from co

143 ogically; 1198 with cervical intraepithelial neoplasia grade 1 (CIN1), 456 with CIN2, and 455 with CI

144 istent infection or cervical intraepithelial neoplasia grade 1 or greater (CIN1+) associated with HPV

145 rmance in detecting cervical intraepithelial neoplasia grade 2 (CIN2) or more severe (CIN2+) diagnose

146 controls (less than cervical intraepithelial neoplasia grade 2 [<CIN2]) or cases (cervical intraepith

147 e cervical disease (cervical intraepithelial neoplasia grade 2 or 3, adenocarcinoma in situ, invasive

148 Cumulative risks of cervical intraepithelial neoplasia grade 2 or greater (CIN-2+; threshold used for

149 or the detection of cervical intraepithelial neoplasia grade 2 or higher (CIN2+) and CIN3+ relative t

150 [<CIN2]) or cases (cervical intraepithelial neoplasia grade 2 or higher [CIN2+]) for disease status.

151 ocarcinoma in situ (cervical intraepithelial neoplasia grade 2 or higher [CIN2+]) in 2008.

152 disease endpoint of cervical intraepithelial neoplasia grade 2 or worse (CIN2+).

153 or the detection of cervical intraepithelial neoplasia grade 2+ (CIN2+) and CIN3+ was assessed relati

154 ified 90 women with cervical intraepithelial neoplasia grade 2+ (CIN2+), including 43 women with CIN3

155 nd invasive cancer (cervical intraepithelial neoplasia grade 2+ [CIN2+]) compared to cytology, but no

156 helial lesions (ie, cervical intraepithelial neoplasia grade 2/3 [CIN 2/3]) and (2) incident transien

157 and vaginal disease (vaginal intraepithelial neoplasia grade 2/3, vaginal cancer) related to HPV 31,

158 oma), vulvar disease (vulvar intraepithelial neoplasia grade 2/3, vulvar cancer), and vaginal disease

159 omen diagnosed with cervical intraepithelial neoplasia grade 3 (CIN3).

160 s from 482 cases of cervical intraepithelial neoplasia grade 3 or cancer (CIN3+) and 3,517 random HC2

161 CI, 3.64 to 12.25) for anal intraepithelial neoplasia grade 3, 4.97 (95% CI, 3.26 to 7.57) for vulva

162 I, 9.69 to 19.25) for vulvar intraepithelial neoplasia grade 3, 86.08 (95% CI, 11.98 to 618.08) for v

163 10.50 to 62.69) for vaginal intraepithelial neoplasia grade 3, and 5.51 (95% CI, 1.22 to 24.84) for

164 in patients with pancreatic intraepithelial neoplasias grade 3 and PDAC lesions relative to matched

165 d HPV 16/18 to find cervical intraepithelial neoplasia (grade >/=2 [CIN2+] or grade >/=3 [CIN3+]).

166 d HPV 16/18 to find cervical intraepithelial neoplasia (grade >/=2 [CIN2+] or grade >/=3 [CIN3+]).

167 ads and the risk of cervical intraepithelial neoplasia grades 2 and 3 (CIN2-3) was evaluated among wo

168 datory reporting of cervical intraepithelial neoplasia grades 2/3 and adenocarcinoma in situ (cervica

169 a history of high-grade anal intraepithelial neoplasia (HGAIN) was associated with a 50% reduction in

170 ncer and high-grade prostate intraepithelial neoplasia (HGPIN).

171 hyperactivation causes hereditary endocrine neoplasias; however, its role in sporadic epithelial can

172 ene could affect the risk of developing this neoplasia hypothesizing a role of TAS2R16 in modulating

173 memory, they also can cause autoimmunity or neoplasia if misdirected or dysregulated.

174 een testicular microlithiasis and testicular neoplasia in a large geographically diverse pediatric po

175 ubjects with IBD undergoing surveillance for neoplasia in Australia (23 with Crohn's colitis, 29 with

176 Ocular surface squamous neoplasia in HIV-positive individuals is aggressive with

177 the development of prostatic intraepithelial neoplasia in mice, demonstrating that JMJD2A can initiat

178 H signaling during development of intestinal neoplasia in mice.

179 egradation of Pten, lung adenocarcinoma, and neoplasia in mouse prostate with aberrantly high levels

180 either ICMT or NOTCH1 accelerates pancreatic neoplasia in Pdx1-Cre;LSL-Kras(G12D) mice, suggesting th

181 Risks for advanced neoplasia in persons at very low, low, intermediate, and

182 ossible risk factors associated with hepatic neoplasia in the white sucker.

183 icular microlithiasis and primary testicular neoplasia in this pediatric population.

184 idence and pathologic severity of colorectal neoplasia in two independent mouse models.

185 development of new approaches for detecting neoplasia in vivo Cancer Res; 76(16); 4637-47.

186 Human colorectal cancer (CRC) is a frequent neoplasia in Western countries, and its metastatic progr

187 A retroviral etiology for malignant neoplasias in koalas has long been suspected.

188 communication between the immune system and neoplasia includes an increasingly complex cellular micr

189 ncluded detection of any adenoma or advanced neoplasia (including CRC) and screening-related harms (i

190 mutant tumors reveals multiple signatures of neoplasia, including altered metabolism and dedifferenti

191 omatic mutations and can initiate intestinal neoplasia, indicating that the crypt base stem cell is n

192 the formation of pancreatic intraepithelial neoplasia induced by mutant Kras(G12D), whereas upregula

193 rveillance mechanism that detects a range of neoplasia-inducing processes.

194 glands, high-grade prostatic intraepithelial neoplasia, invasive adenocarcinoma, or prostate organoid

195 ROUND & AIMS: Intraductal papillary mucinous neoplasias (IPMNs) are precancerous cystic lesions that

196 Prostatic intraepithelial neoplasia is a precursor to prostate cancer.

197 rgical and endoscopic management of duodenal neoplasia is difficult and chemoprevention has not been

198 expression both in prostate intra-epithelial neoplasia lesions as well as malignant adenocarcinoma co

199 cative activity of prostatic intraepithelial neoplasia lesions in the dorsal prostate.

200 M)-a precursor of pancreatic intraepithelial neoplasia lesions that can progress to PDAC.

201 les labeled with a new ligand for colorectal neoplasia, LTTHYKL peptide.

202 in the development of gastrointestinal (GI) neoplasia, made evident from the high degree of associat

203 Neoplasia manifested as transplantable CD8+ lymphoma or

204 Multiple intestinal neoplasia mice were colonized with ETBF for the experime

205 ing oncogene-driven prostate intraepithelial neoplasia (mPIN).

206 perturbed haematopoiesis, myeloproliferative neoplasia (MPN) and leukaemia.

207 ous cell carcinoma or vulvar intraepithelial neoplasia occurred during follow-up in 0 of the complian

208 (MD) is a highly contagious T-cell lymphoid neoplasia of chicken induced by Marek's disease virus (M

209 ecurrent high-grade cervical intraepithelial neoplasia of grade two or worse (CIN2+) and compared it

210 High-grade anal intraepithelial neoplasia or worse (HG-AIN+) was diagnosed in 12.9% (n =

211 ic pancreatitis, pancreatic intra-epithelial neoplasia, or PDAC, as well as hepatic stellate cells (H

212 ions suspected to be ocular surface squamous neoplasia (OSSN) based on the clinical impression.

213 surgical outcomes of ocular surface squamous neoplasia (OSSN) following wide excisional biopsy with a

214 e for distinguishing ocular surface squamous neoplasia (OSSN) from benign conjunctival lesions.

215 Ocular surface squamous neoplasia (OSSN) is an aggressive eye tumour particularl

216 pha2b) treatment for ocular surface squamous neoplasia (OSSN).

217 dysregulated miRNAs specific for colorectal neoplasia (P < 0.05, false discovery rate: 5%, adjusted

218 and 2.4% [95% CI, 1.3% to 3.3%] for advanced neoplasia, P < .001 for both comparisons).

219 and 3.1% [95% CI, 2.0% to 4.1%] for advanced neoplasia, P < .001 for both comparisons; FIT outreach g

220 nd 0.7% [95% CI, -0.2% to 1.6%] for advanced neoplasia, P < .08 and P < .13, respectively), and highe

221 s as early as the pancreatic intraepithelial neoplasia (PanIN) 2 stage.

222 M can progress to pancreatic intraepithelial neoplasia (PanIN) and eventually pancreatic cancer.

223 ominantly through pancreatic intraepithelial neoplasia (PanIN) and intraductal papillary mucinous neo

224 induced in mouse pancreatic intraepithelial neoplasia (PanIN) and pancreatic ductal adenocarcinoma (

225 KRAS, accelerates pancreatic intraepithelial neoplasia (PanIN) formation and the development of invas

226 uctal metaplasia, pancreatic intraepithelial neoplasia (PanIN) formation, and PanIN progression to PD

227 evelop high-grade pancreatic intraepithelial neoplasia (PanIN) lesions and neoplasia accompanied by p

228 early to advanced pancreatic intraepithelial neoplasia (PanIN) lesions, we assessed whether Wnt ligan

229 asia and in early pancreatic intraepithelial neoplasia (PanIN) lesions.

230 for inflammation, pancreatic intraepithelial neoplasia (PanIN), and PDAC.

231 asive precursors, pancreatic intraepithelial neoplasia (PanIN), arise via reprogramming of mature aci

232 n human and mouse pancreatic intraepithelial neoplasia (PanIN), suggesting that N-cadherin may also h

233 the formation of pancreatic intraepithelial neoplasia (PanIN)-derived PDA.

234 nd development of pancreatic intraepithelial neoplasia (PanIN).

235 sion of low-grade pancreatic intraepithelial neoplasia (PanINs), likely through differential expressi

236 features of human pancreatic intraepithelial neoplasia (PanINs), the precursor to pancreatic ductal a

237 duce formation of pancreatic intraepithelial neoplasia (PanINs)-a precursor of PDAC.

238 es (TC) and early pancreatic intraepithelial neoplasia (PanINs).

239 t of premalignant pancreatic intraepithelial neoplasias (PanINs) and cystic lesions in Kras(G12D)-exp

240 metaplasia (ADM), pancreatic intraepithelial neoplasias (PanINs) and ultimately pancreatic ductal ade

241 rms the predisposition of this clade towards neoplasia pathologies already in its basal members.

242 bft gene in mucosal samples from colorectal neoplasia patients (cases, n = 49) to a control group un

243 cluding condyloma and penile intraepithelial neoplasia (PeIN).

244 ice rarely induced prostatic intraepithelial neoplasia (PIN) in dorsal prostates (one out of eight mi

245 Further, prostatic intraepithelial neoplasia (PIN) progressed to carcinoma in rats given ne

246 ce and severity of prostatic intraepithelial neoplasia (PIN), a premalignant lesion.

247 entually developed prostatic intraepithelial neoplasia (PIN).

248 hyperplasia [BPH], prostatic intraepithelial neoplasia [PIN], inflammation, and atrophy) and prostate

249 tise in managing Barrett's esophagus-related neoplasia practicing at centers equipped with high-defin

250 was strongly associated with progression to neoplasia; risk for progression increased greatly when a

251 oncogenic pathways implicated in pancreatic neoplasia, such as MYC, KRAS, VEGFA, and BRD4 Specifical

252 that rats affected by the multiple endocrine neoplasia syndrome MENX, caused by a p27 mutation, devel

253 se (VHL) is one of the most common inherited neoplasia syndromes and is characterized by highly vascu

254 tion, occur more frequently in early colonic neoplasia than previously believed, and identify epigeno

255 d higher grade of pancreatic intraepithelial neoplasias than KC mice, and 1 mouse developed an invasi

256 this gene in a subset of patients with this neoplasia that have poor prognosis.

257 s allows titratable initiation of pancreatic neoplasias that progress into invasive and metastatic PD

258 dendritic melanocytes (hyperplasia or early neoplasia) that generally remain confined to the basal/b

259 cancer cells and pancreatic intraepithelial neoplasia, the early lesion of pancreatic cancer, in a g

260 t zebrafish larval model of Ras(G12V)-driven neoplasia to image the interactions between inflammatory

261 thophysiological progression from APC-mutant neoplasia to submucosal invasive tumor.

262 mmatory signals from Kras-induced pancreatic neoplasia to the CNS.

263 component of the pancreatic intraepithelial neoplasias-to-PDAC route in Kras(G12D)-driven mouse panc

264 suspected, usual-type vulvar intraepithelial neoplasia treatment, including medical and surgical opti

265 Menin, the product of the multiple endocrine neoplasia type 1 (Men1) tumor suppressor gene, mediates

266 Multiple endocrine neoplasia type 1 (MEN1), an autosomal dominant disorder,

267 rt of a syndrome, such as multiple endocrine neoplasia type 1 or hyperparathyroidism-jaw tumor syndro

268 sporadic NETs, and 1 had multiple endocrine neoplasia type 1 syndrome.

269 Multiple endocrine neoplasia type 2 (MEN 2) syndrome is an autosomal domina

270 Patients with multiple endocrine neoplasia type 2 (MEN2) have mutations in the RET protoo

271 (MTC) and pathogenesis of multiple endocrine neoplasia type 2 (MEN2).

272 RET, were found to cause multiple endocrine neoplasia type 2, a dominant inherited cancer syndrome t

273 ine RET mutations causing multiple endocrine neoplasia type 2.

274 the following phenotypes: multiple endocrine neoplasia type 2A (MEN 2A) and multiple endocrine neopla

275 asia type 2A (MEN 2A) and multiple endocrine neoplasia type 2B (MEN 2B) syndromes.

276 enesis in the syndrome of multiple endocrine neoplasia type-1 (MEN1).

277 BACKGROUND & AIMS: The multiple endocrine neoplasia, type 1 (MEN1) locus encodes the nuclear prote

278 s in a second model of toxin-induced hepatic neoplasia, using DEN and 3,3',5,5'-tetrachloro-1,4-bis(p

279 ded VSCC and adjacent vulvar intraepithelial neoplasia (VIN) and VLS specimens, in cancer-free VLS (c

280 n the derivation set, prevalence of advanced neoplasia was 9.4%.

281 Neoplasia was diagnosed within 3 years of neurologic ons

282 ociation between dyslipidemia and colorectal neoplasia was observed for hypertriglyceridemia.

283 formation, whereas no evidence of pancreatic neoplasia was observed for up to 6 months following Kras

284 dation set, corresponding risks for advanced neoplasia were 1.65% (CI, 0.20% to 5.84%), 3.31% (CI, 2.

285 Importantly, no iDPs-derived astrocytes and neoplasia were detected in mouse brains after transplant

286 sitive predictive values (PPVs) for advanced neoplasia were determined weekly, quarterly, and yearly.

287 Patients with multiple endocrine neoplasia were excluded.

288 No differences in OS or second neoplasias were observed in in both trials.

289 In both trials, no differences in second neoplasias were observed.

290 All cancers (except EBV-related neoplasia) were recorded.

291 hematopoiesis, and cervical intraepithelial neoplasia which also serve as models for inherited syndr

292 ve paucity of such knowledge in premalignant neoplasia, which inherently limits the potential to deve

293 oma and 2 for intraductal papillary mucinous neoplasia), while the remaining 35 are under continued s

294 terozygous rb1-/+ adults show no evidence of neoplasia, while homozygous mutant rb1-/- are larval let

295 cial interest in Barrett's esophagus-related neoplasia who is recognized as an expert in this field b

296 stiocytosis (LCH) is an inflammatory myeloid neoplasia with a broad spectrum of clinical manifestatio

297 reatment of mice carrying RZ(-/-) intestinal neoplasia with a small molecule Wnt secretion inhibitor

298 sents a potential therapeutic for colorectal neoplasia with comparable therapeutic efficacy to rapamy

299 esions (high-grade prostatic intraepithelial neoplasia) with striking nuclear atypia and invasive, po

300 The drivers of neoplasia within low-grade luminal breast cancers remain