ライフサイエンスコーパス: IPMN

1 IPMN profiles showed significant lipid pathway alteratio

2 IPMNs involving the MPD harbor a high likelihood of mali

3 IPMNs of the pancreas are estimated to have a better pro

4 IPMNs represent an increasing indication for pancreatic

5 alysis, NLR value higher than 4 (P < 0.001), IPMN cyst of size more than 3 cm (P < 0.001), presence o

6 Ten of 13 IPMNs with moderate dysplasia or malignancy had loss of

7 overy set of 18 surgical samples (11 PDAC, 4 IPMN, 3 C).

8 Set 1-52 surgical samples (24 PDAC, 7 IPMN, 6 chronic pancreatitis, 15 C), and set 2-95 endosc

9 d-guided fine-needle aspirations (60 PDAC, 9 IPMN, 26 C).

10 isplayed detectable chromosomal aberrations, IPMNs with moderate and high-grade dysplasia showed freq

11 f life-long follow-up after resection for an IPMN.

12 ndent risk factors for the development of an IPMN with HGD or an invasive carcinoma in the remnant pa

13 A, invasive adenocarcinoma arising within an IPMN was associated with a lower incidence of (1) advanc

14 biologic and clinical behavior of IPMNs and IPMN-associated adenocarcinomas is different from PDAC i

15 miRNome analysis shows that PDAC and IPMN have differential miRNA profiles with respect to C,

16 ssion is significantly increased in PDAC and IPMN lesions.

17 s were significantly deregulated in PDAC and IPMN versus C.

18 RNAs commonly overexpressed in both PDAC and IPMN were selected for further validation.

19 overall accuracy rate of 92% between SCA and IPMN.

20 SPNs are low-grade malignancies, and IPMNs and MCNs, but not SCAs, have the capacity to progr

21 intraductal papillary mucinous neoplasm (BD IPMN; 67%), whereas also being specific (85 and 88%, res

22 in mucinous cysts, particularly in small BD IPMN.

23 ohort was 68 years, 56% had branch duct (BD)-IPMN and 21% had invasive cancers.

24 BD-IPMN patients are at risk of pancreatic carcinogenesis.

25 o main-duct (MD-IPMN) versus branch-duct (BD-IPMN).

26 eatic and extrapancreatic malignancies in BD-IPMN patients.

27 Invasive cancer arising in BD-IPMN was found in 23 patients of the entire cohort (4%),

28 owever, was similar between institutions (BD-IPMN: P = 0.36, MD-IPMN: P = 0.48).

29 y about surgery of branch-duct type IPMN (BD-IPMN).

30 than 3 cm and in 25% of "Sendai-negative" BD-IPMN.

31 Recurrence of noninvasive BD-IPMN is infrequent and surveillance may be avoided in se

32 Expectant management of BD-IPMN following the old guidelines is safe, whereas cauti

33 uring the study period, the percentage of BD-IPMN resected with >=1 high-risk feature increased (52%

34 ver the 15-year study period, the rate of BD-IPMN resected with high-risk radiographic features incre

35 carcinoma or carcinoma in situ in 67% of BD-IPMN smaller than 3 cm and in 25% of "Sendai-negative" B

36 The diagnosis of BD-IPMN was based on the presence of unilocular or multiloc

37 The percentage of BD-IPMN with >=1 high-risk radiographic feature differed be

38 d worrisome features in the management of BD-IPMN.

39 m 577 patients with suspected or presumed BD-IPMN under surveillance at the Massachusetts General Hos

40 o the revised guidelines, 76% of resected BD-IPMN with carcinoma in situ and 95% of resected BD-IPMN

41 ith carcinoma in situ and 95% of resected BD-IPMN with invasive cancer had high-risk stigmata or worr

42 In 33 patients (9%), a residual BD-IPMN was left in the pancreatic remnant, but none of the

43 , 205 mixed-type (40%), and 233 suspected BD-IPMN (46%).

44 No patient developed unresectable BD-IPMN carcinoma during follow-up.

45 Patients with BD-IPMN are not at risk of extrapancreatic carcinogenesis.

46 ive database identified 563 patients with BD-IPMN.

47 imaging, many IPMNs are misclassified as BD-IPMNs but reveal mixed-type lesions in histopathology.

48 s are not sufficient to reliably diagnose BD-IPMNs, surgical resection for suspected small branch-duc

49 Of 141 Sendai negative BD-IPMNs, a malignancy rate of 18% (high-grade dysplasia an

50 intraductal papillary mucinous neoplasms (BD-IPMNs).

51 alignancy and define a subset of low-risk BD-IPMNs.

52 Most interesting, 29% of suspected BD-IPMNs (67/233) revealed histological involvement of the

53 tcomes of a large cohort of patients with BD-IPMNs to determine risk of malignancy and define a subse

54 a retrospective analysis of patients with BD-IPMNs under surveillance, their overall risk of malignan

55 ardized incidence ratio for patients with BD-IPMNs without worrisome features of malignancy at 5 year

56 rant surgical removal from 'indolent/benign' IPMNs that can be observed.

57 tegrated data modeling discriminated between IPMN and SCN with 100% accuracy and distinguished IPMN L

58 vocally establish it as a suppressor of both IPMNs and MCNs.

59 volutionary analyses, we establish that both IPMNs and MCNs are direct precursors to pancreatic cance

60 pancreatitis, 13 with low-grade side-branch IPMNs, and 15 patients with PDAC; histologically normal

61 cins and have characteristics of side-branch IPMNs.

62 IPMN with an associated invasive carcinoma (IPMN-INV).

63 s the first to use array CGH to characterize IPMNs.

64 t a resection for PDAC and had a concomitant IPMN.

65 efinitive pathological examination confirmed IPMN diagnosis in 95% of patients (n = 77), all except 2

66 gical resection for histologically confirmed IPMN from January 1997 to July 2015.

67 ma from a cohort of pathologically-confirmed IPMN cases of various grades of severity and non-disease

68 (G12D);Pten(DeltaDuct/+) mice, 70% developed IPMN, predominately of the pancreatobiliary subtype, and

69 Pten(DeltaDuct/DeltaDuct) mice developed IPMNs of several subtypes.

70 RNAs (GAS5 and SRA) aided in differentiating IPMNs from controls.

71 and SCN with 100% accuracy and distinguished IPMN LGD or IPMN HGD and invasive cancer with up to 90.0

72 cal features that are similar to branch duct IPMN.

73 d patients with Fukuoka-negative branch-duct IPMN or pancreatic cancer.

74 al resection for suspected small branch-duct IPMN should be considered in patients fit for surgery.

75 ht loss, interval (from isolated branch-duct IPMN) to MPD involvement, diffuse MPD dilation, increase

76 3%), and arose in the setting of a main duct IPMN (96%).

77 idelines, which include redefining main duct IPMN and removing the recommendation for surgical resect

78 ed-type IPMN, and 82 patients with main-duct IPMN alone.

79 N) recommend surgical treatment in main-duct IPMN patients with a main pancreatic duct (MPD) diameter

80 Although many branch-duct IPMNs are small and asymptomatic, they harbor a signific

81 who were surgically resected for branch-duct IPMNs between January 2004 and July 2010 at the Universi

82 the current Sendai criteria for branch-duct IPMNs need to be adjusted.

83 believe that both main-duct and branch-duct IPMNs represent premalignant lesions.

84 onsecutively resected IPMNs, 123 branch-duct IPMNs were identified analyzing preoperative imaging.

85 Some 69 branch-duct IPMNs were less than 3 cm in size, without mural nodules

86 Of all the Sendai negative branch-duct IPMNs, 24.6% (17/69) showed malignant features (invasive

87 Main-duct IPMNs with a MPD between 5 and 9 mm already bear a signi

88 tic subunit of the SWI/SNF complexes, during IPMN-PDA development.

89 Six of the eight IPMNs and three of the eight MCNs harbored mutations of

90 ement of CFIMs may be a surrogate marker for IPMN progression and allow for the identification of hig

91 component and resection margin positive for IPMN were predictors of recurrence (P < 0.05).

92 a on recurrence after surgical resection for IPMN are currently lacking.

93 otal of 223 patients underwent resection for IPMN involving the MPD.

94 Fifty-nine patients underwent resection for IPMN with an associated invasive carcinoma (IPMN-INV).

95 haracteristics, outcomes after resection for IPMN-associated and standard PDA were not significantly

96 5-year survival was 42% after resection for IPMN-associated versus 19% for standard PDA (P < 0.001).

97 avoids inappropriate standard resections for IPMN-mimicking lesions.

98 nsecutive patients who underwent surgery for IPMN between January 2004 and December 2012 were include

99 al of 605 patients who underwent surgery for IPMN, there were 320 patients with MPD involvement, 238

100 whether PDGs are a precursor compartment for IPMNs and the role of Trefoil factor family 2 (TFF2)-a p

101 All patients operated on for IPMNs between January 1, 2007, and December 31, 2012, wi

102 ic screening of 272 patients operated on for IPMNs revealed 1 patient with axial and peripheral polyo

103 from 4 high-volume centers were queried for IPMNs, with invasive components measuring 20 mm or less.

104 cells undergo "ductal retrogression" to form IPMN-PDA.

105 We aimed to identify cells that form IPMNs and mutations that promote IPMN development and pr

106 tic cyst fluid and pre-operative plasma from IPMN and serous cystic neoplasm (SCN) patients in a panc

107 In this study, we analyze 148 samples from IPMNs, MCNs, and small associated invasive carcinomas fr

108 history of pancreatic cancer and high-grade IPMN was identified as risk factors for recurrence in bo

109 arkably, TP53INP1 is down-regulated in human IPMN.

110 metaplasia of the PDG, which resembled human IPMN; these expressed gastric mucins (MUC5AC and MUC6),

111 so observed progressive loss of p16 in human IPMNs of increasing grades.

112 In histologic analyses of human IPMNs, we found PDGs to form the basal segment and possi

113 h histologic and molecular features of human IPMNs.

114 lity as a diagnostic adjunct for identifying IPMNs and their pathology, especially when incorporated

115 surveillance so as not to overlook cancer in IPMN.

116 ncies (EPMs) occur with unusual frequency in IPMN patients.

117 Targeted-NGS on genes commonly mutated in IPMN and PDAC was performed on tumors from (1) 13 patien

118 majority of proteins were down-regulated in IPMN and MCN compared with SCA.

119 l subtypes of invasive carcinomas arising in IPMNs have been described, colloid carcinoma and tubular

120 gh-grade dysplasia and invasive carcinoma in IPMNs with MPD involvement was 68%.

121 gly associated with malignant progression in IPMNs.

122 study to evaluate the significance of UDD in IPMNs and shows it to be a high-risk feature.

123 5-year survival of patients with intestinal IPMNs was significantly better than pancreatobiliary IPM

124 Invasive IPMN recurred in 45% of cases, whereas noninvasive in on

125 In invasive IPMN recurrence depends on N status, pancreatic margin,

126 ter the surgical resection of a non-invasive IPMN.

127 d carcinoma histological subtype of invasive IPMN had a more statistically favorable survival outcome

128 ed the regions with and without the invasive IPMN (control tissue) by immunohistochemistry.

129 Of the 11 patients with invasive IPMN (inv/HG), 9 had high MUC5AC expression in plasma EV

130 Of the 67 invasive IPMNs, 39 were tubular carcinomas (58%) and invasion was

131 Among invasive IPMNs, the majority (58%) were mixed-type lesions accord

132 aDuct/DeltaDuct) mice all developed invasive IPMNs within 1 month.

133 together, these data establish non-invasive IPMNs and MCNs as origins of invasive pancreatic cancer,

134 recommend surgical resection of MPD-involved IPMN in fit patients.

135 As such, the natural history of MPD-involved IPMN is poorly understood.

136 res in distinguishing 'aggressive/malignant' IPMNs that warrant surgical removal from 'indolent/benig

137 By abdominal imaging, many IPMNs are misclassified as BD-IPMNs but reveal mixed-typ

138 eoplasms (IPMNs) involving the main duct (MD IPMNs) or the main and branch ducts (mixed IPMNs) of the

139 MD-IPMN is mainly intestinal-type and malignant.

140 between institutions (BD-IPMN: P = 0.36, MD-IPMN: P = 0.48).

141 Patients were categorized into main-duct (MD-IPMN) versus branch-duct (BD-IPMN).

142 For MD-IPMN, there was not a clear trend towards guideline adhe

143 to preoperative imaging, 74 patients had MD-IPMN (14%), 205 mixed-type (40%), and 233 suspected BD-I

144 In MD-IPMN cohort, the presence of radiographic features such

145 on has led to a redefinition of MPD IPMN (MD-IPMN).

146 Retrospective review of resected MD-IPMN from 1990 to 2013.

147 eveloped clinically significant metachronous IPMNs.

148 ents undergoing resection for an MD or mixed IPMN (59 men [57.3%]; 44 women [42.7%]; median [range] a

149 for a preoperative diagnosis of MD or mixed IPMN and in whom IPMN was confirmed by surgical patholog

150 factor for malignant disease in MD or mixed IPMN.

151 D IPMNs) or the main and branch ducts (mixed IPMNs) of the pancreatic system is a main pancreatic duc

152 ment algorithm for patients with MD or mixed IPMNs.

153 In all models, IPMNs and PDAC expressed the duct-specific lineage traci

154 r exclusion has led to a redefinition of MPD IPMN (MD-IPMN).

155 ss the clonal relationships among multifocal IPMNs.

156 ts with histologically documented multifocal IPMNs were collected and their clinicopathologic feature

157 ts with histologically documented multifocal IPMNs.

158 A majority of multifocal IPMNs (86% synchronous, 100% metachronous) were composed

159 The majority of multifocal IPMNs arise independently and exhibit a gastric-foveolar

160 In addition, thirty multifocal IPMNs arising in 13 patients from 3 hospitals were subje

161 Molecular analysis of multiple IPMNs from 13 patients demonstrated nonoverlapping KRAS

162 ived from an intestinal subtype GNAS-mutated IPMN.

163 : Intraductal papillary mucinous neoplasias (IPMNs) are precancerous cystic lesions that can develop

164 of intraductal papillary mucinous neoplasm (IPMN) and mucinous cystic neoplasm were updated in 2012,

165 BD) intraductal papillary mucinous neoplasm (IPMN) espouse safety of observation of asymptomatic cyst

166 ved intraductal papillary mucinous neoplasm (IPMN) has been established by surgical series.

167 BD) intraductal papillary mucinous neoplasm (IPMN) is infrequent and that extrapancreatic malignancie

168 of intraductal papillary mucinous neoplasm (IPMN) of the pancreas.

169 and intraductal papillary mucinous neoplasm (IPMN) precursor lesions.

170 man intraductal papillary mucinous neoplasm (IPMN) specimens were analyzed by immunohistochemistry.

171 ing intraductal papillary mucinous neoplasm (IPMN) were observed as early as 2 months of age.

172 ion intraductal papillary mucinous neoplasm (IPMN), to find new microRNA (miRNA)-based biomarkers for

173 for intraductal papillary mucinous neoplasm (IPMN).

174 ith intraductal papillary mucinous neoplasm (IPMN).

175 ts (intraductal papillary mucinous neoplasm [IPMN], mucinous cystic neoplasm [MCN]).

176 ed intraductal papillary mucinous neoplasms (IPMN) of the pancreas with respect to risk factors of ma

177 of intraductal papillary mucinous neoplasms (IPMN) recommend surgical treatment in main-duct IPMN pat

178 ic intraductal papillary mucinous neoplasms (IPMN) using targeted next-generation sequencing (NGS).

179 4 intraductal papillary mucinous neoplasms (IPMN), 2 adenocarcinomas, 1 low-grade intraepithelial pa

180 ic intraductal papillary mucinous neoplasms (IPMN).

181 ), intraductal papillary mucinous neoplasms (IPMN, n = 20), and ampulla of Vater carcinomas (AVC, n =

182 in intraductal papillary mucinous neoplasms (IPMNs) and in McCune-Albright syndrome, characterized by

183 Intraductal papillary mucinous neoplasms (IPMNs) and mucinous cystic neoplasms (MCNs) are non-inva

184 as intraductal papillary mucinous neoplasms (IPMNs) and predictors of their pathology/histological cl

185 s, Intraductal Papillary Mucinous Neoplasms (IPMNs) are common lesions that may progress from low-gra

186 Intraductal papillary mucinous neoplasms (IPMNs) are the most frequent cystic pancreatic tumors.

187 of intraductal papillary mucinous neoplasms (IPMNs) involving the main duct (MD IPMNs) or the main an

188 g, Intraductal Papillary Mucinous Neoplasms (IPMNs) of the pancreas are identified with increasing fr

189 th intraductal papillary mucinous neoplasms (IPMNs) of the pancreas.

190 of intraductal papillary mucinous neoplasms (IPMNs), and their management remains controversial.

191 ), intraductal papillary mucinous neoplasms (IPMNs), mucinous cystic neoplasms (MCNs), and solid pseu

192 ct intraductal papillary mucinous neoplasms (IPMNs).

193 ion of IPMN may include development of a new IPMN or ductal adenocarcinoma (PDAC).

194 on-invasive progression was defined as a new IPMN, increased main pancreatic duct (MPD) size, and inc

195 SCA (n = 15), non main-duct and noninvasive IPMN (n = 32), and noninvasive MCN (n = 12) was aspirate

196 nts that underwent resection for noninvasive IPMN were followed for a median of 9.5 years.

197 ients who underwent resection of noninvasive IPMN were reviewed to identify risk factors associated w

198 ected patients, PSP for presumed noninvasive IPMN in experienced hands is highly feasible and avoids

199 insufficiency, and may overtreat noninvasive IPMNs.

200 ted in 91 patients with presumed noninvasive IPMNs, after complete preoperative work-up including com

201 nalysis of the 260 patients with noninvasive IPMNs showed that family history of pancreatic cancer (P

202 G cells and their overlying nonproliferative IPMN cells.

203 The favorable biologic behavior of IPMN-associated compared with standard PDA is based on i

204 tients resected for an invasive component of IPMN were analyzed with detailed pathologic review of hi

205 ergistic effects in promoting development of IPMN and progression to PDAC.

206 or cyst fluid can improve discrimination of IPMN from SCN and within PMNs predict the grade of dyspl

207 Accurate discrimination of IPMN-associated neoplastic grade is an unmet clinical ne

208 Evaluation of IPMN subtypes supports postoperative patient prognosis p

209 sm of neoplastic cells with the expansion of IPMN lesions in Acvr1b(flox/flox);LSL-KRAS(G12D);Pdx1-Cr

210 and histologically analyzed for formation of IPMN, pancreatic intraepithelial neoplasias, and PDAC, i

211 observed that the behavior and management of IPMN and adenocarcinoma in the pancreas graft appears co

212 Surgical management of IPMN based on radiographic criteria is variable between

213 r, underlining its role in the occurrence of IPMN and highlighting the importance of TP53INP1 in the

214 endent predictive marker for the presence of IPMN-associated invasive carcinoma.

215 point system for estimating the presence of IPMN-associated invasive carcinoma.

216 imply a tendency for earlier presentation of IPMN-associated invasive adenocarcinoma.

217 ve data protocol) with histological proof of IPMN who underwent surgery between January 2004 and Dece

218 atic surgery and had a histological proof of IPMN.

219 the remnant pancreas following resection of IPMN may include development of a new IPMN or ductal ade

220 owever, survival outcomes after resection of IPMN-associated and after resection of standard pancreat

221 The 5-year survival after resection of IPMN-associated invasive adenocarcinoma is reported to b

222 the remnant pancreas following resection of IPMN; and (2) 10 patients who underwent a resection for

223 atients who were free of them at the time of IPMN diagnosis.

224 In Pten(DeltaDuct/DeltaDuct) mice, 31.5% of IPMNs became invasive; invasion was associated with spon

225 The biologic and clinical behavior of IPMNs and IPMN-associated adenocarcinomas is different f

226 International consensus guidelines of IPMNs still consider it as a branch-duct, even though it

227 e found evidence for a ductal cell origin of IPMNs.

228 p16 (Cdkn2a) was required for progression of IPMNs to pancreatic ductal adenocarcinomas in Acvr1b(flo

229 activation on initiation and progression of IPMNs.

230 ch duct types), the histological subtypes of IPMNs (ie, intestinal, pancreatobiliary, gastric, and on

231 All subtypes of IPMNs display a relevant risk for malignant transformati

232 later (P < 0.001), but patterns depended on IPMN subtypes.

233 long-term outcome particularly for oncocytic IPMNs.

234 ved between MPD diameter and clinical and/or IPMN features such as age, cyst location, mural nodules,

235 100% accuracy and distinguished IPMN LGD or IPMN HGD and invasive cancer with up to 90.06% accuracy.

236 relationship between the margin and original IPMN using driver gene mutations identified by next-gene

237 the margin was independent from the original IPMN in at least 9 of 32 cases (28%).

238 apillary mucinous neoplasms of the pancreas (IPMN) by histological subtype of the invasive component

239 tes growth of mutant KRAS-induced pancreatic IPMNs in mice; this process appears to involve NOTCH4 an

240 re mice accelerated the growth of pancreatic IPMNs compared with LSL-KRAS(G12D);Pdx1-Cre mice, but di

241 und that the invasive human pancreatobiliary IPMN tissue had lower levels of PTEN and increased level

242 a patient with an invasive pancreatobiliary IPMN and analyzed the regions with and without the invas

243 s significantly better than pancreatobiliary IPMNs (86.6% vs. 35.6%; P < 0.001).

244 165) were obtained from patients with PDAC, IPMN, or from control individuals (C), from Hospital Cli

245 imaging features, the accuracy of predicting IPMN pathological classification improved.

246 Patients with a primary IPMN with HGD or with positive family history are at an

247 s that form IPMNs and mutations that promote IPMN development and progression.

248 ations in GNAS have been reported to promote IPMN formation.

249 Recently, IPMNs have been described as a McCune-Albright syndrome-

250 with an aggressive phenotype even in remote IPMN lesions.

251 This association persisted for remote IPMNs limited to the dorsal pancreas, suggesting UDD may

252 al (MGH) databases were queried for resected IPMN (2000-2015).

253 ld have increased the percentage of resected IPMN with high-risk disease.

254 were identified, comprising 25% of resected IPMN-associated carcinomas (n = 280).

255 Retrospective review of 412 resected IPMNs from 1990 to 2013 who have had near-complete follo

256 We evaluated 78 resected IPMNs (2004-2013).

257 Among a total of 287 consecutively resected IPMNs, 123 branch-duct IPMNs were identified analyzing p

258 449 consecutive patients with resected IPMNs from 1995-2018 were included to the study.

259 es have been developed to identify high-risk IPMN.

260 o distinguish between indolent and high risk IPMNs.

261 We found that SCAs, IPMNs, MCNs, and SPNs contained 10 +/- 4.6, 27 +/- 12, 1

262 A total of 70 small IPMN-associated invasive carcinomas (</=20-mm invasion)

263 i-institutional experience of resected small IPMN-associated carcinoma.

264 atients operated on for presumptive sporadic IPMNs.

265 Synchronous IPMNs were present in 29 patients (85%), whereas 5 (15%)

266 Three synchronous IPMNs (10%) had an associated invasive cancer.

267 providing additional evidence of a syndromic IPMN as a feature of McCune-Albright syndrome, this obse

268 Benign neoplasms most frequent in the IPMN group were colonic polyps (n = 114) and Barrett's n

269 patients (17%) experienced recurrence of the IPMN, and 5- and 10-year disease-free survival (DFS) was

270 In this study, we analyzed the IPMNs from 2 pancreatic cancer referral centers by corre

271 While none of the IPMNs with low-grade dysplasia displayed detectable chro

272 One hundred ninety-three IPMN patients (38%) suffered from invasive carcinoma.

273 trospective review of all surgically treated IPMNs at our institution after 2008 was performed.

274 Patients with invasive tubular IPMN had no statistically significant difference in surv

275 ontroversy about surgery of branch-duct type IPMN (BD-IPMN).

276 lysis of human samples revealed gastric-type IPMN to comprise 2 molecularly distinct layers: a basal

277 Primary surveillance of mixed-type IPMN may be a reasonable strategy in select patients.

278 PD involvement, 238 patients with mixed-type IPMN, and 82 patients with main-duct IPMN alone.

279 urveillance, 70 for MPD-involved, mixed-type IPMN.

280 patients with asymptomatic branch-duct type IPMNs of the pancreas less than 3 cm in diameter without

281 us that main-duct (MD) as well as mixed-type IPMNs should be treated surgically due to a high risk of

282 ve diagnosis of MD or mixed IPMN and in whom IPMN was confirmed by surgical pathologic findings at a

283 ive patients were identified, 132 (10%) with IPMN-associated invasive adenocarcinoma and 1128 (90%) w

284 d imaging data for possible correlation with IPMN-associated carcinoma in the form of a predictive no

285 Patients with IPMN have increased risk of harboring extrapancreatic ne

286 he management and follow-up of patients with IPMN including avoiding unnecessary surgery.

287 re be used in the diagnosis of patients with IPMN or in monitoring disease progression.

288 lected database (1992-2012) of patients with IPMN undergoing primary surveillance was performed.

289 A total of 503 patients with IPMN underwent primary surveillance, 70 for MPD-involved

290 d GNAS mutations in cfDNA from patients with IPMN, but not in patients with serous cystadenoma or con

291 f extrapancreatic neoplasms in patients with IPMN, but these studies focused only on those patients w

292 were significantly elevated in patients with IPMN-associated invasive carcinoma (P < 0.001).

293 py should be considered in all patients with IPMN.

294 us or synchronous neoplasms in patients with IPMN.

295 Cases with IPMNs were identified, and the subtypes were distinguish

296 e some histologic and clinical features with IPMNs of the pancreas, and may represent a carcinogenesi

297 detect lncRNAs in plasma from patients with IPMNs and suggest that an lncRNA-based blood test may ha

298 Subgroup analysis on patients with IPMNs confined to the dorsal portion of the gland (n = 1

299 om peripheral blood drawn from patients with IPMNs.

300 ct the presence of invasive carcinoma within IPMN.