ライフサイエンスコーパス: poorly-differentiated

1 rs that are characterized as morphologically poorly differentiated.

2 , while 14 (15.1%) cases were categorized as poorly differentiated.

3 epithelioid and sarcomatous components), or poorly differentiated.

4 ned antigrowth activity of genistein against poorly differentiated 253J B-V human bladder cancer cell

5 kidney tubular epithelia of KO animals were poorly differentiated, a phenotype reminiscent of human

6 (S175A)-expressing cells formed enlarged and poorly differentiated acini.

7 and natural killer (NK) cells compared with poorly differentiated adenocarcinoma observed in untreat

8 The surgical pathology showed a poorly differentiated adenocarcinoma with signet ring ce

9 Tumors from these mice were poorly differentiated adenocarcinoma, characterized by e

10 Treatment with progesterone did not mitigate poorly differentiated adenocarcinoma, nor did it affect

11 well-differentiated adenocarcinoma, WD; and poorly differentiated adenocarcinoma, PD], the expressio

12 differentiated adenocarcinoma; and grade 5, poorly differentiated adenocarcinoma.

13 SIRT1 expression was increased in mice with poorly differentiated adenocarcinomas and in human prost

14 IRT1 was significantly elevated in mice with poorly differentiated adenocarcinomas compared with thos

15 Poorly differentiated, aggressive cancers often overexpr

16 Poorly differentiated anal neuroendocrine carcinomas (AN

17 r (PTC) was diagnosed in 97% of patients and poorly differentiated/anaplastic TC in 1.1%.

18 Jarid2, like Ezh2, is present in poorly differentiated and actively dividing cells, while

19 r cancers, CD73 is markedly downregulated in poorly differentiated and advanced-stage endometrial car

20 s-c-myc transgene, which on its own produced poorly differentiated and aggressive tumors.

21 ors that metastasized, five of six that were poorly differentiated and all that were assigned a Gleas

22 genes identified in a large series of human poorly differentiated and anaplastic thyroid cancers scr

23 RN-ALK was found with a higher prevalence in poorly differentiated and anaplastic thyroid cancers, an

24 High CYP24A1 protein levels were seen in poorly differentiated and highly advanced stages of pros

25 tein in the tumor cells in 10 of 45 cases of poorly differentiated and highly aggressive carcinoma wi

26 Most notably, forced claudin-7 expression in poorly differentiated and highly metastatic SW620 colon

27 These tumors were highly vascularized, poorly differentiated and invasive and loss of expressio

28 reas no expression of MICA/B was detected in poorly differentiated and invasive colorectal tumors tha

29 nt decrease of PTPRM transcripts was seen in poorly differentiated and moderately differentiated tumo

30 8)Ga-DOTATOC appears promising especially in poorly differentiated and oxyphilic subtypes of DTC.

31 ferentiated human SCCs, Smad2-/- tumors were poorly differentiated and underwent epithelial-mesenchym

32 ion was further elevated with progression to poorly differentiated and undifferentiated carcinoma.

33 prevalence in tall-cell variant PTCs and in poorly differentiated and undifferentiated carcinomas ar

34 metastatic tumors, with the remainder being poorly differentiated and undifferentiated primary cance

35 tissue of origin determination restricted to poorly differentiated and undifferentiated primary cance

36 found to be slightly lower than that of the poorly differentiated and undifferentiated primary tumor

37 Poorly-differentiated and well-differentiated cancer cel

38 expressing wild-type ADAM9 had predominantly poorly differentiated, and in some cases significantly l

39 l-differentiated, moderately differentiated, poorly differentiated, and localized endometrial cancer

40 rm significantly larger, hyperproliferative, poorly differentiated, and locally invasive tumors in nu

41 atients have been found to have larger, more poorly differentiated, and more hormonally insensitive t

42 Histologically, such cancers are poorly differentiated, and most fall into the basal subg

43 HPV-positive cancers are frequently poorly differentiated, and the HPV life cycle depends up

44 illary, 2 follicular, 8 Hurthle cell, and 13 poorly differentiated) approximately 5 d after the thera

45 the nonproductive stage, which arises in the poorly differentiated basal epithelial compartment of a

46 emonstrate that flow cytometric detection of poorly differentiated basal tumor cells (BTCs), as defin

47 lear plasmid in proliferating populations of poorly differentiated (basal-like) human keratinocytes a

48 In contrast, the HPV16 LCR from poorly differentiated, basal cell-like cells contained m

49 However, SUVauto poorly differentiated between responding and nonrespondi

50 ectodermal tumors (CNS-PNET) are aggressive, poorly differentiated brain tumors with limited effectiv

51 asion and induced an epithelial phenotype in poorly differentiated breast cancer cells.

52 breast epithelium and loss of alpha2beta1 in poorly differentiated breast cancer.

53 ated during lactation, and is upregulated in poorly differentiated breast cancer.

54 richment Analysis (GSEA), we discovered that poorly differentiated breast cancers are enriched for th

55 a genotype was significantly associated with poorly-differentiated breast tumors (p = 0.04) in combin

56 ivision cycle 25C (CDC25C) overexpression in poorly differentiated BTCs and determined that CDC25C ex

57 displayed enlarged shoot meristems, open and poorly differentiated buds, and a higher rate of cell di

58 fferentiated cancer (WDC) but not late-stage poorly differentiated cancer (PDC).

59 differentiated PDA but resist progression to poorly differentiated cancer compared with KPC control m

60 t solid tumors, HCCs are believed to contain poorly differentiated cancer stem cell-like cells (CSCs)

61 cified subset analysis, PADT use in men with poorly differentiated cancer was associated with improve

62 ant lesions, well-differentiated cancer, and poorly differentiated cancer.

63 Poorly-differentiated cancer cells were generally more r

64 levels of monoamine oxidase A expression and poorly differentiated cancers by immunohistochemistry.

65 and protein level was almost undetectable in poorly differentiated cancers compared with the moderate

66 Patients with poorly differentiated cancers having more than 11 pelvic

67 26; P < .0001) compared with patients having poorly differentiated cancers with 11 or fewer nodes rem

68 For pN0M0 moderately and poorly differentiated cancers, and all node-positive (pN

69 highly expressed during embryogenesis and in poorly differentiated cancers, and high levels portend a

70 were younger, more often had larger or more poorly differentiated cancers, had more comorbid illness

71 sion, whereas this ratio was reversed in the poorly differentiated cancers.

72 -moderately differentiated PDACs but weak in poorly differentiated cancers.

73 and completely prevented its progression to poorly differentiated carcinoma (74% incidence in contro

74 grade prostatic intraepithelial neoplasia to poorly differentiated carcinoma at a greatly accelerated

75 Reduction of Snail expression in a poorly differentiated carcinoma cell line by RNA interfe

76 Decreased expression of beta1-subunit in poorly differentiated carcinoma cell lines correlated wi

77 Here, we report that poorly differentiated carcinoma cell lines derived from

78 of the dorsolateral prostate occupied by the poorly differentiated carcinoma were significantly lower

79 The poorly differentiated carcinoma with t(15;19)(q13, p13.1

80 imilar regardless of histology (small-cell v poorly differentiated carcinoma) or primary site.

81 r progression of prostate tumorigenesis into poorly differentiated carcinoma.

82 ted carcinoma and in almost all cells of the poorly differentiated carcinoma.

83 ures, 83% areas of invasion, and 48% foci of poorly differentiated carcinoma.

84 ) with striking nuclear atypia and invasive, poorly differentiated carcinoma.

85 follicular carcinomas), in 16 (55.2%) of 29 poorly differentiated carcinomas (PDCs), and in 15 (51.7

86 arly papillomatogenesis and rapidly produced poorly differentiated carcinomas (pdSCCs) with high BrdU

87 mplifying compartment that progresses to the poorly differentiated carcinomas that arise rapidly afte

88 Histologically, these tumors are poorly differentiated carcinomas with occasional cysts a

89 overexpressing Bmi-1 and H-Ras, which formed poorly differentiated carcinomas with spindle cell featu

90 ut its expression is dramatically reduced in poorly differentiated carcinomas, a finding that paralle

91 oiter and invasive PTC, which transitions to poorly differentiated carcinomas.

92 MCF10A-Kras-shHOXA5 cells formed aggressive, poorly differentiated carcinomas.

93 Overexpression of miR-215 in poorly differentiated cell lines causes a decrease in cl

94 concentrated at the luminal edge, whereas in poorly differentiated cells polarity is inverted and exp

95 ptotic pathway prevents the removal of these poorly differentiated cells, resulting in the retention

96 rapeutic strategies for patients affected by poorly differentiated CNS tumors.

97 The poorly differentiated cognate amino acid-binding site in

98 Loss of CDX2 expression is seen in some poorly differentiated colon carcinomas in humans.

99 induced) colitis promoted the development of poorly differentiated colonic adenocarcinoma in mice lac

100 ost with increasing mesenchymal phenotype in poorly differentiated CRC cell lines as a consequence of

101 tiated CRC cells and FOXA1 overexpression in poorly differentiated CRC cells, we identified novel pro

102 expression due to Cdx-1 loss is a feature of poorly differentiated CRCs.

103 ovide a therapeutic benefit, particularly in poorly differentiated cSCC.

104 cantly fewer aberrations than moderately and poorly differentiated cSCCs; yet, despite a lower rate o

105 Improved survival was also observed in poorly differentiated disease.

106 Two false-negative results were related to poorly differentiated duodenal and prostatic NETs (G3).

107 confined cancer of 0.5 cm(3) or less without poorly differentiated elements.

108 us system (CNS-PNETs) are highly aggressive, poorly differentiated embryonal tumors occurring predomi

109 first genetically engineered mouse model of poorly differentiated endometrial adenocarcinoma.

110 These tumors were poorly differentiated endometrial adenocarcinomas with p

111 etion of Dicer1 and Pten in mice resulted in poorly differentiated endometrial adenocarcinomas, which

112 V-infected tumor cells in Kaposi sarcoma are poorly differentiated endothelial cells, expressing mark

113 nd imaging investigations in these otherwise poorly differentiated epilepsies.

114 Expression of ACE2 in poorly differentiated epithelia facilitated SARS spike (

115 NMC) belongs to a class of highly lethal and poorly differentiated epithelial cancers arising mainly

116 Tumors were poorly differentiated ER-alpha and progesterone receptor

117 on revealed a higher mean vessel density and poorly differentiated extracellular matrix (ECM) in MDA-

118 edullary disease is typically an aggressive, poorly differentiated form of MM that confers inferior o

119 PRRT in G3 NENs, especially in well- versus poorly differentiated G3 disease.

120 0% had metastatic disease and two thirds had poorly differentiated gastric or GEJ adenocarcinoma, wer

121 ly produced aggressive, highly branched, and poorly differentiated glandular-like structures in Matri

122 a PSA doubling time of 10 months or less or poorly differentiated (Gleason grade 8 to 10) cancer.

123 The ES signature is also present in poorly differentiated glioblastomas and bladder carcinom

124 nizing hormone gene, Lhb We demonstrate that poorly differentiated gonadotropes express a TET1 isofor

125 ulation was greater (p<0.05) in pathological poorly differentiated grade G3/G4 than in well-different

126 mass diagnoses an invasive ductal carcinoma, poorly differentiated (grade 3), with lymphovascular inv

127 Pathology review indicated a poorly differentiated, grade 3 invasive ductal carcinoma

128 on imbalance map analysis revealed that more poorly differentiated hepatocellular carcinoma contain m

129 and downregulation of IGF1R correlated with poorly differentiated, high-risk hormone receptor-negati

130 ed hazard ratios for stage IV moderately and poorly differentiated histological grade were 1.63 [95%

131 moking exposure, larger tumor size, and more poorly differentiated histological grade.

132 her sites and the exclusion of patients with poorly differentiated histologies from trials focused on

133 MSI colon cancers frequently display a poorly differentiated histology for which the molecular

134 577 CRCs linked loss of villin expression to poorly differentiated histology in MSI and MSS tumors.

135 y sampled nodes, T4 lesions, perforation, or poorly differentiated histology.

136 We found that TCF3 is highly expressed in poorly differentiated human breast cancers, preferential

137 oblasts and histologically closely resembled poorly differentiated human breast carcinomas.

138 When actively dividing poorly differentiated human hepatoma-derived (Huh7) cell

139 a marked reduction in IKKalpha expression in poorly differentiated human SCCs and identified Ikkalpha

140 Consistent with the loss of Smad2 in poorly differentiated human SCCs, Smad2-/- tumors were p

141 xpression is downregulated in many advanced, poorly differentiated, human cancers.

142 ion, DNA damage, and partial polyploidy in a poorly differentiated, immortalized hepatocyte cell line

143 Interestingly, poorly differentiated, including head and neck, cervical

144 sts fostered a microenvironment conducive to poorly differentiated invading tumor cells, whereas feta

145 ere highly invasive, leading us to term them poorly differentiated invasive carcinomas (PDICs).

146 h EZH2 overexpression promotes the growth of poorly differentiated invasive carcinomas remains to be

147 f ERG, it promotes the development of a more poorly differentiated, invasive adenocarcinoma.

148 c overexpression leads to the development of poorly differentiated, invasive prostate cancer that is

149 However, the resulting tumors are poorly differentiated, invasive, and metastatic to the l

150 C), but little or no expression was found in poorly differentiated, later-staged invasive tumors.

151 ary differentiation that is downregulated in poorly differentiated lung adenocarcinoma.

152 ioventricular heart valves, and hypoplastic, poorly differentiated lungs.

153 pathological findings were consistent with a poorly differentiated malignancy, suggestive of metastat

154 lls, which produced highly proliferative and poorly differentiated malignant tumors in mice.

155 entiated epithelial cells are converted into poorly differentiated, migratory and invasive mesenchyma

156 ancies found in unexpected locations or with poorly differentiated morphologies can pose a significan

157 Il24 coincided with the loss of RET/PTC3 in poorly differentiated mouse tumors.

158 Stage IV moderately and poorly differentiated mucinous adenocarcinomas have dist

159 edition's decision to combine moderately and poorly differentiated mucinous adenocarcinomas into a si

160 roximal colon, lymphocytic infiltrate, and a poorly differentiated, mucinous or signet ring appearanc

161 Cancer stem-like cells represent poorly differentiated multipotent tumor-propagating cell

162 ltration of proliferating cells displaying a poorly differentiated myoblastic phenotype.

163 %; moderately differentiated, n = 33; 35.5%; poorly differentiated, n = 26; 27.9%) (P < 0.05).

164 c disorders, preinvasive, microinvasive, and poorly differentiated neoplasms received the most attent

165 ults in preferential formation of metastatic poorly differentiated neoplasms, which are similar to hu

166 However, in poorly differentiated NETs, (18)F-FDG PET/CT plays a sig

167 In 11 (39.2%) of 28 patients with poorly differentiated NETs, the management decision was

168 andidate master transcriptional regulator of poorly differentiated NETs.

169 pho-Akt protein expression was identified in poorly differentiated neuroblastomas.

170 that commonly consist of undifferentiated or poorly differentiated neuroblasts with unfavorable clini

171 Treatment for advanced poorly differentiated neuroendocrine carcinoma should pa

172 pigenetically, NEPC resembles other types of poorly differentiated neuroendocrine tumors (NETs).

173 anding of the tumorigenesis and treatment of poorly differentiated neuroendocrine tumors.

174 rformed, and pathology yields a diagnosis of poorly differentiated non-small cell lung cancer (NSCLC;

175 nd ipsilateral mediastinal nodes confirmed a poorly differentiated non-small-cell carcinoma.

176 ells, BLU stable transfectants, derived from poorly-differentiated NPC HONE1 cells, suppress VEGF165,

177 IC-IIA high-grade serous, clear cell, or any poorly differentiated or grade 3 histological subtype, o

178 53(Deltaosx1) double knockout mice developed poorly differentiated osteosarcomas that resemble human

179 a-DOTATOC PET/CT was significantly higher in poorly differentiated/oxyphilic carcinomas (4/4 patients

180 tion, respectively, are blunted in advanced, poorly differentiated p53-mutant pancreatic tumors.

181 ressed high levels of NGAL but moderately to poorly differentiated PaCa cells (PANC-1 and MIAPaCa-2)

182 pression and chemosensitivity responses in a poorly differentiated pancreatic cancer cell line, MIA P

183 racterized a previously undescribed class of poorly differentiated PanNETs in the RIP1-Tag2 mouse mod

184 In particular, high grade, poorly-differentiated PanNETs have the worst patient pro

185 Poorly differentiated PCECs are uncoupled, and Ca(2+) in

186 s exhibited a high mitotic index, resembling poorly differentiated (PD)-PanNETs in human patients.

187 Our data demonstrate that L1 is expressed in poorly differentiated PDAC cells in situ and that threon

188 Syk expression is lost in poorly differentiated PDAC cells in vitro and in situ, a

189 corresponding to patients with moderately or poorly differentiated PDAC tumors, respectively.

190 idermis and/or squamous papilloma (Hyp/Pap), poorly-differentiated (PDSCC), or well-differentiated (W

191 The Ewing family of tumors are poorly differentiated pediatric solid tumors arising in

192 l translocation in Ewing tumors, a family of poorly differentiated pediatric tumors arising predomina

193 neage cells resulted in hypoplastic kidneys, poorly differentiated peripheral glomeruli, and decrease

194 at Lcn2-expressing breast tumors displayed a poorly differentiated phenotype and showed increased loc

195 stasis, and inhibition of progression to the poorly differentiated phenotype in primary prostatic tum

196 escaped fgfr1 deletion primarily exhibited a poorly differentiated phenotype.

197 Loss of CCN6 is associated with poorly differentiated phenotypes and increased invasion.

198 bigenic mice we did not detect IGF-1(des) in poorly differentiated primary tumors or metastatic lesio

199 loss of AR in both mouse models resulted in poorly differentiated primary tumors with expanded inter

200 rongly expressed in the endothelial cells of poorly differentiated prostate adenocarcinoma but not in

201 vasculature between well-differentiated and poorly differentiated prostate adenocarcinoma suggest th

202 rrow significantly reduced the hemorrhage in poorly differentiated prostate adenocarcinomas with bone

203 ars after diagnosis, men with moderately and poorly differentiated prostate cancer were more likely t

204 fferentiated), or high-GS cohorts (GS >/= 8, poorly differentiated prostate cancer).

205 7 of 13 (54%) control-treated mice developed poorly differentiated prostate cancer.

206 weeks) significantly inhibits progression to poorly differentiated prostate carcinoma and pulmonary m

207 ase in the number of well-differentiated and poorly differentiated prostates, coinciding with a 70% i

208 tion associated with a high Gleason's score, poorly differentiated prostatic adenocarcinoma.

209 parts to be KRAS2 wild type, TP53 wild type, poorly differentiated, proximally located, occur at lowe

210 itivity to the VEGFR2 inhibitor sorafenib in poorly differentiated PTC cells.

211 iated secretory cancer cells, but not in the poorly differentiated quasi-mesenchymal cells that coexi

212 eplicates in vivo than previous models using poorly differentiated rapidly dividing hepatoma cells.

213 e easily treatable, those with anaplastic or poorly differentiated recurrent thyroid carcinomas have

214 [moderately differentiated], and high-grade [poorly differentiated], respectively), chromogranin A, a

215 R-206, which are routinely lost in advanced, poorly differentiated rhabdomyosarcoma (RMS) but charact

216 nancies of the ear, tail, and foot comprised poorly differentiated, round to spindle-shaped cells wit

217 Adult neu(+)/pfp(+) males developed poorly differentiated salivary carcinomas, whereas neu(+

218 of EWS-FLI1 shifted the tumor phenotype to a poorly differentiated sarcoma.

219 development and accelerates the formation of poorly differentiated sarcomas.

220 and results in replacement of neck BAT with poorly differentiated skeletal muscle.

221 s identified as a heterozygous mutation in a poorly differentiated squamous cell carcinoma (SCC) and

222 a) expression in a large proportion of human poorly differentiated squamous cell carcinomas (SCC) and

223 e diffused but broadly expressed in well and poorly differentiated squamous cell carcinomas (SCC), in

224 Biopsy revealed poorly differentiated, squamous cell carcinoma.

225 on of moderately differentiated carcinoma to poorly differentiated state and distant metastasis.

226 g-deficient tumors showed a propensity for a poorly differentiated state with features of epithelial-

227 is required for tumors to reach a primitive, poorly differentiated state.

228 stem cell phenotypes and contributes to GBM poorly differentiated state.

229 al lesions with a propensity to advance to a poorly differentiated state.

230 medicine or as novel therapeutic targets for poorly differentiated, stem-like cancers.

231 HMGA1) gene is highly expressed in hESCs and poorly differentiated, stem-like cancers; however, its r

232 tva transgenic mice, we detected high-grade, poorly differentiated, stroma-rich and ER-negative tumor

233 imilar morphological phenotypes (high grade, poorly differentiated, stroma-rich and ER-negative), irr

234 ocytes, generate neurons poorly, form small, poorly differentiated teratomas, and cannot generate chi

235 Poorly differentiated thyroid cancer (PDTC) and anaplast

236 yroid cancers (PTC) that rapidly progress to poorly differentiated thyroid cancer (PDTC).

237 atic differentiated thyroid cancer (DTC) and poorly differentiated thyroid cancer (PDTC).

238 Patients with poorly differentiated thyroid cancers (PDTC), anaplastic

239 e histological features of human RAS-driven, poorly differentiated thyroid cancers.

240 cally invasive and have well-defined foci of poorly differentiated thyroid carcinoma (PDTC).

241 e thyroid tumors (for example, anaplastic or poorly differentiated thyroid carcinoma) carry several c

242 his pathway may promote redifferentiation in poorly differentiated thyroid carcinomas with constituti

243 0E), the mice developed highly penetrant and poorly differentiated thyroid tumors.

244 and impaired ESC differentiation, as seen in poorly differentiated TKO embryoid bodies (EBs) and tera

245 d no viable retinal tumor; the remainder had poorly differentiated tumor (6 eyes [50%]) or moderately

246 or size > 3 cm (HR 1.34 [range, 1.03-3.12]), poorly differentiated tumor (HR 3.18 [range, 1.31-7.70])

247 erts a strong promyogenic influence on these poorly differentiated tumor cells.

248 g and advanced, aggressive HCC subtypes with poorly differentiated tumor phenotypes.

249 In FaDu xenografts, a poorly differentiated tumor-expressing mutant p53, the c

250 ssion in colorectal carcinoma cell lines and poorly differentiated tumor-tissue specimens.

251 dies of their function have been hampered by poorly-differentiated tumor cell lines and genetically-i

252 r (2% vs 9%) invasions (P < .001), and fewer poorly differentiated tumors (15% vs 28%; P < .001).

253 intake was stronger for serous invasive and poorly differentiated tumors (comparable HR: 0.68; 95% C

254 ake of somatostatin analog usually indicates poorly differentiated tumors (G3).

255 imilar risk estimate was observed for serous/poorly differentiated tumors (n = 176 cases; comparable

256 expression, CRKI and CRKII were increased in poorly differentiated tumors (P<0.05).

257 s stage I), larger (T(2-4) versus T(1)), and poorly differentiated tumors and in tumors from patients

258 When compared with wild-type mice, poorly differentiated tumors arising in FGF(+/-) and FGF

259 1 loss strongly accentuated the formation of poorly differentiated tumors characterized by increased

260 atients undergoing APR were older, with more poorly differentiated tumors evidencing less response to

261 Poorly differentiated tumors exhibited greater microvess

262 Poorly differentiated tumors have fewer mutations than w

263 Poorly differentiated tumors in non-small cell lung canc

264 ller and well-differentiated compared to the poorly differentiated tumors in wild-type mice.

265 present with advanced-stage disease and have poorly differentiated tumors or tumors with an unfavorab

266 In Id-deficient TRAMP mice, the poorly differentiated tumors show extensive hemorrhage,

267 We find that histologically poorly differentiated tumors show preferential overexpre

268 Poorly differentiated tumors showed a trend toward decre

269 d c-Myc are more frequently overexpressed in poorly differentiated tumors than in well-differentiated

270 l carcinomas (ECs) are estrogen independent, poorly differentiated tumors that behave in an aggressiv

271 on of TCGA cutaneous melanoma and found that poorly differentiated tumors were predicted to have incr

272 cer, but curative treatments are elusive for poorly differentiated tumors where survival is just 15%

273 ia that progresses to highly pleomorphic and poorly differentiated tumors with basal characteristics.

274 tic impact and was enriched in patients with poorly differentiated tumors with high AFP levels as wel

275 of mice heterozygous for Ini1 presented with poorly differentiated tumors with variable rhabdoid feat

276 Twenty-eight patients (26.9%) had poorly differentiated tumors, and 76 (73.1%) had well-di

277 stage, pN+ stage tumors, larger tumor size, poorly differentiated tumors, and R1/2 resections were m

278 h pT3/4 stage, N+ tumors, larger tumor size, poorly differentiated tumors, and R1/2 resections.

279 al reactivity of each protein was reduced in poorly differentiated tumors, and there was a positive a

280 malignant progression, which is enriched in poorly differentiated tumors, and was highly predictive

281 "signature" phenotypes of highly malignant, poorly differentiated tumors, including hepatomas, is th

282 ming adenocarcinomas, and for characterizing poorly differentiated tumors, including neuroendocrine c

283 a mesenchymal phenotype, similar to well and poorly differentiated tumors, respectively.

284 with a more advanced stage, and to have more poorly differentiated tumors.

285 s, male sex, distant/metastatic disease, and poorly differentiated tumors.

286 Similar diminishing effects were found for poorly differentiated tumors.

287 d 25.6% (95% CI, 23.7%-28.3%) for those with poorly differentiated tumors.

288 tion regulators that are highly expressed in poorly differentiated tumors.

289 popharyngeal primary sites and patients with poorly differentiated tumors.

290 ted tumors express lower levels of pp32 than poorly differentiated tumors.

291 well-differentiated tumors, it was absent in poorly differentiated tumors.

292 , and its low expression can be a marker for poorly differentiated tumors.

293 rmore, we were able to successfully classify poorly differentiated tumours using miRNA expression pro

294 -1 negativity is pathognomonic of high-grade poorly differentiated tumours.

295 relation studies documented progression from poorly differentiated viable HCC tissues before treatmen

296 could be attributable to low visual acuity, poorly differentiated visual brain areas, or small absol

297 tly higher proportion of HCC cases graded as poorly differentiated (well-differentiated, n = 34; 36.6

298 nd pertuzumab expressed EMT markers and were poorly differentiated, whereas tumors exposed to the com

299 he gastric tumors from the GS-TGFB mice were poorly differentiated with diffuse morphology and signet

300 is that led to the diagnosis of an ulcerated poorly differentiated (with signet ring cells) adenocarc