ライフサイエンスコーパス: invasive tumor

1 PSCC can occur as either an in situ or invasive tumor.

2 oclonal transformed cells to develop into an invasive tumor.

3 s than in patients with concomitant DCIS and invasive tumor.

4 sion from APC-mutant neoplasia to submucosal invasive tumor.

5 ular evidence for the progression of DCIS to invasive tumor.

6 in the clonal progression to the synchronous invasive tumor.

7 oenvironment, ultimately resulting in a more invasive tumor.

8 ihood of progression of superficial tumor to invasive tumor.

9 found in poorly differentiated, later-staged invasive tumors.

10 tu melanomas, and from the RGP and VGP of 29 invasive tumors.

11 junction/cytoskeletal axis is a hallmark of invasive tumors.

12 unger, had higher stage tumors, and had more invasive tumors.

13 erentially expressed between superficial and invasive tumors.

14 st during the cells' transition to malignant invasive tumors.

15 ors have different propensity to progress to invasive tumors.

16 ugh the benefit was more pronounced for less invasive tumors.

17 duced apoptosis that is a hallmark of highly invasive tumors.

18 to a single phenotype at advanced stages of invasive tumors.

19 TAg-expressing cells in preinvasive foci and invasive tumors.

20 gnant epithelial cells in late-stage, highly invasive tumors.

21 -grade lesions but not in those derived from invasive tumors.

22 invariably integrate into the host genome in invasive tumors.

23 eptide, reduced or absent staining in muscle invasive tumors.

24 CA1d cells outcompeted MCF10A, forming invasive tumors.

25 ally increased in human gliomas, notoriously invasive tumors.

26 oplastic stages and a decreased incidence of invasive tumors.

27 pattern of staining to that observed for the invasive tumors.

28 uitary tumor growth and expansion into large invasive tumors.

29 ved in the invasiveness of gliomas and other invasive tumors.

30 Human malignant gliomas are highly invasive tumors.

31 of the end point of carcinomas and number of invasive tumors.

32 nase A on cell surfaces and are expressed in invasive tumors.

33 The bladder remains at risk for new invasive tumors.

34 focus upon their role in high-risk nonmuscle invasive tumors.

35 hroughout tumor progression, and absent from invasive tumors.

36 scription factor that synergizes with FOS in invasive tumors.

37 differentiate between superficial and muscle-invasive tumors.

38 ring mutant p53, leading to the formation of invasive tumors.

39 enetic pathways, resulting in noninvasive or invasive tumors.

40 ficial tumors that are likely to progress to invasive tumors.

41 logy in the absence of features of malignant invasive tumors.

42 articularly estrogen receptor (ER) -positive invasive tumors.

43 i alone were lowest in localized and locally invasive tumors (1/14 and 2/12, respectively) and highes

44 Of 29 invasive tumors, 16 exhibited RGP mutations (55.2%); 22

45 %) relapsed in the bladder with a new muscle-invasive tumor, 18 (53%) were successfully treated with

46 f 16 (100%) HNSCC cell lines, 26 of 29 (90%) invasive tumors, 7 of 7 (100%) dysplastic lesions, and 5

47 y of having an in situ tumor (rather than an invasive tumor) [95% CI: 3.48-4.61], compared to sites o

48 SVER expression resulted in hyperplasias or invasive tumors affecting particular visceral smooth mus

49 ped hyperplastic ductal trees and multifocal invasive tumors after several pregnancies, some of which

50 icial bladder tumors, the tumors progress to invasive tumors after treatment.

51 the probability of having an in situ versus invasive tumor among SCCA cases.

52 quencies in 5,724 subjects with at least one invasive tumor and 1,943 subjects with in situ tumors on

53 unger than the screening age, found that 711 invasive tumors and 180 cases of DCIS were overdiagnosed

54 D3S1300, was found in 6 of 16 microdissected invasive tumors and 3 of 6 ductal in situ carcinomas.

55 It is likely that 1 in every 3 invasive tumors and cases of DCIS diagnosed in women off

56 lioma model, PDZ1i resulted in smaller, less invasive tumors and enhanced survival.

57 e small GTPase RhoC is overexpressed in many invasive tumors and is essential for metastasis.

58 longer survival with only 20% penetrance of invasive tumors and no apparent lung or liver metastases

59 have demonstrated that proteases secreted by invasive tumors and pathological microorganisms are capa

60 uld predict the likelihood of progression to invasive tumors and to test the robustness of the expres

61 These sinusoids arose around locally invasive tumors and were associated with more advanced i

62 al cells of the desmoplastic response to the invasive tumor, and four of these genes were specificall

63 ven ovarian carcinoma cell lines, 71% of the invasive tumors, and 92% of the borderline tumor tissues

64 Advanced AJCC T-stage, locally invasive tumors, and more pathologically aggressive tumo

65 n which fingerlike shapes, characteristic of invasive tumor, are observed.

66 sociated form of RalGEF (RalGDS-CAAX) formed invasive tumors as well, demonstrating that activation o

67 omparatively resistant to the development of invasive tumors, as are RT2 C3HB6(F1) hybrid mice.

68 al complete response or the disappearance of invasive tumor at surgery.

69 generally present with small, unresectable, invasive tumors at a site traditionally considered progn

70 Glioblastoma multiforme is a highly invasive tumor bearing a dismal prognosis.

71 clear the breast and axillary lymph nodes of invasive tumor before surgery.

72 ygosity at this locus was observed in 50% of invasive tumors but in none of the borderline tumors.

73 endothelial, and tumor cells in a variety of invasive tumors but is undetectable in the majority of n

74 n family, N-cadherin, is expressed in highly invasive tumor cell lines that lacked E-cadherin express

75 tumor cells and their revertants from highly invasive tumor cell populations, indicating how phenotyp

76 Based on the hypothesis that invasive tumor cells are released more readily upon dige

77 cancer, 3p loss of heterozygosity occurs in invasive tumor cells as well as in morphologically norma

78 that archazolid induced apoptosis in highly invasive tumor cells at nanomolar concentrations which w

79 The invasive tumor cells collected from PyMT mouse mammary t

80 show a pattern like that seen previously in invasive tumor cells from the MTLn3 cell line-derived tu

81 activity significantly reduces migration of invasive tumor cells in vitro.

82 yonic development and for progression of non-invasive tumor cells into malignant, metastatic carcinom

83 To test the hypothesis that invasive tumor cells may block the formation of the fibr

84 cell behavior, which were identified in the invasive tumor cells of cell line-derived tumors, are co

85 ll line-derived tumors, are conserved in the invasive tumor cells of PyMT-derived mouse mammary tumor

86 ng that the enforced expression of PEA-15 in invasive tumor cells reduced invasion.

87 The nuclei in 11 invasive tumor cells were typically round with finely di

88 iform, intense membrane staining of > 30% of invasive tumor cells), a fluorescent in situ hybridizati

89 analogously to the process of chemotaxis in invasive tumor cells, axonal growth cones of Xenopus spi

90 herefore, CD147, which is itself elevated on invasive tumor cells, may make a major contribution to t

91 anched polylactosamine sugars that appear on invasive tumor cells.

92 n of EPLIN may contribute to the motility of invasive tumor cells.

93 ild type is expressed in G2/G3 tumors and in invasive tumor cells.

94 ucial role in the promotion of glycolysis in invasive tumor cells.

95 in, p38 MAPK activity, and uPA expression in invasive tumor cells.

96 on of CXCR4 and activated AKT in primary and invasive tumor cells.

97 d beta1 integrin may serve as a biomarker of invasive tumor cells.

98 ovide a means of targeting mesenchymal-like, invasive tumor cells.

99 several-fold lower than in the corresponding invasive tumors; cells throughout these multilayered pro

100 glutamate release leads to smaller and less invasive tumors compared with saline-treated controls.

101 umors and widespread hypermethylation in the invasive tumors, confirming that the two pathways differ

102 gemistocytic astrocytomas, typically highly invasive tumors, contained high numbers of PLP-positive

103 Invasive tumors demonstrating loss of VHL consistently d

104 The mean diameter of the invasive tumors detected was 10.9 mm.

105 bed that PPARgamma activation suppresses non-invasive tumor development and induces ER-positivity wit

106 and induces ER-positivity without affecting invasive tumor development.

107 combined mammography and MR imaging, median invasive tumor diameters at diagnosis decreased to 1.9,

108 Interestingly, in situ lesions found in invasive tumors displayed LOH.

109 lesions and subgroups within early-stage and invasive tumors displaying different overall survival.

110 TWIST1 and C3 colocalized at the invasive tumor edges, and in the neural crest and limb b

111 Invasive tumors, even if completely resected, require ad

112 risk factors were similar for borderline and invasive tumors, except for age at diagnosis.

113 Overall, 112 of 161 (69.5%) invasive tumors exhibited elevated expression.

114 Highly angiogenic and poorly invasive tumors expressed low levels of beta8 integrin,

115 Mammography depicted 39 (81%) of 48 invasive tumor foci and 14 (88%) of 16 foci of DCIS.

116 US depicted 45 (94%) of 48 invasive tumor foci and seven (44%) of 16 foci of ductal

117 m low- and high-grade dysplastic lesions and invasive tumor foci from 10 fully embedded esophageal re

118 for Ras mutation, and Ras is sufficient for invasive tumor formation in Rb1 family mutant mouse embr

119 lysine demethylase KDM6A were present in non-invasive tumors from females than males.

120 using gene array analysis of preinvasive and invasive tumors from mice, which were then evaluated in

121 vasion of HCC cells in the livers, with more invasive tumor front and increased incidence of venous i

122 ivated in a small subset of SCC cells at the invasive tumor front and predicts for poor prognosis of

123 inated elevation of Twist and Glu-tubulin at invasive tumor fronts, particularly within ductal carcin

124 o isoforms of bFGF may have implications for invasive tumor growth and chemoresistance.

125 red for many pathologic processes, including invasive tumor growth as well as physiologic organ/tissu

126 th a history of previous debulking), lack of invasive tumor growth, and minimal residual disease afte

127 will further facilitate in-depth analysis of invasive tumor growth, angiogenesis, metastasis and tumo

128 including proliferative fibrotic disorders, invasive tumor growth, rheumatoid arthritis, and atheros

129 including proliferative fibrotic disorders, invasive tumor growth, rheumatoid arthritis, and atheros

130 ted in development, tissue regeneration, and invasive tumor growth.

131 teinase (MT1-MMP) mediates proteolysis-based invasive tumor growth.

132 LIN28 expression levels were associated with invasive tumor growth.

133 ol and identify Alk as a genetic modifier of invasive tumor growth.

134 ed through screening were at risk for a more invasive tumor (>/=T3: relative risk [RR] = 1.96; P < .0

135 ly pattern of loss while all foci of CIS and invasive tumor had an advanced pattern.

136 However, all invasive tumors had evidence of ss-galactosidase express

137 ive breast carcinomas than in normal breast; invasive tumors have significantly higher numbers than D

138 luding targeted intervention therapy and non-invasive tumor imaging in vivo.

139 age of pathologic complete response (pCR; no invasive tumor in breast and axillary nodes).

140 pCR was defined as no evidence of invasive tumor in the breast and axillary lymph nodes.

141 plete response was defined as the absence of invasive tumor in the breast.

142 resection of the mass showed large masses of invasive tumor in the resection site, with small foci of

143 cinoma in situ (DCIS) of the breast is a non-invasive tumor in which cells proliferate abnormally, bu

144 , Notch1 loss could accelerate the growth of invasive tumors in a manner associated with increased ex

145 which TbetaRIII had been knocked down formed invasive tumors in athymic nude mice, whereas the contro

146 lized MCF-7 cells overexpressing IQGAP1 form invasive tumors in immunocompromised mice, whereas tumor

147 s are transformed in vivo, forming large and invasive tumors in immunocompromised mice.

148 rprisingly, were fully capable of initiating invasive tumors in NOD SCID gamma (NSG) mice.

149 ferative, poorly differentiated, and locally invasive tumors in nude mice compared with WT EREG-expre

150 genes, grow in soft agar and develop ectopic invasive tumors in recipient mice, indicating that the c

151 vival with a bladder, frequency of recurrent invasive tumors in the bladder, and survival after salva

152 senchymal transition, and production of more invasive tumors in xenograft assays.

153 Invasive tumors, including gliomas, utilize proteinases

154 carcinomas revealed a new categorization of invasive tumors into basal-like (positive for DeltaNp63

155 high (A2b2) SPARC-secreting clones produced invasive tumors, invading with fingerlike projections an

156 The switch from a quiescent tumor to an invasive tumor is accompanied by the acquisition of angi

157 In invasive tumors, low-level 3q amplification (3 to 4 X co

158 These spaces surrounded only locally invasive tumors (mean diameter, 0.85 mm) that had obstru

159 oportion of detected tumors that were large (invasive tumors measuring >/=2 cm) decreased from 64% to

160 n of detected breast tumors that were small (invasive tumors measuring <2 cm or in situ carcinomas) i

161 ell nutrients, driving shape instability and invasive tumor morphologies, and stabilizing mechanical

162 rms was detected in paraffin sections in all invasive tumors, most prominently in moderately differen

163 s (n=54), carcinoma is situ (CIS) (n=15) and invasive tumors (n=12).

164 aIgTrkB NCM-1 cells form rapidly growing and invasive tumors necessitating euthanasia of all mice by

165 d within one of five distinct regions of the invasive tumors (neoplastic epithelium; angioendothelium

166 In 9 cases, the invasive tumor nests were surrounded by an intact BM; in

167 Glioblastoma is an aggressive, invasive tumor of the central nervous system (CNS).

168 positive SLNs was found in patients who had invasive tumors of increasing size: 18 of 112 patients (

169 thod to automatically identify the extent of invasive tumor on digitized images.

170 nal neural network for detecting presence of invasive tumor on whole slide images.

171 n was scored negative, close or positive for invasive tumor or ductal carcinoma in situ according to

172 lance is eventually overwhelmed by a growing invasive tumor, our findings suggest that productive tum

173 ete loss of Pten was not sufficient to cause invasive tumors, over two thirds of the mutant females d

174 Invasive tumors overexpress the short progesterone recep

175 sk stratification of patients with nonmuscle-invasive tumors permits appropriate timing of intravesic

176 Carcinogen-treated RDEB mice developed invasive tumors phenocopying human RDEB-cSCC, whereas wi

177 ng short hairpin RNA technology to mimic the invasive tumor phenotype and also RAD51 knockdown (RAD51

178 icroenvironment affect the proliferative and invasive tumor phenotype of the earliest stages of tumor

179 hat promote the switch from a noninvasive to invasive tumor phenotype remain obscure.

180 or expression of MMP3 is co-incident with an invasive tumor phenotype.

181 Whether invasive tumor phenotypes like EMT arise from oncogenic

182 therapy may be more effective for minimally invasive tumors rather than advanced-stage disease.

183 Ras/Raf pathway in the eye, or in malignant invasive tumors resulting when Raf activation is combine

184 low-up, while the effect of DCIS adjacent to invasive tumor seemed to remain stable.

185 Therefore, patients with high-grade invasive tumors should be monitored closely, especially

186 significantly associated with sex (P < .01), invasive tumor size (P < .01), T status (P < .01), N sta

187 Median invasive tumor size and proportion of cancers detected a

188 tion of unedited miR-376a* and the extent of invasive tumor spread as measured by magnetic resonance

189 th the presence of lymph node metastases and invasive tumor stages.

190 overexpressed at least 1.5-fold in the more invasive tumor subtype.

191 greater degree in higher grade node-positive invasive tumors than in normal breast tissue or ductal c

192 ncy of copy number alterations was higher in invasive tumors than that in DCIS, with several of them

193 luminal-like cells generated larger and more invasive tumors than their basal-like counterparts.

194 lood vessels, and arterioles and to identify invasive tumor through distinctive patterns in OCME imag

195 f exon 2 solely in the cancer cell lines and invasive tumor tissues.

196 tic tumors and other differentiated and less invasive tumor types.

197 We observed complete loss of KiSS-1 in all invasive tumors under study as compared to their respect

198 This surgery is best suitable for locally invasive tumors unresectable because of location and vas

199 enotypic pathways (superficial papillary non-invasive tumors versus flat carcinoma in situ lesions),

200 Induction of M-severin in an invasive tumor was directly observed in human colon aden

201 No invasive tumor was found in the tracheobronchial tree or

202 Invasive tumors were also divided into 2 groups (>10 mm

203 Invasive tumors were found at significantly higher frequ

204 Fifteen cases were pure DCIS; most invasive tumors were smaller than 1.0 cm.

205 with germ-line mutations in BRCA1 and BRCA2, invasive tumors were studied from 58 Jewish women ascert

206 ncident breast cancer cases (including 5,245 invasive tumors) were ascertained among 89,902 women.

207 oes not express BEHAB/brevican and forms non-invasive tumors when grown as intracranial grafts, can f

208 ls still form progressively growing, locally invasive tumors when injected into mammary fat pads but

209 when grown as intracranial grafts, can form invasive tumors when transfected with a 5' cDNA fragment

210 ults suggest that 10p losses may define less invasive tumors, whereas 10q losses may play a role in t

211 PIK3CA mutations occur almost exclusively in invasive tumors, whereas upstream mutations occur as fre

212 The less common but more aggressive invasive tumors, which have a higher mortality rate, are

213 The association of high-grade invasive tumor with IBTR diminished during follow-up, wh

214 assified normal urothelium, superficial, and invasive tumors with 82.2% accuracy, and stratified blad

215 risk of relapse (P = .04) and patients with invasive tumors with both shorter relapse-free (P = .004

216 ssociations were evident for the majority of invasive tumors with ductal histology and regardless of

217 low levels of beta8 integrin, whereas highly invasive tumors with limited neovascularization expresse

218 loci in 49 noninvasive urothelial tumors, 38 invasive tumors with matched normal-appearing urothelium

219 hnic minority groups more often have larger, invasive tumors with positive lymph nodes.

220 us cell carcinomas (SCCas) are heterogeneous invasive tumors with proliferating outer layers and inne

221 gnef-C-expressing cells formed smaller, less invasive tumors with reduced tyrosine phosphorylation of

222 Rnd3 expression was significantly lower in invasive tumors with satellite nodules.