ライフサイエンスコーパス: colorectal carcinoma

1 for the clinical behavior of posttransplant colorectal carcinoma.

2 ative phosphorylation in 3D Caco-2 models of colorectal carcinoma.

3 at increased frequency also in patients with colorectal carcinoma.

4 particularly high frequency in melanoma and colorectal carcinoma.

5 adjunct to traditional staging strategies in colorectal carcinoma.

6 rozygous mutations of fbw7 observed in human colorectal carcinoma.

7 to predict poor survival in RCC, but not in colorectal carcinoma.

8 ectal adenomas and a potential biomarker for colorectal carcinoma.

9 ancer and MTG8 is a candidate cancer gene in colorectal carcinoma.

10 y initiating step on the serrated pathway to colorectal carcinoma.

11 equently observed in invasive and metastatic colorectal carcinoma.

12 motherapy for peritoneal carcinomatosis from colorectal carcinoma.

13 ng the malignant progression of pancreas and colorectal carcinoma.

14 ctn and the EMT itself in the progression of colorectal carcinoma.

15 tis, are at an increased risk for developing colorectal carcinoma.

16 has potential for development as therapy for colorectal carcinoma.

17 tered to Met, was identified previously in a colorectal carcinoma.

18 tion may be a novel target for metastasis by colorectal carcinoma.

19 il (5-FU) is used widely for chemotherapy of colorectal carcinoma.

20 urden in a chemically induced mouse model of colorectal carcinoma.

21 d in the progression and metastasis of human colorectal carcinoma.

22 ally in breast cancer, hepatocarcinomas, and colorectal carcinoma.

23 tients with metastatic residual or recurrent colorectal carcinoma.

24 n syndrome known as hereditary non-polyposis colorectal carcinoma.

25 t may be a useful anticancer therapeutic for colorectal carcinoma.

26 -line treatment for patients with metastatic colorectal carcinoma.

27 e, less-differentiated and therapy-resistant colorectal carcinoma.

28 enesis is an important therapeutic target in colorectal carcinoma.

29 iation of T lymphocytes infiltrating a human colorectal carcinoma.

30 alterations and dysplastic transformation to colorectal carcinoma.

31 se of cancer-related deaths in patients with colorectal carcinoma.

32 s (range, 1-202/7.5 mL sample) with stage IV colorectal carcinoma.

33 Aspirin use reduces the risk of colorectal carcinoma.

34 about the role of MSI in the development of colorectal carcinoma.

35 e survival in patients underwent surgery for colorectal carcinoma.

36 OX-2 and ANGPTL4 as well STAT1 expression in colorectal carcinomas.

37 observed in many human tumors, most notably colorectal carcinomas.

38 t Rap1GAP expression is decreased in primary colorectal carcinomas.

39 d in colon-cancer cell lines and in sporadic colorectal carcinomas.

40 epithelial carcinomas, including breast and colorectal carcinomas.

41 ut not all, differences were also present in colorectal carcinomas.

42 at are over-expressed in a majority of human colorectal carcinomas.

43 ns an attractive therapeutic possibility for colorectal carcinomas.

44 gene seem to underlie the initiation of many colorectal carcinomas.

45 erplastic polyps (HPs) and increased risk of colorectal carcinomas.

46 essive role for PGE(2) in the development of colorectal carcinomas.

47 ygosity on chromosome 22q13.31 in breast and colorectal carcinomas.

48 tients with metastatic prostate, breast, and colorectal carcinomas.

49 at occurs in a significant fraction of human colorectal carcinomas.

50 wed by analysis of non-neural tumors such as colorectal carcinomas.

51 t, we analyzed CDX2 expression in 45 primary colorectal carcinomas.

52 rmation, Notch activity seems dispensable in colorectal carcinomas.

53 HLA-A2(+) melanomas and breast, ovarian, and colorectal carcinomas.

54 t is shared with human fusobacteria-positive colorectal carcinomas.

55 ately after colonoscopy for the diagnosis of colorectal carcinoma and 6 patients presented with sympt

56 HT-29 colorectal carcinoma and A549 lung adenocarcinoma cells

57 bolism are inversely associated with risk of colorectal carcinoma and adenomas.

58 Twenty-five patients with colorectal carcinoma and bilobar liver metastases receiv

59 Tested on colorectal carcinoma and glioblastoma multiforme cancer

60 ects in cancer stem cells from patients with colorectal carcinoma and glioblastoma multiforme, known

61 and eplin mRNA is frequently associated with colorectal carcinoma and is correlated with poor prognos

62 (CTNNB1) signaling pathway is implicated in colorectal carcinoma and metabolic diseases.

63 with different cultures of tumor cells from colorectal carcinoma and stroma cells showed that the ex

64 EPT vector has been shown to be effective in colorectal carcinoma and that apoptosis and significant

65 anoid biosynthesis, is overexpressed in most colorectal carcinomas and a subset of colorectal adenoma

66 r in many cancers, including the majority of colorectal carcinomas and a subset of ovarian endometrio

67 ynch syndrome have a high risk of developing colorectal carcinomas and adenomas at a young age, due t

68 tly described mechanism for tumorigenesis in colorectal carcinomas and adenomas characterized by meth

69 ly described mechanism for carcinogenesis in colorectal carcinomas and adenomas characterized by meth

70 utation analysis of CS patients and sporadic colorectal carcinomas and comparative aminoacid analysis

71 encing in 53 ACF from patients with sporadic colorectal carcinomas and familial adenomatous polyposis

72 fourth most frequently mutated gene in human colorectal carcinomas and has recently been described as

73 essed in premalignant adenomatous polyps and colorectal carcinomas and is associated with increased e

74 utive stabilization of beta-catenin, such as colorectal carcinomas and ovarian endometrioid adenocarc

75 vels of the Netrin receptors DCC (deleted in colorectal carcinoma) and Neogenin.

76 (Leishmania donovani), cancer (melanoma and colorectal carcinoma), and an autoimmune disease (rheuma

77 eaching 50% in some types of cancer, such as colorectal carcinoma, and 10% in prostate cancers.

78 uding non-small-cell lung carcinoma [NSCLC], colorectal carcinoma, and melanoma) were sequenced in th

79 e bronchoalveolar carcinoma, four (21%) were colorectal carcinoma, and six (32%) were sarcoma less th

80 e genesis of various malignancies, including colorectal carcinomas, and it is a key therapeutic targe

81 rly event in the pathogenesis of a subset of colorectal carcinomas, and that ACF from FAP patients an

82 highly aggressive and undifferentiated human colorectal carcinomas, and that its expression can restr

83 Hepatic metastases of colorectal carcinoma are a leading cause of cancer-relat

84 origins (endometrial, ovarian, prostate, and colorectal carcinomas) are hypersensitive to bleomycin,

85 has also been implicated in promoting human colorectal carcinomas as well as a variety of other canc

86 silenced by DNA hypermethylation in primary colorectal carcinomas as well as colorectal carcinoma-de

87 l carcinoma of the head and neck and 10 HT29 colorectal carcinoma-bearing nude rats were studied.

88 ysis of MCAM and LAMA4 expression in RCC and colorectal carcinoma blood vessels.

89 TC22 is expressed in 100% of colorectal carcinoma but is not expressed in normal colo

90 Fusobacterium spp. are associated with human colorectal carcinoma, but whether this is an indirect or

91 um nucleatum infection is prevalent in human colorectal carcinoma' by Castellarin and colleagues publ

92 iproliferative activity in human ovarian and colorectal carcinoma cell cultures.

93 ntagonize the ability of PPARgamma to induce colorectal carcinoma cell death.

94 We found a colorectal carcinoma cell line harboring the fusion gene

95 ated a DNMT1 conditional allele in the human colorectal carcinoma cell line HCT116 in which several e

96 survival, we generated three isogenic human colorectal carcinoma cell line models in which we can dy

97 table subclones of the high metastatic human colorectal carcinoma cell line, KM20, isolated from a Du

98 sensitivity was measured in HCT-116, a human colorectal carcinoma cell line, using inhibitors of SHP2

99 four human leukemia cell lines and one human colorectal carcinoma cell line.

100 F/5), a fibrosarcoma cell line (HT1080), and colorectal carcinoma cell lines (HCT116, SW480, and SW62

101 xpression of 15-PGDH is decreased in several colorectal carcinoma cell lines and in other human malig

102 tivity parallels reduced EPHB3 expression in colorectal carcinoma cell lines and poorly differentiate

103 on-incompetent adenovirus, Ad.mda-7, several colorectal carcinoma cell lines are resistant to its ant

104 d EBP50 localization to the nucleus of human colorectal carcinoma cell lines at low cell culture dens

105 Knockdown of EBP50 in human colorectal carcinoma cell lines compromised cell cycle p

106 tiproliferative activities against the human colorectal carcinoma cell lines HCT116N and HCT116O, an

107 have shown that it is applicable to 10 human colorectal carcinoma cell lines with a direct correlatio

108 and c-Src is critical for the regulation of colorectal carcinoma cell migration in vitro as well as

109 t with ANGPTL4 recombinant protein increases colorectal carcinoma cell proliferation through effects

110 y highlights a novel mechanism to circumvent colorectal carcinoma cell resistance to TRAIL-mediated a

111 We established RKO (human colorectal carcinoma) cell lines that can be induced by

112 roarray analysis showed that in human HCT116 colorectal carcinoma cells (WT), IR-activated Chk2 trigg

113 PHB3 enhancer activity is highly variable in colorectal carcinoma cells and precisely reflects EPHB3

114 tinue to identify novel PGE2 target genes in colorectal carcinoma cells and report here that an immed

115 pression of functional, endogenous CXCL12 in colorectal carcinoma cells dramatically reduced metastat

116 tic cells, tumor-associated fibroblasts, and colorectal carcinoma cells elicited significant Th1-type

117 death was cell type-dependent, because DLD1 colorectal carcinoma cells exhibited enhanced apoptosis,

118 HEF1 is highly expressed in cultured colorectal carcinoma cells exposed to hypoxia and in the

119 Colorectal carcinoma cells express CYP27B1 and CYP24A1 t

120 nd RhoC were increased 4- to 7-fold in SW480 colorectal carcinoma cells expressing exogenous PRL-1 an

121 733-2E and specifically bound to human SW948 colorectal carcinoma cells expressing the antigen GA733-

122 cell death by comparing the growth of human colorectal carcinoma cells in low fluid shear stress rot

123 sion of Akt2 expression in highly metastatic colorectal carcinoma cells inhibits their ability to met

124 ransactivation of the EGF receptor (EGFR) in colorectal carcinoma cells is mediated by means of a c-S

125 t that E4orf6, stably expressed in RKO human colorectal carcinoma cells or transiently expressed by a

126 Constitutive expression of CXCL12 in human colorectal carcinoma cells reduced orthotopic tumor form

127 Here, we demonstrate that colorectal carcinoma cells secrete VEGFA, which stimulat

128 rough its DNA-binding (DBD) domain in HCT116 colorectal carcinoma cells that express wild-type p53.

129 om cultured human skin fibroblasts and human colorectal carcinoma cells treated with azaserine, a DNA

130 Treatment of COX-2-expressing colorectal carcinoma cells with COX-2-selective NSAIDs-i

131 cell cycle arrest and senescence, mimicking colorectal carcinoma cells with high endogenous RCC1 lev

132 xpression of mda-7/IL-24 enhanced killing of colorectal carcinoma cells with mutated K-ras, but not w

133 -regulated antisense RNA expressed in HCT116 colorectal carcinoma cells, a cellular model of activate

134 , released by or expressed on the surface of colorectal carcinoma cells, also induces activation of c

135 even promoted growth arrest and apoptosis of colorectal carcinoma cells, attenuated their self-renewa

136 influence transformation potential in human colorectal carcinoma cells, by examining the effect of B

137 These studies were performed in human colorectal carcinoma cells, human neuroblastoma cells, a

138 In p53-deficient human colorectal carcinoma cells, ST led to a transcriptional

139 In human RKO colorectal carcinoma cells, this increase was not due to

140 ct apoptotic genes governing the survival of colorectal carcinoma cells, we employed RNAi to silence

141 n breast cancer, acute myeloid leukemia, and colorectal carcinoma cells.

142 t HEF1 mediates hypoxia-induced migration of colorectal carcinoma cells.

143 creasing GC-C activation in intact T84 human colorectal carcinoma cells.

144 nduced apoptosis specifically in nonadherent colorectal carcinoma cells.

145 rmia in vitro were tested in DHD/K12/TRb rat colorectal carcinoma cells.

146 is following reexpression of CXCL12 in human colorectal carcinoma cells.

147 gh-confidence beta-catenin targets in HCT116 colorectal carcinoma cells.

148 ces transcription of a reporter construct in colorectal carcinoma cells.

149 tudied the effects of LM-1685/CAI on CCL-250 colorectal carcinoma cells.

150 mechanism of A5G27 activity using WiDr human colorectal carcinoma cells.

151 roliferation, migration, and invasiveness of colorectal carcinoma cells.

152 been shown to stimulate the growth of human colorectal carcinoma cells.

153 of cell-incorporated 35S-methionine on human colorectal carcinoma cells.

154 which can be activated by targeting Bcl-2 in colorectal carcinoma cells.

155 bsequently down-regulates PPARgamma in human colorectal carcinoma cells.

156 ote cellular adhesion and differentiation of colorectal carcinoma cells.

157 nd high cytostatic potential in BRAF-mutated colorectal carcinoma cells.

158 e report the label-free enumeration of human colorectal-carcinoma cells from blood lymphocytes by usi

159 EP4 expression was also higher in colorectal carcinoma compared with adenoma cell lines an

160 The majority of colorectal carcinomas contain truncating mutations in th

161 to be underexpressed in all stages of human colorectal carcinoma (CRC) and in adenomatous polyps, in

162 Resection of a primary colorectal carcinoma (CRC) can be accompanied by rapid o

163 AR2A, NMDAR2B), only NMDAR2A was silenced in colorectal carcinoma (CRC) cell lines at basal line and

164 nd selective MEK1/2 inhibitor, on a panel of colorectal carcinoma (CRC) cells and found no inhibition

165 such as carcinoembryonic antigen (CEA) from colorectal carcinoma (CRC) cells, has been investigated

166 y modulates the stemness of individual human colorectal carcinoma (CRC) cells.

167 Colorectal carcinoma (CRC) has been described as a subse

168 mopreventive agent, silibinin, against human colorectal carcinoma (CRC) HT29 xenograft growth.

169 iated antitumor responses against metastatic colorectal carcinoma (CRC) in mice.

170 s with synchronous advanced adenoma (AA) and colorectal carcinoma (CRC) is currently unclear.

171 Pediatric colorectal carcinoma (CRC) is rare, but the available da

172 Hepatic resection of colorectal carcinoma (CRC) liver metastases is increasin

173 in a unique collection of eight fresh human colorectal carcinoma (CRC) liver metastases.

174 U) and LV in previously untreated metastatic colorectal carcinoma (CRC) patients.

175 tumor organoid cultures from 20 consecutive colorectal carcinoma (CRC) patients.

176 growth factor receptor (EGFR), in metastatic colorectal carcinoma (CRC) refractory to irinotecan, oxa

177 Colorectal carcinoma (CRC) remains a frequent cause of c

178 Colorectal carcinoma (CRC) risk was 10-fold increased, a

179 cal features of lymphoid cell infiltrates in colorectal carcinoma (CRC) that correlate with clinical

180 lleagues performed a metagenomic analysis of colorectal carcinoma (CRC) to identify potential associa

181 ues (VAT compared with SAT) in patients with colorectal carcinoma (CRC) were investigated by using ma

182 mily protein BCL-W is often overexpressed in colorectal carcinoma (CRC) where it correlates with adva

183 the human gastrointestinal tract, including colorectal carcinoma (CRC).

184 ibutes to the development and progression of colorectal carcinoma (CRC).

185 man colonic mucosa (NR), adenomas (ADs), and colorectal carcinoma (CRC).

186 biological role and mechanism of miR-198 in colorectal carcinoma (CRC).

187 Colorectal carcinomas (CRC) might be organized hierarchi

188 TNM-staging of colorectal carcinomas (CRC) relies on the histopathologi

189 a marked diminution of 15-PGDH expression in colorectal carcinomas (CRC).

190 st or reduced in a significant proportion of colorectal carcinomas (CRCs) but the underlying mechanis

191 Here, we isolated pure TECs from human colorectal carcinomas (CRCs) that exhibited TMEs with ei

192 patients, 2b was particularly potent against colorectal carcinoma CSCs, while 4b, 6a, and the SIRT2-s

193 f the cross-protective tumor Ag GSW11 in the colorectal carcinoma CT26 is increased when ERAAP expres

194 uman prostate adenocarcinoma LNCaP and human colorectal carcinoma CX-1 cells.

195 Similar results were observed in human colorectal carcinoma CX-1 cells.

196 of commissural axons through the Deleted in Colorectal Carcinoma (DCC) family of receptors.

197 , we examined mutants lacking the deleted in colorectal carcinoma (DCC) guidance receptor.

198 Netrin and its receptors Unc5 and deleted in colorectal carcinoma (DCC) regulate axon guidance and ce

199 d DOCK180 and the netrin receptor deleted in colorectal carcinoma (DCC).

200 oding the axon-guidance receptor 'deleted in colorectal carcinoma' (DCC), which has been implicated i

201 In the CT26 BALB/c murine model of colorectal carcinoma, depletion of regulatory T cells (T

202 in primary colorectal carcinomas as well as colorectal carcinoma-derived cell lines.

203 d allogeneic NK cells can recognize and kill colorectal carcinoma-derived CICs whereas the non-CIC co

204 Somatic colorectal carcinoma-derived PTEN missense mutations wer

205 Colorectal carcinoma evolves through a multitude of mole

206 However, unlike other bacteria linked to colorectal carcinoma, F. nucleatum does not exacerbate c

207 oup performance status <or= 1 and measurable colorectal carcinoma for whom standard treatments for me

208 atch repair (MMR) is present in adenomas and colorectal carcinomas from individuals with hereditary n

209 We analyzed data on human colorectal carcinomas from the Cancer Genome Atlas colle

210 in regulating the host microenvironment and colorectal carcinoma growth and metastasis in obese mice

211 Two patients with chemotherapy-refractory colorectal carcinoma had minor regressions, and four pat

212 A genomic analysis of colorectal carcinoma has identified an association betwe

213 crosatellite-stable, near-diploid (MSI-CIN-) colorectal carcinomas have been reported, but it is not

214 teraction and selectively kill p53 wild-type colorectal carcinoma HCT-116 cells but not p53 null cell

215 reatment in four cell lines derived from the colorectal carcinoma HCT116 cells: p53(+/+) (p53-wt), p5

216 In human colorectal carcinoma (HCT116) cells treated with H2O2, e

217 of two cell lines, glioblastoma (U-87MG) and colorectal carcinoma (HCT116), exhibited distinctive evo

218 sregulation of Wnt/beta-catenin signaling in colorectal carcinoma, hepatocellular carcinoma, and panc

219 escribed as a poor prognosis marker in human colorectal carcinoma; however, the molecular mechanism u

220 Angiogenesis was activated in colorectal carcinoma in both groups.

221 ine the clinical and molecular phenotypes of colorectal carcinoma in kidney transplant recipients and

222 luated outcomes for patients with metastatic colorectal carcinoma in relation to KRAS mutational stat

223 The behavior and mechanisms of colorectal carcinoma in solid organ transplantation have

224 MMP9 contribute to the growth of metastatic colorectal carcinoma in the liver and that postresection

225 interference, was tested in human breast and colorectal carcinoma in vitro and in vivo.

226 st and colon cancer cells and in noninvasive colorectal carcinomas in situ in which EGFR signaling fa

227 rkedly reduced in approximately 40% of human colorectal carcinomas in vivo.

228 was used to compute hazard ratios (HRs) for colorectal carcinoma incidence according to BRAF mutatio

229 The tumor microenvironment of colorectal carcinoma is a complex community of genomical

230 Colorectal carcinoma is one of the most common cancers i

231 or its receptors [Unc5b and DCC (deleted in colorectal carcinoma)] may be useful therapeutic targets

232 on status can distinguish between metastatic colorectal carcinoma (mCRC) patients who may benefit fro

233 including some mesothelioma, breast cancer, colorectal carcinoma, melanoma and glioblastoma.

234 amplified and its message is up-regulated in colorectal carcinoma metastases.

235 his limits the therapeutic value of TNKSi in colorectal carcinomas, most of which express high LEF1 l

236 re: hepatocellular carcinoma (HCC; N = 210), colorectal carcinoma (N = 40), miscellaneous liver metas

237 of multiple types of colorectal polyp, with colorectal carcinoma occurring in a high proportion of a

238 activity, the primary transforming events in colorectal carcinoma, occurs through induction of the Wn

239 Bs) would be found in patients with familial colorectal carcinomas of an undefined genetic basis (UFC

240 ring mice by potently limiting metastasis of colorectal carcinoma or murine melanoma.

241 egulation of an anti-tumorigenic response in colorectal carcinoma or whether both cytokines cooperate

242 om patients with renal cell carcinoma (RCC), colorectal carcinoma, or colorectal liver metastasis.

243 Like most human colorectal carcinomas, our murine Rb-deficient tumors de

244 potential from the low migratory SW480 human colorectal carcinoma parental cell line were biologicall

245 however, the precise role of Fusobacteria in colorectal carcinoma pathogenesis requires further inves

246 sion of S100A4 and SAA in tumor samples from colorectal carcinoma patients significantly correlated w

247 rvival rates in tumor-bearing animals and in colorectal carcinoma patients treated with an anti-VEGF

248 nuclear cell (PBMCs) from healthy donors and colorectal carcinoma patients.

249 ent capecitabine in patients with metastatic colorectal carcinoma refractory to FU showed no objectiv

250 diagnostic tool for hereditary nonpolyposis colorectal carcinoma-related cancers.

251 ty are significantly down-regulated in human colorectal carcinomas relative to matched normal tissue.

252 Higher risks were observed in patients with colorectal carcinoma (relative risk 3.10, 95% CI 1.26-7.

253 patients with peritoneal carcinomatosis from colorectal carcinoma remains to be established.

254 Colorectal carcinoma represents a heterogeneous entity,

255 in/+) mice (CD4-TLR4-APC(Min/+)), a model of colorectal carcinoma, resulted in a dramatic drop in tum

256 Late diagnosis of colorectal carcinoma results in a significant reduction

257 an-Meier analysis of beta6 expression in 488 colorectal carcinomas revealed a striking reduction in m

258 In a mouse model of colorectal carcinoma, RLI as a stand-alone treatment cou

259 D44, LRG5, and SOX2 messenger RNAs) in human colorectal carcinoma samples.

260 3 is detected, then patients with metastatic colorectal carcinoma should not receive anti-EGFR antibo

261 Colorectal carcinoma specimens and matched normal tissue

262 Incidence of colorectal carcinoma subclassified by F nucleatum status

263 nosis and clinical outcome in PIK3CA-mutated colorectal carcinoma, suggesting somatic PIK3CA mutation

264 uced expression of Dsc2 has been reported in colorectal carcinomas, suggesting that Dsc2 may play a r

265 entified levels of genomic rearrangements in colorectal carcinoma that can lead to essential gene fus

266 tant non-small cell lung cancers (NSCLC) and colorectal carcinomas that harbor wild-type TP53.

267 study, we conducted a systematic analysis of colorectal carcinomas that integrated genomic copy numbe

268 elopment as a therapeutic agent for treating colorectal carcinoma, though form B shows equal efficacy

269 and 5-carboxy-2'-deoxycytidine were lower in colorectal carcinoma tissue (ca. 2.5- and 3.5-fold, resp

270 an experimental model of colitis-associated colorectal carcinoma to investigate the contribution of

271 mutation testing in patients with metastatic colorectal carcinoma to predict response to anti-epiderm

272 )-2'-deoxycytidine level was 5-fold lower in colorectal carcinoma tumor in comparison with the normal

273 ween Smad4 and claudin-1 expression in human colorectal carcinoma tumor samples and in human colon ca

274 that Netrin signals through DCC (Deleted in Colorectal Carcinoma)/UNC-40/Frazzled (Fra) to mediate C

275 dline cells, signals through DCC (Deleted in Colorectal Carcinoma)/UNC40/Frazzled receptors to attrac

276 were 749 patients who underwent surgery for colorectal carcinoma under general anesthesia with or wi

277 ed nontumor liver tissues from patients with colorectal carcinoma undergoing surgery for liver metast

278 terized the composition of the microbiota in colorectal carcinoma using whole genome sequences from n

279 Colorectal carcinoma was more prevalent and exhibited a

280 A xenograft model of colorectal carcinoma was used to test the efficacy of ta

281 ocarcinoma (non-small cell lung cancers) and colorectal carcinoma was well tolerated and produced inc

282 5 homolog B, C. elegans) and DCC (deleted in colorectal carcinoma), was found in Muller cells and ast

283 hanisms involved in the clinical behavior of colorectal carcinoma, we compared the tumoral expression

284 tors that influence esophageal, gastric, and colorectal carcinoma were also shown to influence inflam

285 Kidney transplant recipients with colorectal carcinoma were diagnosed and followed up from

286 or moderate risk factors for development of colorectal carcinoma were recruited and placed into thre

287 properties in a preclinical mouse model for colorectal carcinoma, whereas antibodies raised with pep

288 ant literature, all patients with metastatic colorectal carcinoma who are candidates for anti-EGFR an

289 patients with locally advanced or metastatic colorectal carcinoma who had experienced treatment failu

290 of capecitabine in patients with metastatic colorectal carcinoma who progressed despite previous FU

291 X), characterized by hereditary nonpolyposis colorectal carcinoma with no mismatch repair defects.

292 Colorectal carcinomas with adjacent normal tissues were

293 Nonetheless, comparison of colorectal carcinomas with their adjacent normal tissues

294 AP1 regulation on BRAF is conserved in human colorectal carcinomas, with the two proteins being frequ

295 patients undergoing treatment for metastatic colorectal carcinoma, women treated within the past 6 mo

296 model (ED50 = 2.6 mg/kg QD) and the HCT-116 colorectal carcinoma xenograft model (ED50 = 10 mg/kg QD

297 owth inhibition in an APC mutant SW620 human colorectal carcinoma xenograft model after oral administ

298 vivo imaging of tumor vasculature in a HT29 colorectal carcinoma xenograft.

299 Nude mice bearing SW1222 human colorectal carcinoma xenografts were administered (64)Cu

300 at its expression can restrict the growth of colorectal carcinoma xenografts.