ライフサイエンスコーパス: colorectal carcinoma

1 lically repressed cytotoxic T cells in human colorectal carcinoma.

2 iation of T lymphocytes infiltrating a human colorectal carcinoma.

3 alterations and dysplastic transformation to colorectal carcinoma.

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

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

6 Aspirin use reduces the risk of colorectal carcinoma.

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

8 e survival in patients underwent surgery for colorectal carcinoma.

9 for the clinical behavior of posttransplant colorectal carcinoma.

10 at increased frequency also in patients with colorectal carcinoma.

11 to reduce the substantial long-term risk of colorectal carcinoma.

12 particularly high frequency in melanoma and colorectal carcinoma.

13 adjunct to traditional staging strategies in colorectal carcinoma.

14 rozygous mutations of fbw7 observed in human colorectal carcinoma.

15 ectal adenomas and a potential biomarker for colorectal carcinoma.

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

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

18 equently observed in invasive and metastatic colorectal carcinoma.

19 motherapy for peritoneal carcinomatosis from colorectal carcinoma.

20 ng the malignant progression of pancreas and colorectal carcinoma.

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

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

23 has potential for development as therapy for colorectal carcinoma.

24 RAS from a patient with extremely aggressive colorectal carcinoma.

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

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

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

28 -line treatment for patients with metastatic colorectal carcinoma.

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

30 enesis is an important therapeutic target in colorectal carcinoma.

31 rmation, Notch activity seems dispensable in colorectal carcinomas.

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

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

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

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

36 t Rap1GAP expression is decreased in primary colorectal carcinomas.

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

38 epithelial carcinomas, including breast and colorectal carcinomas.

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

40 -functional Apc truncation commonly found in colorectal carcinomas.

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

42 iling is capable of detection of early-stage 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 gnaling pathway contribute to development of colorectal carcinomas.

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

50 HT-29 colorectal carcinoma and A549 lung adenocarcinoma cells

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

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

53 g noncoding RNA SATB2-AS1 is dysregulated in colorectal carcinoma and correlates with poor survival a

54 Tested on colorectal carcinoma and glioblastoma multiforme cancer

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

72 noma, a duodenal carcinoma, two metachronous colorectal carcinomas, and multi-regional sampling in a

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

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

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

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

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

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

79 mutated within specific sequence contexts in colorectal carcinomas but the underlying mechanism is no

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

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

82 7-ethyl-10-hydrocamptothecin (SN38) on human colorectal carcinoma cancer cells (HCT 116) was used as

83 ed as first-line treatment for some types of colorectal carcinoma, causes peripheral neuropathic pain

84 ned from three very different sources (human colorectal carcinoma cell culture, raw bovine milk, and

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

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

87 In contrast, the human C2Bbe1 colorectal carcinoma cell line expresses little caspase-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

105 Mixed xenograft experiments using HCT8 colorectal carcinoma cells and primary MSC of different

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

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

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

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

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

111 Colorectal carcinoma cells express CYP27B1 and CYP24A1 t

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

113 733-2E and specifically bound to human SW948 colorectal carcinoma cells expressing the antigen GA733-

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

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

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

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

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

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

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

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

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

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

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

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

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

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

128 proximately 100-fold lower relative to human colorectal carcinoma cells, the levels of both - 5fC and

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

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

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

132 nduced apoptosis specifically in nonadherent colorectal carcinoma cells.

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

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

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

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

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

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

139 ote cellular adhesion and differentiation of colorectal carcinoma cells.

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

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

142 Fusions were present in 5% of MSI-H/MMR-D colorectal carcinoma compared with 0.4% of MSS/MMR-P col

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

144 The majority of colorectal carcinomas contain truncating mutations in th

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

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

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

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

149 as SV40, JCV, BKV and EBV in patient-derived colorectal carcinoma (CRC) cells typifying all molecular

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

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

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

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

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

155 To identify the mechanisms underlying colorectal carcinoma (CRC) invasion, we collected live h

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 antly upregulated in about half of the human colorectal carcinomas (CRC) and in other cancers.

172 Colorectal carcinomas (CRC) might be organized hierarchi

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

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

175 en rat sarcoma viral oncogene homolog (Kras) colorectal carcinomas (CRCs) and serve as a reservoir fo

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

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

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

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

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

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

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

183 The Deleted in Colorectal Carcinoma (Dcc) receptor plays a critical rol

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

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

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

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

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

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

190 Somatic colorectal carcinoma-derived PTEN missense mutations wer

191 Colorectal carcinoma evolves through a multitude of mole

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

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

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

195 Overall 57% (12/21) of colorectal carcinoma fusions were MSI-H/MMR-D.

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

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

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

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

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

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

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

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

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

205 Angiogenesis was activated in colorectal carcinoma in both groups.

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

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

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

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

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

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

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

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

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

215 Colorectal carcinoma is one of the most common cancers i

216 orthotopic murine glioma (GL261) and a human colorectal carcinoma (LS147T), and perform sensitivity a

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

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

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

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

221 giogenesis and tumor growth in a CT26 murine colorectal carcinoma model.

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

223 In B16-F10 melanoma and MC38 colorectal carcinoma mouse models, reprogramming nanopar

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

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

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

227 kinase fusions in BRAF/RAS wild-type, MSI-H colorectal carcinoma offers a rationale for routine scre

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

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

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

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

232 al carcinoma compared with 0.4% of MSS/MMR-P colorectal carcinoma (P < 0.001) and 15% of MSI-H/MMR-D

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

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

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

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

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

238 ed in epigenetic modification that regulates colorectal carcinoma progression.See related article by

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

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

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

242 Colorectal carcinoma represents a heterogeneous entity,

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

244 Late diagnosis of colorectal carcinoma results in a significant reduction

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

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

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

248 3 is detected, then patients with metastatic colorectal carcinoma should not receive anti-EGFR antibo

249 Colorectal carcinoma specimens and matched normal tissue

250 Incidence of colorectal carcinoma subclassified by F nucleatum status

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

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

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

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

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

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

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

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

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

260 )-2'-deoxycytidine level was 5-fold lower in colorectal carcinoma tumor in comparison with the normal

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

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

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

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

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

266 es were conducted in a murine model of human colorectal carcinoma using an immunoconjugate of the huA

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

268 Colorectal carcinoma was more prevalent and exhibited a

269 hepatic metastasis of malignant melanoma and colorectal carcinoma was significantly reduced.

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

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

272 5 homolog B, C. elegans) and DCC (deleted in colorectal carcinoma), was found in Muller cells and ast

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

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

275 Kinase fusions in MSI-H colorectal carcinoma were associated with sporadic MLH1p

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

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

278 s (10 hepatocellular carcinoma, 3 metastatic colorectal carcinoma) were included.

279 of pERK and pSRC, present in the metastatic colorectal carcinoma, were better preserved with the rap

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

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

282 d kinase fusions from patients with advanced colorectal carcinoma who had MSK-IMPACT testing of their

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

284 ) in microsatellite instability-high (MSI-H) colorectal carcinoma with fusions were investigated.

285 hese findings identify a molecular subset of colorectal carcinoma with kinase fusions that may be res

286 routine screening to identify patients with colorectal carcinoma with kinase fusions that may be res

287 -viral HCC, neuroendocrine tumors (NET), and colorectal carcinoma with liver metastases (CRLM), but n

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

289 carcinoma (P < 0.001) and 15% of MSI-H/MMR-D colorectal carcinoma with wild-type RAS/BRAF.

290 Colorectal carcinomas with adjacent normal tissues were

291 Of 24 total MLH1-deficient colorectal carcinomas with MLH1ph and wild-type RAS/BRAF

292 Of 2,314 colorectal carcinomas with MSK-IMPACT testing, 21 harbor

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

300 fusions are rare and poorly characterized in colorectal carcinoma, yet they present unique opportunit