ライフサイエンスコーパス: colorectal

1 four common cancers (lung, prostate, breast, colorectal).

2 icity of so-obtained BRJ to human epithelial colorectal adenocarcinoma (Caco-2) and human non-maligna

3 levels, and patient survival times from 456 colorectal adenocarcinoma cases, and a separate set of 5

4 obar distribution of hepatic metastases from colorectal adenocarcinoma may not be associated with the

5 tigate the impact of the primary location of colorectal adenocarcinoma on the lobar distribution of i

6 ed mucosa of human IBD patients and in human colorectal adenocarcinoma, accounting for the epithelial

7 We found colorectal adenocarcinomas to express mutant forms of CE

8 cases, and a separate set of 594 samples of colorectal adenocarcinomas, in The Cancer Genome Atlas.

9 d A643T in the B3 domain of human CEACAM5 in colorectal adenocarcinomas; structural studies indicated

10 n, 45-75 y of age, recently diagnosed with a colorectal adenoma, were randomly assigned to 1000 IU/d

11 pectroscopy in 15 patients with a dysplastic colorectal adenoma.

12 Colorectal anastomotic leakage (CAL) is the single most

13 OXP3(+) T-cell counts and increased risks of colorectal and breast cancer (overall and ER- subtype).

14 een the clinically adopted strategy to treat colorectal and breast cancers as well as age-related mac

15 75 matched controls from the Prostate, Lung, Colorectal and Ovarian (PLCO) Cancer Screening Trial.

16 nts aged 15-84 years, diagnosed with breast, colorectal, and oesophageal cancer between Jan 1, 2010,

17 inal cancers, including esophageal, gastric, colorectal, and pancreatic cancers.

18 o enhance immunotherapy outcome in melanoma, colorectal, and potentially other cancers.

19 untry in question) or one such record plus a colorectal biopsy report with a morphology code suggesti

20 ) is positively associated with the risks of colorectal, breast, and prostate cancer, but evidence fo

21 tor for several common cancers (e.g., liver, colorectal, breast, pancreas).

22 ing after breast cancer (2.1 million cases), colorectal cancer (0.8 million) and lung cancer (0.7 mil

23 lasia were associated with increased risk of colorectal cancer (adjusted hazard ratios 9.25; 95% conf

24 testinal inflammation and colitis-associated colorectal cancer (CAC).

25 rld's highest recorded incidence of sporadic colorectal cancer (CRC) (~91:100,000), whereas rural Afr

26 The long-term risks of colorectal cancer (CRC) and CRC-related death following

27 ly screen for Lynch syndrome (LS)-associated colorectal cancer (CRC) and endometrial cancer (EC), but

28 a better prognosis among male patients with colorectal cancer (CRC) and the role of open surgery in

29 il (5-FU) is a standard treatment option for colorectal cancer (CRC) but its rapid metabolism and sys

30 A significant proportion of colorectal cancer (CRC) cases have familial aggregation

31 the release of Cas9 RNP into 293T cells and colorectal cancer (CRC) cells, thus displaying high geno

32 ing sites at nucleotide resolution in intact colorectal cancer (CRC) cells.

33 nical tissues from 146 patients in a Chinese colorectal cancer (CRC) cohort, among which 70 had metas

34 Patients with stage II or III colorectal cancer (CRC) exhibit various clinical outcome

35 us molecular subtype (CMS) classification of colorectal cancer (CRC) has been established, which may

36 Approximately 35% of patients with colorectal cancer (CRC) have a family history of the dis

37 nical efforts, patients affected by advanced colorectal cancer (CRC) have still a poor prognosis.

38 In contrast to the decreasing incidence of colorectal cancer (CRC) in older populations, the incide

39 ite advances in the detection and therapy of colorectal cancer (CRC) in recent years, CRC has remaine

40 Colorectal cancer (CRC) incidence and mortality are incr

41 Colorectal cancer (CRC) incidence is increasing among yo

42 idence that colonoscopy surveillance reduces colorectal cancer (CRC) incidence or mortality is weak.

43 treatment options available to patients with colorectal cancer (CRC) is increasing, with a parallel r

44 Colorectal cancer (CRC) is the second deadliest cancer i

45 Colorectal cancer (CRC) is the second most common malign

46 of memory T cell response is inefficient in colorectal cancer (CRC) liver metastasis following exist

47 teria and inflammagens, and is implicated in colorectal cancer (CRC) pathogenesis.

48 RAS mutations in the blood of colorectal cancer (CRC) patients are emerging as biomark

49 tly, recurrence-free and overall survival of colorectal cancer (CRC) patients negatively correlates w

50 We recently identified a subset of colorectal cancer (CRC) patients who are heterozygous fo

51 Radioembolization is a treatment option for colorectal cancer (CRC) patients with inoperable, chemor

52 cleatum is an oral bacterium associated with colorectal cancer (CRC) proliferation, chemoresistance,

53 ontaining protein 1 (CDCP1) is predictive of colorectal cancer (CRC) recurrence and poor patient surv

54 ues, its roles in intestinal homeostasis and colorectal cancer (CRC) remain controversial.

55 Accurate colorectal cancer (CRC) risk prediction models are criti

56 Some guidelines recommend starting colorectal cancer (CRC) screening before age 50 years fo

57 Women have a lower incidence of colorectal cancer (CRC) than men, however, they have a h

58 ate microRNA-34a gene (MIR34A) expression in colorectal cancer (CRC) tissues compared with non-cancer

59 Colorectal cancer (CRC) tumors can be partitioned into f

60 lected from 2019 patients with stage I - III colorectal cancer (CRC) using convolutional neural netwo

61 The gut microbiota has been associated with colorectal cancer (CRC), but causal alterations precedin

62 immunity in syngeneic and genetic models of colorectal cancer (CRC), which can be attributed to defe

63 The incidence of early-onset colorectal cancer (CRC), which occurs in individuals <50

64 d with tumor relapse and reduced survival in colorectal cancer (CRC).

65 their metabolites affect the development of colorectal cancer (CRC).

66 Colonoscopy is commonly used to screen for colorectal cancer (CRC).

67 ic driver in several solid tumors, including colorectal cancer (CRC).

68 etes is associated with an increased risk of colorectal cancer (CRC).

69 owel disease (IBD) have an increased risk of colorectal cancer (CRC).

70 microbiota is influenced by sex hormones and colorectal cancer (CRC).

71 microbiota-related metabolites) and risk of colorectal cancer (CRC).

72 Here, we investigate FOXA1 function in human colorectal cancer (CRC).

73 h the transcript and protein levels in human colorectal cancer (CRC).

74 reshold with a 99% sensitivity (>= 2.12) for colorectal cancer (CRC).

75 led how netrin interacts with the deleted in colorectal cancer (DCC) receptor, other receptors, and c

76 Deleted in colorectal cancer (DCC), the receptor for the multifunct

77 n therapy (SIRT) in patients with metastatic colorectal cancer (mCRC), when informed by radiobiologic

78 The Molecular Epidemiology of Colorectal Cancer (MECC) study had information about ove

79 [HR: 0.80 (0.66, 0.98); P-trend = 0.01] and colorectal cancer [HR: 0.41 (0.21, 0.79); P-trend = 0.01

80 rovide new insights into the pathogenesis of colorectal cancer and a novel potential therapeutic targ

81 synthetic pathway, as a target in APC mutant colorectal cancer and also have implications for the cli

82 le agent in primary and metastatic models of colorectal cancer and enabled identification of novel mi

83 anism underlying a case of highly aggressive colorectal cancer and illustrates the importance of robu

84 re, generating tetraploid isogenic clones in colorectal cancer and in non-transformed cells, we show

85 We identified 396 patients with primary colorectal cancer and known somatic mutation status by n

86 ry for malignant lesions), prevents incident colorectal cancer and mortality.

87 We find that the reported lifetime risk of colorectal cancer can be recovered using a mathematical

88 ge II, 30% of stage III, and 32% of stage IV colorectal cancer cases.

89 ase and alpha-glucosidase activities and ii) colorectal cancer cell line (HT29) growth was also studi

90 analyzed RNA sequencing (RNA-seq) data from colorectal cancer cell lines (HCT116, RKO, and SW48) tha

91 FL3 response was diminished in colorectal cancer cell lines and human colorectal cancer

92 ression of these mutants in SW480 and HCT116 colorectal cancer cell lines increased their anchorage-i

93 tants were overexpressed in SW480 and HCT116 colorectal cancer cell lines, which were analyzed by imm

94 changes in DNA methylation to determine the colorectal cancer cell phenotype following loss of Apc f

95 fication of ERK1/2 signaling in KRAS-mutated colorectal cancer cells affects the cytokine milieu of t

96 Here we find that, in colorectal cancer cells and in developing mouse forelimb

97 y amplified ERK1/2 signaling in KRAS-mutated colorectal cancer cells as a driver of tumor-stroma inte

98 inhibitor) efficiently promoted apoptosis in colorectal cancer cells in response to Nutlin-3A, which

99 ion in paired primary/metastatic melanoma or colorectal cancer cells than those that are not.

100 We found that 5-FU resistance in DLD-1/5-FU colorectal cancer cells was mainly associated with SM in

101 hibitors) compounds are selectively toxic to colorectal cancer cells with APC mutations, although the

102 We incubated LS174T colorectal cancer cells with PGE(2) or without (control)

103 NA most highly up-regulated by incubation of colorectal cancer cells with PGE(2).

104 itor was mitochondria toxic and cytotoxic to colorectal cancer cells, but not to normal colon epithel

105 In colorectal cancer cells, FL3 treatment blocked phosphory

106 ne ANGPT2 and the cytokine receptor CXCR4 in colorectal cancer cells, which facilitated development o

107 signaling pathway, which is often altered in colorectal cancer cells.

108 xpression and inhibits the aggressiveness of colorectal cancer cells.

109 deep proteomic profiling of two independent colorectal cancer cohorts using mass spectrometry showed

110 mproves survival of patients with metastatic colorectal cancer compared with doublets + bevacizumab a

111 Furthermore, clinical colorectal cancer data set analysis showed that down-reg

112 ylation profiles are considered hallmarks of colorectal cancer development, the precise timing at whi

113 was to examine whether the increased risk of colorectal cancer due to cigarette smoking differed by a

114 ein (BMP) gradients drive this polarity, and colorectal cancer fundamentally reflects disruption of t

115 en associated with lower risks of breast and colorectal cancer in epidemiological studies; however, i

116 er incidence, but an increasing incidence of colorectal cancer in formerly low-incidence regions duri

117 ceptor (EGFR), and E-cad are associated with colorectal cancer in humans [10-17], our findings may sh

118 For low-risk adenoma individuals, colorectal cancer incidence was 0.55% (95% confidence in

119 t highly activated fibroblasts in metastatic colorectal cancer increase tissue stiffness and angiogen

120 Here we develop a mathematical model of colorectal cancer initiation through inactivation of two

121 n be recovered using a mathematical model of colorectal cancer initiation together with experimentall

122 monstrate that the order of driver events in colorectal cancer is determined primarily by the fitness

123 Colorectal cancer is the third most common cancer worldw

124 variants may prove predictive of early-onset colorectal cancer known an MUTYH-associated polyposis.

125 disease, yet how RAS-ERK signaling regulates colorectal cancer metastasis remains unknown.

126 all survival for patients after diagnosis of colorectal cancer metastatic disease, yet how RAS-ERK si

127 In a syngeneic colorectal cancer model, the inhibitor increased immune

128 Wnt signaling in Wnt-addicted pancreatic and colorectal cancer models.

129 These analyses by colorectal cancer molecular subtypes potentially explain

130 RBD variants, we stratified patient-derived colorectal cancer organoids with known Ras mutational st

131 des the longest overall survival reported in colorectal cancer patient with nonresectable liver metas

132 Over 50% of colorectal cancer patients develop resistance after a tr

133 selective biomarker that is able to identify colorectal cancer patients who are responding to anti-an

134 e Atlas Database indicates that KRAS mutated colorectal cancer patients with low intratumor ferritin

135 owards a disease-like configuration occur in colorectal cancer patients, thereby masking disease sign

136 n support of a potential role of ferritin in colorectal cancer progression, an analysis of The Cancer

137 Patients with nonresectable colorectal cancer receiving palliative chemotherapy has

138 ted from the prospectively collected Swedish Colorectal Cancer Registry.

139 dolescent obesity and its associated risk of colorectal cancer reinforces the urgent need to elucidat

140 Thus, colorectal cancer remains a heavy burden on society and

141 oscopic surgery, mortality and morbidity for colorectal cancer resections by Lapco delegates and non-

142 biopsies of 20 independent patients with MSI colorectal cancer revealed that a median number of 31 FS

143 d the impact of colonoscopist performance on colorectal cancer risk after adenoma removal.

144 tion to polyp characteristics in determining colorectal cancer risk after colonoscopy screening.

145 Cox models to identify associations between colorectal cancer risk and patient and adenoma character

146 rocessed meat has been suspected to increase colorectal cancer risk potentially via endogenous format

147 en dietary fruit or fiber intake and overall colorectal cancer risk that have previously been reporte

148 Compared with the general population, colorectal cancer risk was higher or comparable only for

149 res the effect of physician notification for colorectal cancer screening and cancer detection on pati

150 hysicians to increase their participation in colorectal cancer screening, which could, in turn, motiv

151 own intestinal disease who were referred for colorectal cancer screening.

152 physicians and nonphysicians are overdue for colorectal cancer screening.

153 ts of measuring and improving the quality of colorectal cancer screening.

154 afflicted with pancreatic, breast, colon and colorectal cancer show that our proposed method is compe

155 eveloped a deep-learning system that detects colorectal cancer specimens with dMMR or MSI using H&E-s

156 1 and further repressed CD24 translation and colorectal cancer stemness.

157 nd identify prevalent genetic alterations in colorectal cancer stromal cell populations.

158 vels of EMGS expression were detected in the colorectal cancer subsets consensus molecular subtype (C

159 ktE17K tumors resemble the human mesenchymal colorectal cancer subtype (CMS4), which is characterized

160 Colorectal cancer surgeries-prioritized as emergency, ur

161 Lapco increased the rate of laparoscopic colorectal cancer surgery and reduced mortality and morb

162 nts were recruited from medical oncology and colorectal cancer surgery departments in three hospitals

163 k of tumor recurrence in patients undergoing colorectal cancer surgery.

164 ogene, accounting for the well-known path to colorectal cancer through loss of tumor suppressors APC

165 PHB1 deficiency in mice or in human colorectal cancer tumoroids abolished FL3-induced expres

166 ed in colorectal cancer cell lines and human colorectal cancer tumoroids harboring a mutation at S45

167 ation to real data collected from metastatic colorectal cancer tumors, more associations between gene

168 rrence and reduced survival in patients with colorectal cancer tumors.

169 Patients with MMR-deficient colorectal cancer were excluded.

170 Patients with melanoma, thyroid, or colorectal cancer were excluded; patients with non-small

171 onic antigen (CEA, an important biomarker in colorectal cancer), integrated in the electrical circuit

172 583 patients with breast cancer, 24 975 with colorectal cancer, 6744 with oesophageal cancer, and 29

173 rian cancer, medulloblastoma, breast cancer, colorectal cancer, and lung cancer.

174 y mutations in gastric cancer, liver cancer, colorectal cancer, and pancreatic cancer were 5% (95% CI

175 longer survival in patients with early stage colorectal cancer, especially longer disease-free surviv

176 nt signaling has been intensively studied in colorectal cancer, it remains unclear whether activity i

177 Finally, APC mutations in colorectal cancer, KRAS in gastric cancer, and pancreati

178 Colorectal cancer, liver cancer, stomach cancer, pancrea

179 r types (different grades of breast cancers, colorectal cancer, melanoma, and insulinoma) and other d

180 cancer, five gynaecological malignancy, four colorectal cancer, one melanoma, and seven multiple myel

181 d to treat breast cancer, pancreatic cancer, colorectal cancer, or non-small cell lung cancer.

182 r adult intestinal stem cell homeostasis and colorectal cancer, relatively little is known about its

183 0 is overexpressed in many cancers including colorectal cancer, where overexpression is associated wi

184 formulate oral cetuximab (CTX) for targeting colorectal cancer, which is reported to express somatost

185 ence for Wnt-induced functional diversity of colorectal cancer-associated fibroblasts, representing a

186 2 and NOX1 in inflammatory bowel disease and colorectal cancer.

187 microsatellite stable subtype or late stage colorectal cancer.

188 nt peptide, in a population at high risk for colorectal cancer.

189 1-dependent proteomic ECM signature in human colorectal cancer.

190 mutated in human cancers, including ~30% of colorectal cancer.

191 diseases including breast cancer, glioma and colorectal cancer.

192 es was demonstrated in preclinical models of colorectal cancer.

193 levels and lower risks of breast cancer and colorectal cancer.

194 clear cell renal cell carcinoma (ccRCC) and colorectal cancer.

195 ons by identifying those at greatest risk of colorectal cancer.

196 CC/UICC TNM classification for patients with colorectal cancer.

197 malignant mutational genotypes on the way to colorectal cancer.

198 patitis B virus infection, and screening for colorectal cancer.

199 evidence for increased risks of prostate or colorectal cancer.

200 n tumor-bearing mice and patients with human colorectal cancer.

201 lities of stage II/III rectal and metastatic colorectal cancer.

202 mbats Wnt pathway-dependent cancers, such as colorectal cancer.

203 marking it a potential therapeutic target in colorectal cancer.

204 oplasia, including polyps, the precursor for colorectal cancer.

205 sser increases in risk for breast (1.05) and colorectal cancers (1.20).

206 e its importance in human cancers, including colorectal cancers (CRC), oncogenic KRAS has been extrem

207 aberrations (CNA) are frequently observed in colorectal cancers (CRC).

208 In all, we captured 31,587 colectomies, 5608 colorectal cancers (CRCs) 6608 cholecystectomies, and 41

209 e the prominent CD73(hi) population in human colorectal cancers (CRCs) and two CD73(-) murine tumor m

210 The majority of colorectal cancers (CRCs) initiate following APC mutatio

211 me NAT2 at 8p22, which is frequently lost in colorectal cancers and has a common variant with 10-fold

212 ach for treating patients with PIK3CA-mutant colorectal cancers and warrants further clinical evaluat

213 We identified 130 colorectal cancers in individuals who had adenomas remov

214 Analysis of human colorectal cancers revealed an inverse correlation betwe

215 excised hormone receptor-positive breast and colorectal cancers to predict overall patient survival.

216 n proposed as a candidate oncogene for human colorectal cancers with microsatellite instability and a

217 Using examples of breast and colorectal cancers, we show that individual cells evolve

218 th of PIK3CA-mutant, but not wild-type (WT), colorectal cancers.

219 ity and mortality from prostate, breast, and colorectal cancers.

220 ntibody therapy, and microsatellite instable colorectal cancers.

221 ) signaling pathway plays a critical role in colorectal carcinogenesis.

222 d alter the intestinal microbiome to promote colorectal carcinogenesis.

223 Colorectal carcinoid tumor IRs increased more steeply th

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

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

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

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

228 RAS from a patient with extremely aggressive colorectal carcinoma.

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

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

231 Expression of the APC IDR in colorectal cells promotes Axin puncta formation and beta

232 The discovery of colorectal (CR) cancer stem cell (CSC) as the cell compa

233 In the context of the colorectal crypt, we see that mutations in APC can lead

234 athways on the migration of cells within the colorectal crypt.

235 Visceromotor responses to colorectal distension, an indicator of VH, were recorded

236 emarkably alleviated naturally occurring and colorectal distension-induced AD.

237 ment or those who develop colitis-associated colorectal dysplasia or cancer, still require restorativ

238 ession of CD2 in the majority of people with colorectal, endometrial or ovarian cancer.

239 cause genetic and epigenetic alterations in colorectal epithelial cells but also affect the gut micr

240 cluding hip/knee replacement, hepatobiliary, colorectal, gynecology oncology, bariatric, general, and

241 wed significantly higher fluorescence in the colorectal lesions than in surrounding tissue, with a ta

242 uppression of untreated benign and malignant colorectal lesions.

243 %, P = 0.001), preoperative chemotherapy for colorectal liver metastases (70%, 82%, 89%, P < 0.001) a

244 gy of tumor-associated macrophages (TAMs) in colorectal liver metastasis (CLM) represents a correlate

245 Patients who had colorectal, liver, and pancreas operations abstracted in

246 lth and different types of cancer, including colorectal, lung, pancreatic, and oral malignancies.

247 Non-colorectal Lynch syndrome cancers were reported in 36 pa

248 HIV transmission via genital and colorectal mucosa are the most common routes of dissemin

249 bution and retention in a subcutaneous flank colorectal murine tumor, and therapeutic response charac

250 red with breast (n = 1904), lung (n = 1629), colorectal (n = 1080), and prostate (n = 1055) cancer.

251 identify all prognostic factors for advanced colorectal neoplasia (aCRN, high-grade dysplasia, or CRC

252 Endoluminal surgery for the treatment of colorectal neoplasia is typically carried out using elec

253 recognized carcinogens, are risk factors for colorectal neoplasia, including polyps, the precursor fo

254 overy phase (n = 39) and individuals without colorectal neoplasms (controls, n = 39).

255 ly associated with the risk of lung, breast, colorectal, or prostate cancers (OR range 0.78-1.10; P >

256 opy-based, case-control study, the Tennessee Colorectal Polyp Study.

257 Nerve endings arising from two classes of colorectal-projecting DRG neuron were identified.

258 high in fat, is a modifiable risk factor for colorectal recurrence after curative resection.

259 es in the microbiome, in mice that underwent colorectal resection.

260 Colorectal resections and anastomoses were then performe

261 to further increase with the introduction of colorectal screening programs throughout Europe.

262 igh-risk survivors, adherence to COG breast, colorectal, skin, and cardiac surveillance was 12.6% (95

263 We reviewed the pathology records of 152 colorectal specimens from 2010 to 2012 (46 CRCs, 74 adva

264 k of surgical site infection (SSI) following colorectal surgery as noncarriers.

265 secutive series of adult patients undergoing colorectal surgery with primary anastomosis was enrolled

266 uded were adult patients undergoing elective colorectal surgery with the American-Society-of-Anesthes

267 copy has demonstrated a protective effect in colorectal surgery, but these effects have not been gene

268 With increased use of robotic technology in colorectal surgery, there is a burden to demonstrate the

269 t denominator of postoperative outcome after colorectal surgery.

270 BNP increases with iv-fluid volumes given to colorectal surgical patients, and the level of NT-Pro-BN

271 frequency, and then the association between colorectal testing in family physicians and their patien

272 Uptake of colorectal tests by family physicians was associated wit

273 th experimentally measured mutation rates in colorectal tissues and proliferation rates of premaligna

274 s and 96 genes (928 RNA probes) in lymphoid, colorectal tumor and autoimmune tissues by using the nCo

275 NA expression profiling of 124 fresh, paired colorectal tumor and nontumor samples (30 CRC; 32 AAs) f

276 ted the effect of platelet interactions with colorectal tumor cells.

277 Prostaglandin E(2) (PGE(2)) promotes colorectal tumor formation and progression by unknown me

278 e was no correlation between postcolonoscopy colorectal tumor size and time to diagnosis after index

279 Colorectal tumor subtypes might therefore be used in det

280 damage, and cell proliferation and increases colorectal tumorigenesis in 11G5-infected Apc(Min/+) mic

281 5 inhibition attenuates lipid metabolism and colorectal tumorigenesis in mice.

282 lipid metabolism, and the susceptibility to colorectal tumorigenesis.

283 beta-catenin, a driver of proliferation and colorectal tumorigenesis.

284 ic, and phenotypic information from 12 human colorectal tumors (11 carcinomas, 1 adenoma) obtained th

285 a(2+)/Li(+) exchanger NCLX (SLC8B1) in human colorectal tumors and its association with advanced-stag

286 ls significant heterogeneity between primary colorectal tumors and their liver metastases.

287 Patients with type 2 colorectal tumors had significantly shorter time of DSS

288 7], our findings may shed light on how human colorectal tumors progress.

289 ts into the different molecular subgroups of colorectal tumors that develop via each of these differe

290 of 473 families, including 488 patients with colorectal tumors that had normal expression of mismatch

291 Colorectal tumors were found in 88% of mice fed the West

292 Ps) are precursors to 20% to 30% of cases of colorectal tumors, but patients' long-term risk after re

293 that MDFI is up- and MDFIC downregulated in colorectal tumors.

294 , and somatic mutations in APC and CTNNB1 in colorectal tumors.

295 in RSPO genes have been identified in human colorectal tumors.

296 ere reviewed for the primary location of the colorectal tumour, and the side and number of hepatic me

297 as no significant difference in terms of the colorectal tumours' primary location (p = 0.325).

298 iotics in adult patients undergoing elective colorectal, upper gastrointestinal, transplant, or hepat

299 g magnetic resonance imaging (MRI) data from colorectal xenograft models.

300 propargyl derivative of 5-FU was shown in a colorectal zebrafish xenograft model that led to signifi