ライフサイエンスコーパス: colorectal cancer

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

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

3 1-dependent proteomic ECM signature in human colorectal cancer.

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

5 diseases including breast cancer, glioma and colorectal cancer.

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

7 es was demonstrated in preclinical models of colorectal cancer.

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

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

10 malignant mutational genotypes on the way to colorectal cancer.

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

12 tion and the incidence of and mortality from colorectal cancer.

13 evidence for increased risks of prostate or colorectal cancer.

14 copy is crucial in reducing the mortality of colorectal cancer.

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

16 a chemotherapeutic drug widely used to treat colorectal cancer.

17 om two independent cohorts, predominantly in colorectal cancer.

18 atherosclerosis, and inflammation-associated colorectal cancer.

19 colorectal lesions in high-risk patients for colorectal cancer.

20 egy as compared with PIK3CA WT patients with colorectal cancer.

21 se metastasis and orthotopic models of human colorectal cancer.

22 el syndrome, inflammatory bowel disease, and colorectal cancer.

23 ith disease-specific and overall survival in colorectal cancer.

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

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

26 marking it a potential therapeutic target in colorectal cancer.

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

28 2 and NOX1 in inflammatory bowel disease and colorectal cancer.

29 microsatellite stable subtype or late stage colorectal cancer.

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

31 ntibody therapy, and microsatellite instable colorectal cancers.

32 olyposis coli (APC) is frequently mutated in colorectal cancers.

33 he second most frequent in head-and-neck and colorectal cancers.

34 whom with early stage and 91 with late stage colorectal cancers.

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

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

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

38 583 patients with breast cancer, 24 975 with colorectal cancer, 6744 with oesophageal cancer, and 29

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

40 implicated in initiation and progression of colorectal cancer along with major players such as intes

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

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

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

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

45 describes a distinct mutational signature in colorectal cancer and implies that the underlying mutati

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

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

48 ent levels of classification in samples from colorectal cancer and melanoma cell lines.

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

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

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

52 The ESRP1 transcript is reduced in primary colorectal cancer, and its expression correlates with th

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

54 (LS) predisposes to endometrial cancer (EC), colorectal cancer, and other cancers through inherited p

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

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

57 n tested for Wnt-dependent cancers including colorectal cancer, but are unsuccessful due to severe ad

58 n human pancreatic ductal adenocarcinoma and colorectal cancer by impairing the function of the chemo

59 Detection rates were similar for colorectal cancer.(C) RSNA, 2020See also the editorial b

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

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

62 y is aberrantly activated in the majority of colorectal cancer cases due to somatic mutations in the

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

64 sues and of cancers, including datasets from colorectal cancer (CC), prostate cancer (PC), lung cance

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

66 human pancreatic cancer MIAPaCa-2, and human colorectal cancer cell line WiDr.

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

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

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

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

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

72 inoculated with hFcRn-expressing HT-29 human colorectal cancer cell xenografts, compared to CRISPR/Ca

73 The expression of full-length APC in SW480 colorectal cancer cells (SW480+APC) not only reduces Wnt

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

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

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

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

78 graft model, overexpression of miR-1185-1 in colorectal cancer cells substantially reduced tumor grow

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

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

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

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

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

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

85 In colorectal cancer cells, FL3 treatment blocked phosphory

86 issue of Science, Russo et al. observe that colorectal cancer cells, when exposed to the pressure of

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

88 mulated and MDFIC inhibited growth of HCT116 colorectal cancer cells.

89 metastatic potential of Wnt-dependent human colorectal cancer cells.

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

91 xpression and inhibits the aggressiveness of colorectal cancer cells.

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

93 participants who received aspirin developed colorectal cancer compared with 58 (13%) of 434 who rece

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

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

96 inical experience with mt-sDNA screening for colorectal cancer (CRC) and compare results with CT colo

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

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

99 rium nucleatum is implicated in accelerating colorectal cancer (CRC) and is found within metastatic C

100 igher proportion of patients with vs without colorectal cancer (CRC) and promote colorectal carcinoge

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

102 Estimates of absolute risk of colorectal cancer (CRC) are needed to facilitate communi

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

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

105 We previously showed that mutant KRAS colorectal cancer (CRC) cells release sEVs containing Ra

106 types but is abundant in well-differentiated colorectal cancer (CRC) cells where it functions to inhi

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

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

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

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

111 of nuclear beta-catenin and a suppressor of colorectal cancer (CRC) growth in cell culture and mouse

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

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

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

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

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

117 Colorectal cancer (CRC) incidence and mortality are incr

118 Colorectal cancer (CRC) incidence is increasing among yo

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

120 Oncogenic transformation in colorectal cancer (CRC) is driven by mutations in APC, K

121 Screening for colorectal cancer (CRC) is effective in the population a

122 The incidence of colorectal cancer (CRC) is increasing worldwide.

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

124 Colorectal cancer (CRC) is prevalent with high mortality

125 Colorectal cancer (CRC) is the most common gastrointesti

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

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

128 Colorectal cancer (CRC) is the third most commonly diagn

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

130 Here we show that in a colorectal cancer (CRC) model, primary tumors release in

131 The primary tumors of colorectal cancer (CRC) often metastasize to the liver.

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

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

134 At diagnosis, 22% of colorectal cancer (CRC) patients have metastases, and 50

135 sue samples from a cohort of 432 chemo-naive colorectal cancer (CRC) patients iteratively labeled wit

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

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

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

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

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

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

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

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

144 pheroid traps, into which multiple pre-grown colorectal cancer (CRC) spheroids were loaded.

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

146 ddress these deficiencies with biofabricated colorectal cancer (CRC) tissue equivalents, which are bu

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

148 Inactivation of DNA mismatch repair propels colorectal cancer (CRC) tumorigenesis.

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

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

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

152 bolism has been linked to the development of colorectal cancer (CRC), but the underlying mechanism is

153 re analysis (TA) for differentiating between colorectal cancer (CRC), colonic lesions caused by infla

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

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

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

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

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

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

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

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

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

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

164 nes and associated with an increased risk of colorectal cancer (CRC).

165 S), have been associated with development of colorectal cancer (CRC).

166 has been used as a diagnostic biomarker for colorectal cancer (CRC).

167 ling dysregulation promotes tumorigenesis in colorectal cancer (CRC).

168 ative colitis (UC), Crohn's disease (CD) and colorectal cancer (CRC).

169 itor vemurafenib in patients with metastatic colorectal cancer (CRC).

170 (GWASs) implicate 16q22.1 locus in risk for colorectal cancer (CRC).

171 igh BMI is associated with increased risk of colorectal cancer (CRC).

172 and induce drug resistance and recurrence in colorectal cancer (CRC).

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

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

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

176 eostasis and is aberrantly activated in most colorectal cancers (CRC) through mutation of the tumor s

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

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

179 illous histology or high-grade dysplasia, or colorectal cancer [CRC]) and assessed whether baseline c

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

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

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

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

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

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

186 n 7.1 years and information was collected on colorectal cancer development and death.

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

188 arting point for the development of new anti-colorectal cancer drugs.

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

190 Early-onset colorectal cancer (EOCRC) incidence rates (IRs) are risi

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

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

193 several modifier candidates were depleted in colorectal cancer genomes, suggesting that similar mecha

194 [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

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

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

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

198 more than 3-fold, without increasing risk of colorectal cancer in patients with adenomas.

199 ted a total of 2666 newly diagnosed cases of colorectal cancer in these cohorts.

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

201 osphate (NADPH) production, lipogenesis, and colorectal cancers in which ME1 transcripts are upregula

202 d carcinoid tumors (which are classified as "colorectal cancer" in SEER [Surveillance, Epidemiology,

203 evelop a risk classification system based on colorectal cancer incidence and mortality following aden

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

205 e its predictions to epidemiological data on colorectal cancer incidence.

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

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

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

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

210 Colorectal cancer is a heterogeneous disease that develo

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

212 Carcinoma development in colorectal cancer is driven by genetic alterations in nu

213 Colorectal cancer is the third most common cancer worldw

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

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

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

217 Colorectal cancer, liver cancer, stomach cancer, pancrea

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

219 oved as a first-line treatment in metastatic colorectal cancer (mCRC).

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

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

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

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

224 wed a trend that PIK3CA-mutant patients with colorectal cancer might derive greater benefit from this

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

226 e (AOM)/dextran sodium sulfate (DSS)-induced colorectal cancer model.

227 Colorectal cancer models were carried out in villin-TLR4

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

229 These analyses by colorectal cancer molecular subtypes potentially explain

230 Oncogenic mutations in PIK3CA render colorectal cancers more dependent on glutamine.

231 o significant inverse trend was observed for colorectal cancer mortality.

232 observed between yogurt consumption and the colorectal cancer mortality.

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

234 rval [CI]: 0.27 to 0.98, P-value = 0.04) and colorectal cancer (OR: 0.66, 95% CI: 0.48 to 0.90, P-val

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

236 (2020) employ intravital microscopy of colorectal cancer organoid xenografts to investigate the

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

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

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

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

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

242 his prospective (SECA-II) study, we included colorectal cancer patients with nonresectable liver-only

243 y unclear role of steroid hormones in female colorectal cancer patients, our findings suggest a tumor

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

245 spital database was utilised to identify the colorectal cancer patients.

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

247 and inflammation are a critical component of colorectal cancer progression, and they are used as reli

248 Patients with nonresectable colorectal cancer receiving palliative chemotherapy has

249 ted from the prospectively collected Swedish Colorectal Cancer Registry.

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

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

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

253 a biomarker of patient outcome after primary colorectal cancer resection by directly analysing scanne

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

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

256 Analysis of human colorectal cancers revealed an inverse correlation betwe

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

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

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

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

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

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

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

264 Using data from the Polish National Colorectal Cancer Screening Program, we developed a risk

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

266 physicians and nonphysicians are overdue for colorectal cancer screening.

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

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

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

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

271 1 and further repressed CD24 translation and colorectal cancer stemness.

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

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

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

275 The 3.2% proportion of LS-EC is similar to colorectal cancer, supporting unselected screening of EC

276 Colorectal cancer surgeries-prioritized as emergency, ur

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

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

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

280 ancolonic chromoendoscopy is recommended for colorectal cancer surveillance in patients with Lynch sy

281 Colorectal cancer survivors relied on oncology professio

282 This study explores associations between colorectal cancer survivors' healthcare experiences and

283 are an important histopathologic feature of colorectal cancer that confer prognostic information.

284 T-Alg are a promising platform for targeting colorectal cancer through GIT.

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

286 ion of miR-1185-1 was downregulated in human colorectal cancer tissues, whereas expression of CD24 wa

287 needed to stratify patients with early-stage colorectal cancer to refine selection of adjuvant therap

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

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

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

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

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

293 F screening guidelines for lung, breast, and colorectal cancer via their website, and reviewed all re

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

295 Patients with MMR-deficient colorectal cancer were excluded.

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

297 0 is overexpressed in many cancers including colorectal cancer, where overexpression is associated wi

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

299 The case for prevention of colorectal cancer with aspirin in Lynch syndrome is supp

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