ライフサイエンスコーパス: colorectal

1 including 46 solid-organ cancers (renal, 11; colorectal, 11; prostate, 7; breast, 5; pancreas, 5; ova

2 mbled to deliver CO to a suspension of human colorectal adenocarcinoma cells (HT-29) under the contro

3 In contrast, PD-L1 on MC38 colorectal adenocarcinoma cells is sufficient to suppres

4 ke, and inhibited the proliferation of DLD-1 colorectal adenocarcinoma cells to a greater extent than

5 To study the regulation of colorectal adenocarcinoma progression by O-GlcNAc, we ha

6 ioembolization for liver-dominant metastatic colorectal adenocarcinoma.

7 In summary, we demonstrated that both colorectal adenoma and CRC are monoclonal in origin, and

8 of vitamin D3 or calcium supplementation on colorectal adenoma recurrence.

9 l therapeutic strategy to target KRAS mutant colorectal and lung cancers.

10 is instead used almost exclusively to treat colorectal and other gastrointestinal cancers.

11 ng cancer deaths) and 80,672 Prostate, Lung, Colorectal and Ovarian Cancer Screening Trial (PLCO) eve

12 andardized incidence ratios of lung, breast, colorectal, and all second cancers in HL survivors with

13 ld, and 1.8-fold differences shown for lung, colorectal, and breast cancers, respectively.

14 iac, orthopedic joint replacement, vascular, colorectal, and hysterectomy procedures during the perio

15 cer mortality, but the PLCO (Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial) found no

16 most common cancers (breast, lung, prostate, colorectal, and stomach).

17 ctal cancer resections in the Dutch Surgical Colorectal Audit in 2011 were extended with additional t

18 The C statistics for colorectal (C = 0.607), colon (C = 0.603), and rectal (C

19 tly lower risks, per 10000 person-years, for colorectal cancer (-6 cases [95% CI, -9 to -1]), diabete

20 confidence intervals (95%CI) for developing colorectal cancer (2,636 incident cases) were estimated

21 ), Hodgkin disease (41 patients, 182 scans), colorectal cancer (70 patients, 286 scans), melanoma (69

22 of more than ten types of cancer, including colorectal cancer (and advanced adenomas), endometrial c

23 or 7 to 9 months (n = 1335) for risk of any colorectal cancer (cases per 1000 8-30 days, 30; 2 month

24 Interval colorectal cancer (CRC) accounts for 3% to 8% of all cas

25 , and their relatives have similar risks for colorectal cancer (CRC) as those diagnosed with serrated

26 CKGROUND & AIMS: Among subjects screened for colorectal cancer (CRC) by the guaiac fecal occult blood

27 Here, using several clinically relevant colorectal cancer (CRC) gene expression signatures, we a

28 n dietary inflammatory potential and risk of colorectal cancer (CRC) in 87,042 postmenopausal women r

29 d safety of screening colonoscopy to prevent colorectal cancer (CRC) in persons aged 70 to 74 and tho

30 Colorectal cancer (CRC) is a leading cause of death in t

31 Human colorectal cancer (CRC) is a major cause of cancer morta

32 Colorectal cancer (CRC) is a worldwide health concern wi

33 Colorectal cancer (CRC) is characterized by genome-wide

34 what extent the proteomic landscape of human colorectal cancer (CRC) is maintained in established CRC

35 tigated the role of Akt survival proteins in colorectal cancer (CRC) metastasis and explored potentia

36 of MIIP-S303 phosphorylation correlates with colorectal cancer (CRC) metastasis and prognosis.

37 the highest incidence and mortality rates of colorectal cancer (CRC) of any ethnic group in the Unite

38 hat has been difficult to delineate in human colorectal cancer (CRC) patients.

39 Here we show that in a cell culture model of colorectal cancer (CRC) progression, we observe accumula

40 central, although poorly understood, role in colorectal cancer (CRC) progression.

41 archically organized cell compartment drives colorectal cancer (CRC) progression.

42 Advanced colorectal cancer (CRC) remains a critical health care c

43 Hereditary factors play an important role in colorectal cancer (CRC) risk, yet the prevalence of germ

44 of more than forty genetically diverse human colorectal cancer (CRC) specimens.

45 ancer diagnosis in an orthotopically induced colorectal cancer (CRC) xenograft model.

46 has been associated with a decreased risk of colorectal cancer (CRC), but the association may be rela

47 on beta-catenin activity in mouse models of colorectal cancer (CRC), CRC cell lines, and mouse and h

48 Colorectal cancer (CRC), the second leading cause of can

49 mpacts the transcriptional classification of colorectal cancer (CRC), with clinical and biological im

50 rtant role in the susceptibility to sporadic colorectal cancer (CRC).

51 ty to 5-fluorouracil (5-FU)-chemotherapy for colorectal cancer (CRC).

52 Wnt pathway are a characteristic feature of colorectal cancer (CRC).

53 asis-associated in colon cancer 1 (MACC1) in colorectal cancer (CRC).

54 that in humans, Netrin receptor, Deleted in Colorectal Cancer (DCC), is a master regulator of axonal

55 Chemotherapy-naive patients with metastatic colorectal cancer (WHO performance status 0 or 1) with l

56 BRAF was mutated in 7.6% (484 of 6353) of colorectal cancer and 9.1% (29 of 317) of SBA samples, b

57 mplex mechanisms that underlie metastasis in colorectal cancer and a potential novel biomarker for th

58 gh ADR is associated inversely with interval colorectal cancer and colorectal cancer death, the effec

59 cts of increased ADR on the risk of interval colorectal cancer and death.

60 eillance interval included family history of colorectal cancer and detection of 1-2 serrated polyps a

61 t large-scale genomic comparison of SBA with colorectal cancer and gastric carcinoma.

62 ameter values, including those estimated for colorectal cancer and glioblastoma multiforme, the distr

63 n suppressor, is frequently downregulated in colorectal cancer and other cancers.

64 of truncating MLH1 mutations presented with colorectal cancer at later ages than those with other mu

65 ey (among 276 patients with and survivors of colorectal cancer between October 15, 2015, and November

66 een shown to promote inflammation-associated colorectal cancer by accumulation of CD11b(+)Gr-1(+) imm

67 s, and immune reactions using data from 1380 colorectal cancer cases: 690 cases with proximal colon c

68 genetic screen in an isogenic pair of human colorectal cancer cell lines harboring mutant or wild-ty

69 Similarly, human colorectal cancer cell lines with increased KRAS mutant

70 LOX overexpression in colorectal cancer cells also induced a robust production

71 -Cy nanoparticles can be efficiently destroy colorectal cancer cells by inducing apoptosis as well as

72 ion of LOX activity blocked dissemination of colorectal cancer cells in the bone marrow and tumor-dri

73 ment of drug resistance to 5-fluorouracil in colorectal cancer cells is the primary cause of chemothe

74 ntal studies show that LOX overexpression in colorectal cancer cells or systemic delivery of the cond

75 e conditioned medium from LOX-overexpressing colorectal cancer cells promoted tumor cell disseminatio

76 Silencing CNOT3 in colorectal cancer cells resulted in replication arrest.

77 istant cells, we exposed cetuximab-sensitive colorectal cancer cells to cetuximab in three-dimensiona

78 Here we investigated whether LOX/HIF1 endows colorectal cancer cells with full competence for aggress

79 ntly, RT-activated CAFs promoted survival of colorectal cancer cells, as well as a metabolic switch f

80 were compared with wild-type EPHB1 in DLD-1 colorectal cancer cells, they decreased ephrin B1-induce

81 d gene expression profiles characteristic of colorectal cancer cells.

82 hogenetic protein (BMP) signaling pathway in colorectal cancer cells.

83 synergistic activity with leucovorin against colorectal cancer cells.

84 y, both miRNAs synergized with the frontline colorectal cancer chemotherapy drug irinotecan.

85 eucovorin, is the most commonly used drug in colorectal cancer chemotherapy, yet development of drug

86 In 90 colorectal cancer clinical specimens, a significant posi

87 group (11 patients with early and metastatic colorectal cancer convened during a teleconference in Au

88 nversely with interval colorectal cancer and colorectal cancer death, the effects of an increasing AD

89 About 25% of patients with colorectal cancer develop liver metastases after resecti

90 inues to provide substantial protection from colorectal cancer diagnosis and death, with protection l

91 tulated to be genotoxic and to contribute to colorectal cancer formation.

92 tify veterans having surgery for stage I-III colorectal cancer from 1999 to 2010.

93 d 21,152 patients diagnosed with stage I-III colorectal cancer from 2001 to 2011.

94 , and miR-23b individually could distinguish colorectal cancer from NCE.

95 rd-line or subsequent therapy for metastatic colorectal cancer has clinical benefit in patients with

96 n cancer, but its role in the development of colorectal cancer has yet to be fully examined.

97 ovarian cancer in 28 (10%) of 279 women; and colorectal cancer in 239 (50%) 479 men and women.

98 iers, mutations in MLH1 were associated with colorectal cancer in 249 (61%) of 409 men and women; end

99 INTERPRETATION: We found the risk of colorectal cancer in Asian patients with ulcerative coli

100 The risk of sporadic colorectal cancer in Asian populations is considered low

101 uR as a small-molecule target for preventing colorectal cancer in high-risk groups such as those with

102 ty diets are associated with a lower risk of colorectal cancer in most racial/ethnic subgroups.

103 ard ratio for subsequent detection of HGD or colorectal cancer in patients with fLGD and aneuploidy w

104 vailable for the epidemiology and outcome of colorectal cancer in relation to the three main surgical

105 Hazard ratios (HRs) and 95% CIs for colorectal cancer incidence and mortality were estimated

106 Removal of adenomas reduces colorectal cancer incidence and mortality; however, the

107 We estimated colorectal cancer incidence and standardised incidence r

108 We examined heterogeneity in colorectal cancer incidence in intermediate-risk patient

109 e associated with a significant reduction in colorectal cancer incidence rate (adjusted hazard ratio

110 ontrast, in patients without these features, colorectal cancer incidence was lower than that of the g

111 k patients and the effect of surveillance on colorectal cancer incidence.

112 eneity and unexpectedly remains regulated in colorectal cancer irrespective of KRAS mutation status.

113 Colorectal cancer is the commonest gastrointestinal carc

114 Colorectal cancer is the third most common cancer worldw

115 ologically confirmed recurrent or metastatic colorectal cancer locally assessed as dMMR/MSI-H from 31

116 ximal colon cancer and 690 cases with distal colorectal cancer matched by age and sex.

117 To find mutations involved in the colorectal cancer metastatic process, we performed deep

118 therapeutic interventions, which target the colorectal cancer microenvironment.

119 llowed by IGF1R neutralization in orthotopic colorectal cancer models reduced the number of mice with

120 NO2 was positively associated with colorectal cancer mortality [HR per 6.5 ppb=1.06 (95% CI

121 deline, cardiovascular disease mortality and colorectal cancer mortality were significantly reduced a

122 al number of edges, n = 173) than the distal colorectal cancer network (n = 95) (P < 0.0001 in permut

123 colon cancer network and 0.30 in the distal colorectal cancer network, indicating the greater cluste

124 Patients with lung or colorectal cancer often exhibit leukocytosis.

125 ods Eligible survivors had curable breast or colorectal cancer or melanoma, had completed treatment (

126 Colorectal cancer originates within immunologically comp

127 into clinical management and may ameliorate colorectal cancer patient outcomes.

128 iRNA-6883-5p encoding the clock gene PER1 in colorectal cancer patient samples.

129 hese findings were validated using data from colorectal cancer patients (n = 261).

130 e, there is no basis to prescribe statins to colorectal cancer patients who do not have cardiovascula

131 essed by tumor cells in the bone marrow from colorectal cancer patients with bone metastases.

132 ew loci whose expression correlates with the colorectal cancer patients' overall survival.

133 o 2012, we identified 1,265,684 hospitalized colorectal cancer patients.

134 CK levels correlate with reduced survival of colorectal cancer patients.

135 naling initiated by RT-activated CAF worsens colorectal cancer progression, establishing a preclinica

136 that paracrine IGF1/IGF1R signaling promotes colorectal cancer progression, establishing a preclinica

137 se was not associated with a reduced rate of colorectal cancer recurrence, but it was associated with

138 ions is considered low and risk estimates of colorectal cancer related to ulcerative colitis from Asi

139 loration as a pre-clinical model to evaluate colorectal cancer response to novel therapies.

140 and trunk fat percentage) measurements with colorectal cancer risk among 472,526 men and women follo

141 y Approaches to Stop Hypertension score) and colorectal cancer risk in the Multiethnic Cohort.

142 sed meat, refined grains, and desserts) with colorectal cancer risk may differ according to the prese

143 , the benefit of surveillance colonoscopy on colorectal cancer risk remains unclear.

144 rend = 0.005) was positively associated with colorectal cancer risk.

145 Ptrend = 0.002) were associated with greater colorectal cancer risk.

146 e of alcohol and whole grains in relation to colorectal cancer risk.

147 BRAF, KRAS and PIK3CA oncogenes in archival colorectal cancer samples to precisely map the spatial a

148 detected advanced neoplasms (AN) in a single colorectal cancer screening study.

149 We examined colorectal cancer screening tests according to quartiles

150 testing is the most commonly used method for colorectal cancer screening worldwide.

151 conomic approaches could increase uptake for colorectal cancer screening.

152 tests (FITs) for hemoglobin (Hb) are used in colorectal cancer screening.

153 ssue outcomes on an independent set of human colorectal cancer specimens (n = 37) revealed the model

154 Human colorectal cancer stem cells (CSCs) are tumour initiatin

155 dependent activation of RAS more potently in colorectal cancer than in melanoma and causes resistance

156 fied several novel oncogenic gene fusions in colorectal cancer that may drive malignant development a

157 adioimmunotherapy regimen for GPA33-positive colorectal cancer tumors in humans.

158 breast cancer was 5.7%, and the incidence of colorectal cancer was 1.6%.

159 ression in primary tumors from patients with colorectal cancer was associated with poor clinical outc

160 and upregulation of INHBB and AXL in primary colorectal cancer was associated with poor patient survi

161 l elective resections for a T1-3N0-2M0 stage colorectal cancer were included between 2010 and 2012 in

162 s of deceased patients with advanced lung or colorectal cancer who were enrolled in the Cancer Care O

163 with newly diagnosed advanced or metastatic colorectal cancer whose tumour was wild-type for BRAF, P

164 omly assigned to be invited to screening for colorectal cancer with FS or CT colonography.

165 ltrate on EGFR activation was also seen in a colorectal cancer xenograft.

166 trin-1 guidance cue receptor DCC (deleted in colorectal cancer) appear to confer resilience or suscep

167 There were 546 men and women with colorectal cancer, 162 women with endometrial cancer, an

168 -treated patients with dMMR/MSI-H metastatic colorectal cancer, and could be a new treatment option f

169 ealed their importance in the development of colorectal cancer, and studies from animal models have p

170 istics, health history, and risk factors for colorectal cancer, and were followed from index colonosc

171 nce of associations between AF and breast or colorectal cancer, but there have been no longitudinal s

172 signaling pathway drives the development of colorectal cancer, but understanding of this pathway rem

173 nificant association between AF and incident colorectal cancer, but we did see a 19% excess risk of i

174 r signaling is altered during development of colorectal cancer, models of study, interaction of pathw

175 of 676 genes in 107 stages II to IV primary colorectal cancer, of which half had metastasized.

176 also modeled a known functional risk SNP of colorectal cancer, rs6983267, in HCT-116 cells.

177 To guide immunotherapy in colorectal cancer, simulation of immunotherapy in preest

178 ith KRAS wt untreated advanced or metastatic colorectal cancer, there was no significant difference i

179 sly unrecognized chemoresistance mediator in colorectal cancer, thereby establishing the microbiota a

180 Notably, miR-23b, which was increased in colorectal cancer, was predicted to target the SC-expres

181 H1-HES1 molecular axis as a CSC regulator in colorectal cancer, with potential implications to improv

182 recently identified as a tumor suppressor in colorectal cancer, yet its potential role in PCa has not

183 osed them to specific-pathogen-free (SPF) or colorectal cancer-associated bacteria.

184 In the current work, we report a novel colorectal cancer-associated FEN1 mutation, L209P.

185 es (DQIs) have been related to lower risk of colorectal cancer-mostly among whites.

186 w primary endpoint in patients with advanced colorectal cancer.

187 rce in fiber and vitamin D increase risks of colorectal cancer.

188 s a commonly accepted surgical procedure for colorectal cancer.

189 r, 24% in prostate cancer, and 16% to 30% in colorectal cancer.

190 port the efforts of ICHOM's working group in colorectal cancer.

191 onal role of a novel circRNA, circCCDC66, in colorectal cancer.

192 ed survival time of patients with metastatic colorectal cancer.

193 bit potential for therapeutic development in colorectal cancer.

194 e homeostasis and various cancers, including colorectal cancer.

195 osa associated with WD and predisposition to colorectal cancer.

196 present valid targets for chemoprevention of colorectal cancer.

197 .06) but not for AIAN patients with lung and colorectal cancer.

198 deaths from any cause, and 4,066 deaths from colorectal cancer.

199 ilitating symptoms in patients with advanced colorectal cancer.

200 n advanced or metastatic KRAS wild-type (wt) colorectal cancer.

201 helial to mesenchymal transition and promote colorectal cancer.

202 rs, especially hepatocellular carcinoma, and colorectal cancer.

203 , a tumor-associate antigen (TAA) related to colorectal cancer.

204 ed adenomas, and 189 participants (1.2%) had colorectal cancer.

205 cosa and universally expressed by metastatic colorectal cancer.

206 ng cell-free DNA of 59 patients with lung or colorectal cancer.

207 ) is critical for the accumulation of CSC in colorectal cancer.

208 is of colitis-associated cancer and sporadic colorectal cancer.

209 en EPHB receptor mutations and metastasis in colorectal cancer.

210 t this novel combinatorial treatment against colorectal cancer.

211 atory bowel diseases (IBD) increase risk for colorectal cancer.

212 adversely affects survival in patients with colorectal cancer.

213 antioxidant enzyme in APC-mutation-positive colorectal cancer.2-Cys peroxiredoxin (Prx) enzymes are

214 implicated in inflammatory bowel disease and colorectal cancer; however, colonization alone is insuff

215 nhibitors is not replicated in most cases of colorectal cancer; therefore, different strategies are u

216 rongly resistant to experimental colitis and colorectal cancer; this is mainly through a remodelled g

217 Through genomic analysis of colorectal cancers and cell lines, we find frequent loss

218 Approximately 15% of colorectal cancers exhibit microsatellite instability (M

219 bution of somatic mutations to metastasis of colorectal cancers is currently unknown.

220 splayed elevated expression in primary human colorectal cancers that was associated with lymph-node m

221 Here the authors show that in colorectal cancers with APC mutation, PrxII binds to tan

222 Here we show that colonization of human colorectal cancers with Fusobacterium and its associated

223 active histone mark H3K4me2 in primary human colorectal cancers, as compared with corresponding benig

224 had diagnoses of metastatic appendiceal and colorectal cancers, respectively.

225 efore, ER stress poses a promising target in colorectal cancers, which develop as a result of Wnt act

226 erative colitis with a total of 293 reported colorectal cancers.

227 ofiles observed in mismatch repair-deficient colorectal cancers.

228 also at sites modulated in certain types of colorectal cancers.

229 maintenance of liver metastasis derived from colorectal cancers.

230 ose aspirin (ASA) reduces heart diseases and colorectal cancers.

231 l radiosensitizers have never been tested on colorectal cancers.

232 ative mortality risks for lung, gastric, and colorectal cancers.

233 dy shed further light into the complexity of colorectal carcinogenesis, but it also puts forward a po

234 hese cells or the CX3CR1 receptor may affect colorectal carcinogenesis.

235 ptor (EGFR) signaling is a known mediator of colorectal carcinogenesis.

236 ht be a useful chemopreventive agent against colorectal carcinogenesis.

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

238 Incidence of colorectal carcinoma subclassified by F nucleatum status

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

240 t efficiency of Cu-Cy nanoparticles on SW620 colorectal cells and elucidate the underlying mechanisms

241 tumorigenic potential and survival of human colorectal CSCs by epigenetically activating Wnt target

242 origenic growth and chemoresistance of human colorectal CSCs.

243 nvestigation of the role of mesentery fat in colorectal diseases.

244 f individuals with Lynch syndrome-associated colorectal, endometrial, and/or ovarian cancers whose me

245 the azoxymethane (AOM)-induced precancerous colorectal lesion model in rats.

246 in patients who had a complete resection of colorectal liver metastases (CLM).

247 preoperative chemotherapy and resection for colorectal liver metastases (CLM).

248 nant liver ischemia (RLI) after resection of colorectal liver metastases (CLMs) is unknown to date.

249 was to evaluate outcomes after resection of colorectal liver metastases (CRLM) and concurrent extrah

250 KRAS-mutated colorectal liver metastases (CRLM) are known to be more

251 e as a catalyst for photothermal ablation of colorectal liver metastases by increasing ablation zones

252 om 16 centers, a shift in indications toward colorectal liver metastases from 53% to 77% and a revers

253 of laparoscopic and open liver resection for colorectal liver metastases in the elderly.

254 Intraarterial therapy options for colorectal liver metastases include chemoinfusion via a

255 cancer has clinical benefit in patients with colorectal liver metastases with liver-dominant disease

256 ated tumor regressions in primary tumors and colorectal liver metastases.

257 For colorectal liver metastasis (CRLM), intrahepatic lymph i

258 istar rats were implanted with 5 x 10(6) rat colorectal liver metastasis cell line cells.

259 We included melanoma, breast, colorectal, lung, esophageal, and hepato-pancreato-bilia

260 eview summarizes current evidence for FIT in colorectal neoplasia detection and the comparative effec

261 t and indicate that risk of serrated pathway colorectal neoplasms could be reduced with lifestyle cha

262 A detailed case study on breast neoplasms, colorectal neoplasms, lung neoplasms, and 32 other disea

263 rsons newly diagnosed with cancer (prostate, colorectal, non-small-cell lung, non-Hodgkin lymphoma, b

264 or patients diagnosed with breast, prostate, colorectal, or lung cancer between 2000 and 2013 for eac

265 sed in CRC screening, effectively identifies colorectal polyps >/=10 mm and cancers.

266 recently diagnosed adenoma and no remaining colorectal polyps after complete colonoscopy.

267 en poultry consumption and the prevalence of colorectal polyps in this study.

268 who underwent EMR for large sessile or flat colorectal polyps or laterally spreading lesions, we ass

269 ong patients undergoing hepato-pancreatic or colorectal procedures.

270 et populations: patients undergoing elective colorectal resection and patients undergoing emergency h

271 ntified who underwent a hepato-pancreatic or colorectal resection and received >/=1 unit of PRBCs bet

272 a prospective cohort study in adult elective colorectal resection patients after conventional (n = 46

273 Among patients undergoing colorectal resection, ERAS implementation was associated

274 In the hands of experienced colorectal specialists treating selected patients, LP ma

275 ration in FAP patients significantly altered colorectal stem cell dynamics, which might explain the c

276 In colorectal surgery specifically, small studies have show

277 In an ERP for colorectal surgery, staff-directed facilitation of early

278 ents undergoing elective, clean contaminated colorectal surgery, the use of IPA failed to meet criter

279 ine-alcohol for elective, clean-contaminated colorectal surgery.

280 site infection (SSI) prevention in elective colorectal surgery.

281 -fold higher in primary tumors of metastatic colorectal than in nonmetastatic cases and preferentiall

282 Using DNAm assayed in whole blood and colorectal tissue of 132 admixed individuals from Colomb

283 -164 cells but also heterologous C51 or CT26 colorectal tumor cells in a CD8(+) T-cell-dependent proc

284 of RP-MDM2 binding significantly accelerated colorectal tumor formation while having no discernable e

285 hed 5-FU therapeutic response in a syngeneic colorectal tumor model consistent with increased DPYD-ac

286 expression of EGFR in myeloid cells from the colorectal tumor stroma associates with tumor progressio

287 ly up-regulated ( approximately 70 times) in colorectal tumor tissues compared with their normal pair

288 -MDM2-p53 pathway, is a critical mediator of colorectal tumorigenesis following APC loss.

289 ssion of chronic intestinal inflammation and colorectal tumorigenesis.

290 e (LS) have high lifetime risk of developing colorectal tumors (CRTs) because of a germline mutation

291 ts using single-cell RNA-seq from 11 primary colorectal tumors and matched normal mucosa.

292 analysis of transcriptional heterogeneity in colorectal tumors and their microenvironments using sing

293 We screened human colorectal tumors for EGFR-positive myeloid cells and in

294 Colorectal tumors from patients had increased levels of

295 es with the development of human right-sided colorectal tumors with epigenetic loss of MLH1.

296 ns are the most prevalent genetic changes in colorectal tumors, but it is unknown whether these mutat

297 subsets of pancreatic, ovarian, gastric, and colorectal tumors.

298 hibit the progression of neoantigen-specific colorectal tumors.

299 me sequencing data bank, cancer registry and colorectal tumour bank we determine the prevalence of Ly

300 We engineered compartmentalized biomimetic colorectal tumouroids with stromal surrounds that compri