ライフサイエンスコーパス: colorectal cancer

1 ing the terms FOLFOXIRI and bevacizumab and (colorectal cancer).

2 w primary endpoint in patients with advanced colorectal cancer.

3 ed survival time of patients with metastatic colorectal cancer.

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

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

6 bit potential for therapeutic development in colorectal cancer.

7 e homeostasis and various cancers, including colorectal cancer.

8 osa associated with WD and predisposition to colorectal cancer.

9 present valid targets for chemoprevention of colorectal cancer.

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

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

12 ilitating symptoms in patients with advanced colorectal cancer.

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

14 helial to mesenchymal transition and promote colorectal cancer.

15 rs, especially hepatocellular carcinoma, and colorectal cancer.

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

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

18 tive Wnt signaling is frequently observed in colorectal cancer.

19 t is linked to multiple human infections and colorectal cancer.

20 AF and the development of invasive breast or colorectal cancer.

21 of proximal colon cancer, but not in distal colorectal cancer.

22 APC) tumor suppressor is frequently found in colorectal cancer.

23 a clinic-based cohort of 1,058 patients with colorectal cancer.

24 vely suppress ERK-driven growth of resistant colorectal cancer.

25 6 individuals in the control group died from colorectal cancer.

26 ily members activin and TGF-beta in advanced colorectal cancer.

27 ary outcomes were incidence and mortality of colorectal cancer.

28 ients during initial treatment of metastatic colorectal cancer.

29 ull cataloging of the true targets of MSI in colorectal cancer.

30 cosa and universally expressed by metastatic colorectal cancer.

31 en EPHB receptor mutations and metastasis in colorectal cancer.

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

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

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

35 t this novel combinatorial treatment against colorectal cancer.

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

37 adversely affects survival in patients with colorectal cancer.

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

39 s a commonly accepted surgical procedure for colorectal cancer.

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

41 maintenance of liver metastasis derived from colorectal cancers.

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

43 l radiosensitizers have never been tested on colorectal cancers.

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

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

46 ofiles observed in mismatch repair-deficient colorectal cancers.

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

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

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

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

51 We found that in colorectal cancers, 30% of alterations identified as clo

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

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

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

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

56 Risk of any colorectal cancer and advanced-stage disease (defined as

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

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

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

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

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

62 ion was also observed in cetuximab-resistant colorectal cancer and head and neck squamous cell cancer

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

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

65 Cancer Registry, we identified 168 interval colorectal cancers and 44 interval cancer deaths.

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

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

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

69 n non-small-cell lung cancer, breast cancer, colorectal cancer, and pancreatic cancer published betwe

70 ncer, 36 (33%) in breast cancer, 25 (23%) in colorectal cancer, and six (6%) in pancreatic cancer.

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

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

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

74 BRAF V600E colorectal cancers are insensitive to RAF inhibitor mono

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

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

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

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

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

80 naling, which might be a candidate oncogenic colorectal cancer biomarker.

81 lpha1D of CaV1.3 channel is overexpressed in colorectal cancer biopsies compared to normal tissues.

82 d with a lower risk for F nucleatum-positive colorectal cancer but not F nucleatum-negative cancer, s

83 ients with IBD, IBD-cancer, FAP-adenoma, and colorectal cancer, but not in patients with IBD-dysplasi

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

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

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

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

88 ods using two different examples (breast and colorectal cancers) by merging gene expression data from

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

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

91 ctively, our findings show that LOX supports colorectal cancer cell dissemination in the bone marrow

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

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

94 endogenous levels in HCT116, HT29, and SW480 colorectal cancer cell lines.

95 endogenous colonic malignancies and of human colorectal cancer cell xenografts.

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

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

98 EPHB1 mutations, we demonstrated that DLD-1 colorectal cancer cells expressing EPHB1 form aggregates

99 m through which LOX-driven IL6 production by colorectal cancer cells impairs bone homeostasis.

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

101 g PrxII inhibits the expansion of APC-mutant colorectal cancer cells in vitro and in vivo tumor xenog

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

103 mapping, and expression analysis to examine colorectal cancer cells lacking one or both ARID protein

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

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

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

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

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

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

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

111 d gene expression profiles characteristic of colorectal cancer cells.

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

113 synergistic activity with leucovorin against colorectal cancer cells.

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

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

116 In 90 colorectal cancer clinical specimens, a significant posi

117 Colorectal cancers comprise a complex mixture of maligna

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

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

120 hereditary syndrome leading to high risks of colorectal cancer (CRC) and endometrial cancer mainly as

121 varepsilon (Polvarepsilon) cause hereditary colorectal cancer (CRC) and have been found in many spor

122 The global change in protein abundance in colorectal cancer (CRC) and its contribution to tumorige

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

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

125 entified discriminative splicing profiles of colorectal cancer (CRC) cells compared to adjacent norma

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

127 32 in tumorigenesis and tumor progression in colorectal cancer (CRC) has not been fully elucidated.

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

129 BACKGROUND & AIMS: The incidence of colorectal cancer (CRC) in individuals younger than 50 y

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

131 human cancers; however, the role of MLK3 in colorectal cancer (CRC) invasion is unknown.

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

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

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

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

136 s among unselected patients with early-onset colorectal cancer (CRC) is largely undetermined.

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

138 Colorectal cancer (CRC) is one of the most common malign

139 Among cancer diagnoses, colorectal cancer (CRC) is prevalent, with a lifetime ri

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

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

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

143 ulk whole-exome sequencing (bulk WES) on two colorectal cancer (CRC) patients with normal or adenomat

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

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

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

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

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

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

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

151 yte-to-monocyte ratio (LMR) in patients with colorectal cancer (CRC) undergoing curative resection an

152 ties in survival among elderly patients with colorectal cancer (CRC) were because of differences in t

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

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

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

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

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

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

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

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

161 ted with improved survival for patients with colorectal cancer (CRC).

162 a set of defined mutations toward metastatic colorectal cancer (CRC).

163 velopment of colon polyps in mouse models of colorectal cancer (CRC).

164 Aberrant WNT signaling drives colorectal cancer (CRC).

165 s strongly associated with the occurrence of colorectal cancer (CRC).

166 great number of non-coding risk variants for colorectal cancer (CRC).

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

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

169 , but associations with kidney, bladder, and colorectal cancer death warrant further investigation.

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

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

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

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

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

175 e also been implicated in several aspects of colorectal cancer formation.

176 primary invasive breast, prostate, lung, or colorectal cancer from 1997 to 2015.

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

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

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

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

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

182 About 40% of colorectal cancers have mutations in KRAS accompanied by

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

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

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

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

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

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

189 egulation of beta-catenin by GSK-3beta cause colorectal cancer in humans.

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

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

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

193 ary Prevention of Cardiovascular Disease and Colorectal Cancer" in 2016.

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

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

196 We estimated colorectal cancer incidence and standardised incidence r

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

198 Without surveillance, colorectal cancer incidence in patients with a suboptima

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

200 14.We assessed the effect of surveillance on colorectal cancer incidence using Cox regression with ad

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

202 In intention-to-treat analyses, colorectal cancer incidence was reduced by 26% (HR 0.74

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

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

205 Colorectal cancer is a major cancer type worldwide.

206 Colorectal cancer is the commonest gastrointestinal carc

207 Colorectal cancer is the third most common cancer worldw

208 he relationship between diet and the risk of colorectal cancer is unknown.

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

210 We found that human colorectal cancer liver metastases and murine gastrointe

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

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

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

214 therapeutic interventions, which target the colorectal cancer microenvironment.

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

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

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

218 ervention group versus the control group and colorectal cancer mortality was reduced by 30% (0.70 [0.

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

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

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

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

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

224 Patients with lung or colorectal cancer often exhibit leukocytosis.

225 g anti-EGF receptor therapy of patients with colorectal cancer or in patients resistant to EGF recept

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

227 nations at 10 to 12 months (n = 748) for any colorectal cancer (OR, 1.48 [95% CI, 1.05-2.08]; 49 case

228 s) and more than 12 months (n = 747) for any colorectal cancer (OR, 2.25 [95% CI, 1.89-2.68]; 76 case

229 Colorectal cancer originates within immunologically comp

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

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

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

233 us cell cancer cell lines and in tumors from colorectal cancer patients that progressed on cetuximab.

234 S was a recurrent mechanism of resistance in colorectal cancer patients that was not seen in similarl

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

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

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

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

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

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

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

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

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

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

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

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

247 and procedural characteristics identified as colorectal cancer risk factors.

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

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

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

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

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

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

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

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

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

257 We examined colorectal cancer screening tests according to quartiles

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

259 conomic approaches could increase uptake for colorectal cancer screening.

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

261 The association of prudent diet with colorectal cancer significantly differed by tissue F nuc

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

263 ed all-cause and prostate, breast, lung, and colorectal cancer-specific mortality among AIAN (n = 582

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

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

266 MMARY OF BACKGROUND DATA: Recent advances in colorectal cancer surgery are introduction of laparoscop

267 ent can reduce postoperative morbidity after colorectal cancer surgery, as compared to laparoscopic a

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

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

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

271 herapeutics has emerged for the treatment of colorectal cancer, their use is significantly impacted b

272 We screened international colorectal cancer therapeutic guidelines and determined

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

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

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

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

277 Using primary colorectal cancer tissues, xenograft models, and MAPK re

278 u-Cy nanoparticles have a good potential for colorectal cancer treatment and the discovery of autopha

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

280 e relationship between adult weight gain and colorectal cancer, using data from a prospective nested

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

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

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

284 easures to inform value-based health care in colorectal cancer was developed.

285 ening and a median of 17.1 years' follow-up, colorectal cancer was diagnosed in 1230 individuals in t

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

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

288 n follow-up of 7.9 years (IQR 5.6-11.1), 210 colorectal cancers were diagnosed.

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

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

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

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

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

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

295 By contrast, in lung and colorectal cancers with class 3 BRAF mutants, RAS is typ

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

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

298 d incident rate ratios by lung, gastric, and colorectal cancers, with manufacturing used as the refer

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

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