ライフサイエンスコーパス: gastrointestinal cancer

1 uals are predisposed to colorectal and upper gastrointestinal cancer.

2 r the correction of chronic constipation and gastrointestinal cancer.

3 major cancers: breast cancer, melanoma, and gastrointestinal cancer.

4 dentify novel ways to both prevent and treat gastrointestinal cancer.

5 ine differentiation frequently seen in human gastrointestinal cancer.

6 y predisposition to hamartomatous polyps and gastrointestinal cancer.

7 ced risk of certain malignancies, especially gastrointestinal cancer.

8 s associated with an increased risk of upper gastrointestinal cancer.

9 target of the Wnt pathway and a promoter of gastrointestinal cancer.

10 6 (CEACAM6) is widely overexpressed in human gastrointestinal cancer.

11 ed in a variety of human neoplasms including gastrointestinal cancer.

12 s in inflammatory bowel disease and possibly gastrointestinal cancer.

13 netic disorder, nor do they bestow a risk of gastrointestinal cancer.

14 optotic gene BAX is a mutational hot spot in gastrointestinal cancer.

15 teral IMN in patients undergoing surgery for gastrointestinal cancer.

16 hat cyclooxygenase-2 (COX-2) is important in gastrointestinal cancer.

17 uvenile polyps and are at increased risk for gastrointestinal cancer.

18 escape from apoptosis in the MMP pathway for gastrointestinal cancer.

19 (MAb), were assessed in patients in advanced gastrointestinal cancer.

20 a predisposition to hamartomatous polyps and gastrointestinal cancer.

21 of the gastrointestinal tract and a risk of gastrointestinal cancer.

22 e importance of the escape from apoptosis in gastrointestinal cancer.

23 practice in patients undergoing surgery for gastrointestinal cancer.

24 important in the majority of these types of gastrointestinal cancer.

25 b plus the ICI durvalumab in chemorefractory gastrointestinal cancer.

26 onic inflammation is a known risk factor for gastrointestinal cancer.

27 py to a much broader subset of patients with gastrointestinal cancer.

28 o monitor clinical outcomes in patients with gastrointestinal cancer.

29 lizations and related costs in patients with gastrointestinal cancer.

30 h symptoms mandating investigation for upper gastrointestinal cancer.

31 p, 445 control group) undergoing surgery for gastrointestinal cancer.

32 om FO-enriched nutrition during treatment of gastrointestinal cancer.

33 of genes in the mouse QTL are implicated in gastrointestinal cancer.

34 s those in melanoma, breast, pancreatic, and gastrointestinal cancer.

35 harmacodynamic responses in a mouse model of gastrointestinal cancer.

36 tervention in inflammatory bowel disease and gastrointestinal cancer.

37 treatment of inflammatory bowel disease and gastrointestinal cancer.

38 YAP and Notch inhibitors as therapeutics for gastrointestinal cancer.

39 ents with involuntary weight loss (IWL) have gastrointestinal cancer.

40 ases such as inflammatory bowel diseases and gastrointestinal cancers.

41 trial treatment for gastrointestinal and non-gastrointestinal cancers.

42 ll and disease-free survival in a variety of gastrointestinal cancers.

43 nd has significant therapeutic potential for gastrointestinal cancers.

44 le grain foods seem to protect against lower gastrointestinal cancers.

45 tases for many types of cancer, particularly gastrointestinal cancers.

46 in (ELF), are prominent tumor suppressors in gastrointestinal cancers.

47 ral dietary compounds for chemoprevention of gastrointestinal cancers.

48 , and guide therapeutic intervention in many gastrointestinal cancers.

49 vance the standard of care for patients with gastrointestinal cancers.

50 profiles is on the horizon for patients with gastrointestinal cancers.

51 ethylation-specific test for colon and other gastrointestinal cancers.

52 se agents for the treatment of patients with gastrointestinal cancers.

53 iated by a high-level expression of PRAJA in gastrointestinal cancers.

54 xic prevention and/or treatment strategy for gastrointestinal cancers.

55 tumor suppressor, is often mutated in human gastrointestinal cancers.

56 er agents for the treatment or prevention of gastrointestinal cancers.

57 A]) in the treatment of colorectal and other gastrointestinal cancers.

58 cancer and defining poor prognosis groups in gastrointestinal cancers.

59 CVR2 as a candidate tumor suppressor gene in gastrointestinal cancers.

60 in which patients are at risk for developing gastrointestinal cancers.

61 al to have clinical effects on patients with gastrointestinal cancers.

62 nase A (AURKA) are often detected in luminal gastrointestinal cancers.

63 surgery for the management of selected early gastrointestinal cancers.

64 al activity (PA) during the life course with gastrointestinal cancers.

65 genes are associated with susceptibility to gastrointestinal cancers.

66 hich will improve early diagnosis to prevent gastrointestinal cancers.

67 re is a high risk of overlooked EoE or upper gastrointestinal cancers.

68 hanisms implicated in the risk of developing gastrointestinal cancers.

69 t by expanding treatment options in advanced gastrointestinal cancers.

70 rapy with curative intent, and 157 (57%) had gastrointestinal cancers.

71 bitors in advanced solid cancers, especially gastrointestinal cancers.

72 metastasis is the leading cause of death for gastrointestinal cancers.

73 models underperform in cohorts with lung and gastrointestinal cancers.

74 st exclusively to treat colorectal and other gastrointestinal cancers.

75 ex and gut microbiota, bile acids (BAs), and gastrointestinal cancers.

76 to the mutations found in p53 gene of human gastrointestinal cancers.

77 ial role as chemopreventive agents for upper gastrointestinal cancers.

78 ence of colorectal, esophageal, stomach, and gastrointestinal cancers.

79 ions between inflammatory microorganisms and gastrointestinal cancers.

80 l, are a hallmark of many cancers, including gastrointestinal cancers.

81 cle abnormalities with a special emphasis on gastrointestinal cancers.

82 uld be developed to prevent or treat certain gastrointestinal cancers.

83 ry disease associated with increased risk of gastrointestinal cancers.

84 hysical activity, are known risk factors for gastrointestinal cancers.

85 al resection is the main curative option for gastrointestinal cancers.

86 othesis that antioxidants reduce the risk of gastrointestinal cancers.

87 is frequently amplified and overexpressed in gastrointestinal cancers.

88 g IMCs and might be a therapeutic target for gastrointestinal cancers.

89 cancer, including gastric cancers and other gastrointestinal cancers.

90 pment of Crohn's disease, Blau syndrome, and gastrointestinal cancers.

91 oenvironment and metastasis, with a focus on gastrointestinal cancers.

92 toxic and can cause liver damage and promote gastrointestinal cancers.

93 he best area under the curve (AUC), both for gastrointestinal cancer (0.746, CI: 0.691-0.794), and co

94 all solid cancers, 0.69, 0.54-0.88, p=0.003; gastrointestinal cancers, 0.41, 0.26-0.66, p=0.0001).

95 cancers, hazard ratio [HR] 0.66, 0.50-0.87; gastrointestinal cancers, 0.46, 0.27-0.77; both p=0.003)

96 solid cancers, HR 0.80, 0.72-0.88, p<0.0001; gastrointestinal cancers, 0.65, 0.54-0.78, p<0.0001), an

97 ancers combined (HR 1.40, 95% CI 1.24-1.58), gastrointestinal cancers (1.31, 1.11-1.55), and respirat

98 Of these participants, 201 (61%) had gastrointestinal cancer, 127 (39%) had lung cancer, and

99 8,000, 25%), cervix (210,000, 20%) and upper-gastrointestinal cancers (136,000, 13%), and most occurr

100 on-Hispanic White patients; 245 [34.7%] with gastrointestinal cancer; 175 [24.8%] with lung cancer; m

101 The most common cancer types were gastrointestinal cancer (228 [37.4%]) and lung cancer (1

102 a quarter had cancer, of which 22 (7.6%) had gastrointestinal cancer (8 gastric cancer, 1 ileum cance

103 e with haematological cancers (67% [55-82]), gastrointestinal cancers (89% [81-97]), and other solid

104 Despite recent advances in chemotherapy for gastrointestinal cancer, a crucial factor related to poo

105 Gastrointestinal cancers account for 20% of all incident

106 Bile acids, endogenous promoters of gastrointestinal cancer, activate protein kinase C (PKC)

107 e were RRs of 18.7 (95% CI, 5.8 to 43.5) for gastrointestinal cancer after mixed-modality treatment,

108 y, we examined incidence rates of 3 types of gastrointestinal cancer among non-Hispanic AI/AN (NH-AI/

109 eloped in 18 of the 34 patients: 10 cases of gastrointestinal cancer and 16 cases of extraintestinal

110 .0 person-years, 5324 (0.5%) developed upper gastrointestinal cancer and 4465 (0.4%) died from such c

111 Colorectal cancer (CRC) is a severe gastrointestinal cancer and a leading cause of cancer-re

112 een a positive family history (FH+) of upper gastrointestinal cancer and germline BRCA2 mutations.

113 by which peptide hormones regulate growth of gastrointestinal cancer and ways in which this informati

114 Tennessee had advanced lung or noncolorectal gastrointestinal cancer and were identified by an automa

115 food is associated with an increased risk of gastrointestinal cancer and, in infants, methemoglobinem

116 hort of 42 patients with molecularly defined gastrointestinal cancers and acquired resistance to targ

117 st loss of CDK inhibitors, are all linked to gastrointestinal cancers and are often associated with l

118 vascular endothelial growth factor in human gastrointestinal cancers and discuss the development and

119 his Review, we focus on interactions between gastrointestinal cancers and elements of the central and

120 ting lymphocytes of patients with metastatic gastrointestinal cancers and incorporated the TCR alpha

121 prostaglandin synthesis, is up-regulated in gastrointestinal cancers and is a key mediator of epithe

122 cancer target because it is overexpressed in gastrointestinal cancers and plays an important role in

123 of cell-cycle abnormalities in patients with gastrointestinal cancers and provide a preclinical and c

124 e underlying disease under study (metastatic gastrointestinal cancer) and related complications (10 p

125 predisposes patients to an increased risk of gastrointestinal cancer, and pancreatic cancer has been

126 n patients with breast cancer, melanoma, and gastrointestinal cancer, and these defects may represent

127 t gastrointestinal complaints and diagnoses, gastrointestinal cancers, and deaths from common liver d

128 Gastrointestinal cancers are a leading cause of mortalit

129 epeats that are known to be disrupted in MI+ gastrointestinal cancers are also disrupted in MI+ endom

130 Gastrointestinal cancers are frequently associated with

131 Although the majority of gastrointestinal cancers are generally considered poorly

132 Gastrointestinal cancers are increasingly being treated

133 atellites that are frequently mutated in MI+ gastrointestinal cancers are rarely mutated in MI+ endom

134 other advanced technologies for detection of gastrointestinal cancers are undergoing a major revoluti

135 xaliplatin, a chemotherapeutic used to treat gastrointestinal cancers, are observed in about 20% of p

136 ly 1 member B10 (AKR1B10), down-regulated in gastrointestinal cancers, as a pivotal metastasis suppre

137 tigations of gastrointestinal metaplasia and gastrointestinal cancers associated with chronic inflamm

138 ng systemic anticancer therapies for lung or gastrointestinal cancers at 1 metropolitan and 4 regiona

139 Data were obtained from the Dutch Upper Gastrointestinal Cancer Audit (DUCA) on all gastrectomie

140 The completeness of the Dutch Upper gastrointestinal Cancer Audit was estimated at 99.8%.

141 2016 and were registered in the Dutch Upper gastrointestinal Cancer Audit were included.

142 and 2017 were selected from the Dutch Upper gastrointestinal Cancer Audit.

143 were selected from the national Dutch Upper Gastrointestinal Cancer Audit.

144 Data was acquired from the Dutch Upper Gastrointestinal Cancer Audit.

145 ial in predicting immunotherapy outcomes for gastrointestinal cancers based on genetic mutation featu

146 e pooled results of AI model performance for gastrointestinal cancers based on genetic mutation featu

147 decided to report on the mortality trend of gastrointestinal cancers, based on crude and age-standar

148 orouracil is widely used for chemotherapy of gastrointestinal cancer, but response rates are poor.

149 rage (SSB) intake is associated with various gastrointestinal cancers, but its association with OCC h

150 ial for predicting immunotherapy outcomes in gastrointestinal cancers by analyzing genetic mutation p

151 tate, head and neck, breast, pancreatic, and gastrointestinal cancers by peripheral nerves similarly

152 , p=0.0006), with largest effects on risk of gastrointestinal cancers (case-control studies, OR 0.62,

153 ent decrease in ELF and Smad4 expression, in gastrointestinal cancer cell lines (P < 0.05).

154 In studies of gastrointestinal cancer cell lines with activated KRAS,

155 at the K19 promoter is active in a subset of gastrointestinal cancer cells derived from esophageal an

156 y and in vivo mechanism of action of EF24 in gastrointestinal cancer cells have not been investigated

157 r, in mice xenograft tumors grown from human gastrointestinal cancer cells with mutant, activated for

158 Unexpectedly, we show here that, in gastrointestinal cancer cells, glucose activates AMPK to

159 gulator of mitosis, after 17AAG treatment in gastrointestinal cancer cells.

160 ncologists overall and within the breast and gastrointestinal cancer cohorts in predicting 3-month mo

161 endoscopy had a 55% decreased risk of upper gastrointestinal cancer compared with those who did not

162 ignal transduction pathway are found in many gastrointestinal cancers, confirming its importance as a

163 s) from 9 out of 10 patients with metastatic gastrointestinal cancers contained CD4(+) and/or CD8(+)

164 at the cytotoxicity of 5-FU in patients with gastrointestinal cancer could be compromised by its intr

165 However, the involvement of PTTG1 in gastrointestinal cancer development and progression rema

166 ase-2-prostaglandin E(2) pathway can promote gastrointestinal cancer development.

167 oles in cell growth or survival in aneuploid gastrointestinal cancer (e.g., APC, K-ras, and p53) are

168 hat drive progression and chemoresistance in gastrointestinal cancers, epidermal growth factor recept

169 ctal adenocarcinoma (PDA), which, with other gastrointestinal cancers, exhibits frequent inactivation

170 In some tumor types, especially in gastrointestinal cancers, expression of ACE2 and TMPRSS2

171 nfirm these findings after examining >50 MMP gastrointestinal cancers for mutations in eight SMT loci

172 icacy of immune checkpoint inhibitors in MSS gastrointestinal cancers from the CARIS database, a Memo

173 ead and neck cancer, breast cancer, sarcoma, gastrointestinal cancer, genitourinary cancer, gynaecolo

174 ll lines (HepG2, SNU398, SNU449 and SNU475), gastrointestinal cancer (GI) cell lines (Caco2 and HCT11

175 on and suicidal ideation among patients with Gastrointestinal Cancer (GIC).

176 er had the highest number of incident cases, gastrointestinal cancers had the fastest-growing inciden

177 From 2010 to 2019, gastrointestinal cancers had the fastest-growing inciden

178 us, a high frequency of patients with common gastrointestinal cancers harbor immunogenic mutations th

179 Treatment of early-stage upper gastrointestinal cancers has evolved tremendously.

180 Although therapeutic strategies for gastrointestinal cancer have previously focused on the e

181 dequate, and associated disorders, including gastrointestinal cancers, have high morbidity and mortal

182 ; 95% CI, 0.39 to 0.84) but a higher risk of gastrointestinal cancer (hazard ratio, 2.70; 95% CI, 1.6

183 olescent body size was associated with total gastrointestinal cancers (hazard ratio [HR] = 1.09; 95%

184 olescent body size was associated with total gastrointestinal cancers (hazard ratio, HR: 1.09; 95% co

185 hat neuronal signaling molecules can promote gastrointestinal cancers, however, the mechanisms remain

186 itamin E has anticarcinogenic properties for gastrointestinal cancers; however, few studies have exam

187 , NDMA was associated with increased risk of gastrointestinal cancers (HR: 1.13; 95% CI: 1.00, 1.28),

188 l evaluations of these antigens as potential gastrointestinal cancer immunotherapeutic agents have be

189 ecreases in incidence and mortality in upper gastrointestinal cancer in patients with GERD.

190 o assess the ability of ferritin to rule out gastrointestinal cancer in patients with involuntary wei

191 Ampullary adenocarcinoma is a rare gastrointestinal cancer in which WNT signalling dysregul

192 actory mismatch repair proficient metastatic gastrointestinal cancers in a schema with lymphodepletin

193 common cancers are lung, head and neck, and gastrointestinal cancers in both sexes, and cervix and b

194 fit from immune checkpoint inhibitors in MSS gastrointestinal cancers in the CARIS cohort (n=95, medi

195 Antioxidants do not aid in the prevention of gastrointestinal cancers in the general population; howe

196 tary NOC (NDMA) was associated with a higher gastrointestinal cancer incidence, specifically of recta

197 n described in renal papillary carcinoma and gastrointestinal cancers including hepatocellular carcin

198 n and women older than 18 years with 5 major gastrointestinal cancers, including colorectal, esophage

199 ling has been identified in several types of gastrointestinal cancers, including esophageal, gastric,

200 ne/threonine kinase that is overexpressed in gastrointestinal cancers, including esophageal, gastric,

201 population-based case-control study of upper gastrointestinal cancers, including gastric cardia (n =

202 gnaling is aberrantly activated in different gastrointestinal cancers, including hepatocellular carci

203 gnaling is aberrantly activated in different gastrointestinal cancers, including hepatocellular carci

204 9741, a National Cancer Institute-funded and Gastrointestinal Cancer Intergroup-sponsored study coord

205 as not yet attained an age at which risk for gastrointestinal cancer is greatest.

206 f using them as prognostic markers for human gastrointestinal cancers is discussed.

207 A fundamental trait of virtually all gastrointestinal cancers is genomic and epigenomic DNA a

208 al activity (PA) during the life course with gastrointestinal cancers is inconclusive.

209 f Wnt/beta-catenin signaling and its role in gastrointestinal cancers is now emerging as divergent ph

210 The age-standardized rate and the number of gastrointestinal cancers is rising, highlighting the imp

211 isorders, sometimes in association only with gastrointestinal cancer [juvenile polyposis syndrome (JP

212 ll lung cancer (EGFR T790M), and imatinib in gastrointestinal cancer (KIT V654A).

213 air defect and are predisposed to developing gastrointestinal cancer, lymphomas and tumors of other o

214 oth alleles of Msh2 gene predisposes mice to gastrointestinal cancer, lymphomas and tumors of the ski

215 en (PSA) and CA 19-9 (a human pancreatic and gastrointestinal cancer marker) ELISAs in serum are enha

216 The increased risk of gastrointestinal cancers may relate particularly to mixe

217 on and apparent trends in diagnosis of upper gastrointestinal cancers merit further exploration.

218 In the management of gastrointestinal cancers, molecular profiling is convent

219 Childhood cancer survivors develop gastrointestinal cancer more frequently and at a younger

220 151), non-small cell lung cancer (n = 225), gastrointestinal cancer (n = 50), and melanoma (n = 89).

221 e for Cancer Immunotherapy, the NCI SPORE in Gastrointestinal Cancers, NCI grant (R50CA243627 to LD),

222 omly generated networks as well as a 17-gene gastrointestinal cancer network, which, if not reduced,

223 ed Program of Research Excellence (SPORE) in Gastrointestinal Cancers; NIH Center Core Grant (P30 CA0

224 t, although epithelial malignancies (largely gastrointestinal cancers) occur more frequently than exp

225 Hereditary and sporadic gastrointestinal cancer of the microsatellite mutator ph

226 y at simple repeated sequences characterizes gastrointestinal cancer of the microsatellite mutator ph

227 bility characterizes hereditary and sporadic gastrointestinal cancer of the microsatellite mutator ph

228 ng recurrent missense mutations, not only in gastrointestinal cancer of the MMP but also in gastroint

229 tions in genes that are typically mutated in gastrointestinal cancer of the mutator pathway, includin

230 efects, and it has become apparent that many gastrointestinal cancers originate from a state of chron

231 of CCA, hepatobiliary cancer, liver cancer, gastrointestinal cancer, pancreatic cancer, CRC, total c

232 CTC)-based liquid biopsy was used to monitor gastrointestinal cancer patients during treatment to det

233 serially obtained from a cohort of advanced gastrointestinal cancer patients enrolled in a trial wit

234 Brain and gastrointestinal cancer patients had the highest SMRs (>

235 sing bioelectrical impedance analysis in 128 gastrointestinal cancer patients provided with or withou

236 apy tolerance and prognosis, particularly in gastrointestinal cancer patients with a modified Glasgow

237 efore diagnosis, termed post-endoscopy upper gastrointestinal cancers (PEUGIC).

238 Colorectal cancer (CRC) is a prevalent gastrointestinal cancer posing significant clinical chal

239 a gastric adenocarcinoma but not other upper gastrointestinal cancers, possibly by inducing a hypochl

240 hose receptor is mutated in a rare inherited gastrointestinal cancer predisposition syndrome, was the

241 mall but appreciable proportion of inherited gastrointestinal cancer predisposition syndromes; patien

242 The majority of patients with upper gastrointestinal cancer present with advanced disease, r

243 Among gastrointestinal cancers, primary liver cancer had the h

244 recruit patients (adults with advanced stage gastrointestinal cancer receiving systemic cancer-direct

245 ative IMN in patients undergoing surgery for gastrointestinal cancer reduced infectious complications

246 instability determines whether patients with gastrointestinal cancer respond exceptionally well to im

247 NAT for gastrointestinal cancers results in overall lower LN yie

248 struct to vaccinate patients with metastatic gastrointestinal cancer.RESULTSThe vaccine was safe and

249 An analysis of gastrointestinal cancers revealed a decreasing trend for

250 species diversity has been linked to reduced gastrointestinal cancer risk and all-cause mortality.

251 Gastrointestinal cancer risk was greatest after mixed-mo

252 Cognizance of these disparities in gastrointestinal cancer risk, as well as approaches that

253 e association of fish consumption with upper gastrointestinal cancer risk, but the associations with

254 rum cysteine and cysteinylglycine with upper gastrointestinal cancer risk.

255 0), 50-60 (RS:+ 134, SP:4.02), 2) history of gastrointestinal cancers (RS:+ 173, SP:5.19), 3) male ge

256 r normal-risk individuals regarding diet and gastrointestinal cancer should probably emphasize the im

257 eloproliferative diseases (SIR = 6.0), lower gastrointestinal cancer (SIR = 3.3), and urinary tract c

258 onsumption, IBS diagnosis, family history of gastrointestinal cancer, smoking status, previous negati

259 convened by the National Cancer Institute's Gastrointestinal Cancer Steering Committee to discuss th

260 convened by the National Cancer Institute's Gastrointestinal Cancer Steering Committee to identify t

261 ns are protective against cancer, especially gastrointestinal cancers such as gastric and colon can-c

262 this process usually lead to tissue-specific gastrointestinal cancers such as hepatocellular cancers,

263 as been successful in the treatment of early gastrointestinal cancers, such as oesophageal cancer, an

264 ess the incidence, growth, and metastasis of gastrointestinal cancer supports the concept that a nons

265 y affected a tenth of patients who underwent gastrointestinal cancer surgery and was associated with

266 reoperative nutrition in patients undergoing gastrointestinal cancer surgery in LMICs demonstrated co

267 colorectal, hepatopancreatobiliary and upper gastrointestinal cancer surgery using the raw mean diffe

268 Among adults undergoing complex gastrointestinal cancer surgery, increasing familiarity

269 mixed population of patients undergoing all gastrointestinal cancer surgery.

270 addressing the emerging awareness of CF as a gastrointestinal cancer syndrome.

271 enting and controlling human obesity-related gastrointestinal cancers that often exhibit sex differen

272 predictive value of 99% (96-100%), while for gastrointestinal cancer, the sensitivity was lower (89%,

273 es the oncogenic effects of secondary BAs in gastrointestinal cancers, the targeting of which may enh

274 t of the major advances in the screening for gastrointestinal cancers this year were in the area of c

275 Among gastrointestinal cancers, those with the fastest-growing

276 receptors with an upregulated expression in gastrointestinal cancers to various extents, and LGR5 is

277 In gastrointestinal cancer, tumor suppressor and promoter g

278 associated with family history (FH) of upper gastrointestinal cancer (UGI) cancer in cases with ESCC.

279 inhibits expression of a variety of genes in gastrointestinal cancers, we sought to determine whether

280 The incidence and mortality in upper gastrointestinal cancer were assessed using parametric f

281 ears (range, 5.5 to 30.2 years), 45 cases of gastrointestinal cancer were identified.

282 f hematopoietic stem cells, 15 patients with gastrointestinal cancers were administered a tracer dose

283 Pooled gastrointestinal cancers were associated with gallstone

284 endoscopies were performed, and 284,844 new gastrointestinal cancers were diagnosed.

285 e to gynaecological, lung, or upper or lower gastrointestinal cancers were included and gave a blood

286 , early stage cancer, and those with lung or gastrointestinal cancers were less likely to be enrolled

287 Six patients with advanced gastrointestinal cancers were studied.

288 rgo curative resection for hepatobiliary and gastrointestinal cancers, were English speaking, and wer

289 life course might differently affect risk of gastrointestinal cancers, whereas occupational PA was as

290 stic state during tumorigenesis for multiple gastrointestinal cancers, which have important implicati

291 life course might differently affect risk of gastrointestinal cancers, while occupational PA was foun

292 clinical trial of individuals with lung and gastrointestinal cancers who were stratified by risk sco

293 Ten percent of patients with an upper gastrointestinal cancer will have received an esophagoga

294 for MeAT were obtained from patients who had gastrointestinal cancer with cachexia.

295 Overall, there were 1345 deaths from gastrointestinal cancers with an average age of 69.11 +/

296 fter removal of dysplastic lesions and early gastrointestinal cancers with endoscopic submucosal diss

297 stinal cause of death and is the most common gastrointestinal cancer, with an incidence of 54 per 100

298 Like the majority of gastrointestinal cancers, with some notable exceptions,

299 strointestinal cancer of the MMP but also in gastrointestinal cancer without the MMP.

300 le dietary factors play in the prevention of gastrointestinal cancers, yet evidence regarding the pot