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1 y predisposition to hamartomatous polyps and gastrointestinal cancer.
2 ced risk of certain malignancies, especially gastrointestinal cancer.
3 s associated with an increased risk of upper gastrointestinal cancer.
4 target of the Wnt pathway and a promoter of gastrointestinal cancer.
5 6 (CEACAM6) is widely overexpressed in human gastrointestinal cancer.
6 ed in a variety of human neoplasms including gastrointestinal cancer.
7 s in inflammatory bowel disease and possibly gastrointestinal cancer.
8 netic disorder, nor do they bestow a risk of gastrointestinal cancer.
9 optotic gene BAX is a mutational hot spot in gastrointestinal cancer.
10 hat cyclooxygenase-2 (COX-2) is important in gastrointestinal cancer.
11 uvenile polyps and are at increased risk for gastrointestinal cancer.
12 escape from apoptosis in the MMP pathway for gastrointestinal cancer.
13 (MAb), were assessed in patients in advanced gastrointestinal cancer.
14 a predisposition to hamartomatous polyps and gastrointestinal cancer.
15 of the gastrointestinal tract and a risk of gastrointestinal cancer.
16 e importance of the escape from apoptosis in gastrointestinal cancer.
17 important in the majority of these types of gastrointestinal cancer.
18 of genes in the mouse QTL are implicated in gastrointestinal cancer.
19 s those in melanoma, breast, pancreatic, and gastrointestinal cancer.
20 harmacodynamic responses in a mouse model of gastrointestinal cancer.
21 tervention in inflammatory bowel disease and gastrointestinal cancer.
22 treatment of inflammatory bowel disease and gastrointestinal cancer.
23 YAP and Notch inhibitors as therapeutics for gastrointestinal cancer.
24 om FO-enriched nutrition during treatment of gastrointestinal cancer.
25 ents with involuntary weight loss (IWL) have gastrointestinal cancer.
26 uals are predisposed to colorectal and upper gastrointestinal cancer.
27 r the correction of chronic constipation and gastrointestinal cancer.
28 major cancers: breast cancer, melanoma, and gastrointestinal cancer.
29 dentify novel ways to both prevent and treat gastrointestinal cancer.
30 ine differentiation frequently seen in human gastrointestinal cancer.
31 st exclusively to treat colorectal and other gastrointestinal cancers.
32 , and guide therapeutic intervention in many gastrointestinal cancers.
33 vance the standard of care for patients with gastrointestinal cancers.
34 profiles is on the horizon for patients with gastrointestinal cancers.
35 ethylation-specific test for colon and other gastrointestinal cancers.
36 se agents for the treatment of patients with gastrointestinal cancers.
37 iated by a high-level expression of PRAJA in gastrointestinal cancers.
38 xic prevention and/or treatment strategy for gastrointestinal cancers.
39 tumor suppressor, is often mutated in human gastrointestinal cancers.
40 er agents for the treatment or prevention of gastrointestinal cancers.
41 A]) in the treatment of colorectal and other gastrointestinal cancers.
42 cancer and defining poor prognosis groups in gastrointestinal cancers.
43 CVR2 as a candidate tumor suppressor gene in gastrointestinal cancers.
44 in which patients are at risk for developing gastrointestinal cancers.
45 ial role as chemopreventive agents for upper gastrointestinal cancers.
46 al to have clinical effects on patients with gastrointestinal cancers.
47 ence of colorectal, esophageal, stomach, and gastrointestinal cancers.
48 ions between inflammatory microorganisms and gastrointestinal cancers.
49 l, are a hallmark of many cancers, including gastrointestinal cancers.
50 ex and gut microbiota, bile acids (BAs), and gastrointestinal cancers.
51 cle abnormalities with a special emphasis on gastrointestinal cancers.
52 uld be developed to prevent or treat certain gastrointestinal cancers.
53 hysical activity, are known risk factors for gastrointestinal cancers.
54 to the mutations found in p53 gene of human gastrointestinal cancers.
55 al resection is the main curative option for gastrointestinal cancers.
56 othesis that antioxidants reduce the risk of gastrointestinal cancers.
57 is frequently amplified and overexpressed in gastrointestinal cancers.
58 g IMCs and might be a therapeutic target for gastrointestinal cancers.
59 cancer, including gastric cancers and other gastrointestinal cancers.
60 pment of Crohn's disease, Blau syndrome, and gastrointestinal cancers.
61 oenvironment and metastasis, with a focus on gastrointestinal cancers.
62 toxic and can cause liver damage and promote gastrointestinal cancers.
63 ases such as inflammatory bowel diseases and gastrointestinal cancers.
64 trial treatment for gastrointestinal and non-gastrointestinal cancers.
65 ll and disease-free survival in a variety of gastrointestinal cancers.
66 nd has significant therapeutic potential for gastrointestinal cancers.
67 le grain foods seem to protect against lower gastrointestinal cancers.
68 tases for many types of cancer, particularly gastrointestinal cancers.
69 in (ELF), are prominent tumor suppressors in gastrointestinal cancers.
70 ral dietary compounds for chemoprevention of gastrointestinal cancers.
71 he best area under the curve (AUC), both for gastrointestinal cancer (0.746, CI: 0.691-0.794), and co
72 all solid cancers, 0.69, 0.54-0.88, p=0.003; gastrointestinal cancers, 0.41, 0.26-0.66, p=0.0001).
73 cancers, hazard ratio [HR] 0.66, 0.50-0.87; gastrointestinal cancers, 0.46, 0.27-0.77; both p=0.003)
74 solid cancers, HR 0.80, 0.72-0.88, p<0.0001; gastrointestinal cancers, 0.65, 0.54-0.78, p<0.0001), an
75 a quarter had cancer, of which 22 (7.6%) had gastrointestinal cancer (8 gastric cancer, 1 ileum cance
76 Despite recent advances in chemotherapy for gastrointestinal cancer, a crucial factor related to poo
79 e were RRs of 18.7 (95% CI, 5.8 to 43.5) for gastrointestinal cancer after mixed-modality treatment,
80 eloped in 18 of the 34 patients: 10 cases of gastrointestinal cancer and 16 cases of extraintestinal
81 een a positive family history (FH+) of upper gastrointestinal cancer and germline BRCA2 mutations.
82 by which peptide hormones regulate growth of gastrointestinal cancer and ways in which this informati
83 food is associated with an increased risk of gastrointestinal cancer and, in infants, methemoglobinem
84 st loss of CDK inhibitors, are all linked to gastrointestinal cancers and are often associated with l
85 vascular endothelial growth factor in human gastrointestinal cancers and discuss the development and
86 prostaglandin synthesis, is up-regulated in gastrointestinal cancers and is a key mediator of epithe
87 cancer target because it is overexpressed in gastrointestinal cancers and plays an important role in
88 of cell-cycle abnormalities in patients with gastrointestinal cancers and provide a preclinical and c
89 predisposes patients to an increased risk of gastrointestinal cancer, and pancreatic cancer has been
90 n patients with breast cancer, melanoma, and gastrointestinal cancer, and these defects may represent
91 t gastrointestinal complaints and diagnoses, gastrointestinal cancers, and deaths from common liver d
93 epeats that are known to be disrupted in MI+ gastrointestinal cancers are also disrupted in MI+ endom
95 atellites that are frequently mutated in MI+ gastrointestinal cancers are rarely mutated in MI+ endom
96 other advanced technologies for detection of gastrointestinal cancers are undergoing a major revoluti
97 tigations of gastrointestinal metaplasia and gastrointestinal cancers associated with chronic inflamm
99 orouracil is widely used for chemotherapy of gastrointestinal cancer, but response rates are poor.
100 , p=0.0006), with largest effects on risk of gastrointestinal cancers (case-control studies, OR 0.62,
102 at the K19 promoter is active in a subset of gastrointestinal cancer cells derived from esophageal an
103 y and in vivo mechanism of action of EF24 in gastrointestinal cancer cells have not been investigated
105 ignal transduction pathway are found in many gastrointestinal cancers, confirming its importance as a
106 s) from 9 out of 10 patients with metastatic gastrointestinal cancers contained CD4(+) and/or CD8(+)
107 at the cytotoxicity of 5-FU in patients with gastrointestinal cancer could be compromised by its intr
109 oles in cell growth or survival in aneuploid gastrointestinal cancer (e.g., APC, K-ras, and p53) are
110 hat drive progression and chemoresistance in gastrointestinal cancers, epidermal growth factor recept
111 ctal adenocarcinoma (PDA), which, with other gastrointestinal cancers, exhibits frequent inactivation
112 nfirm these findings after examining >50 MMP gastrointestinal cancers for mutations in eight SMT loci
113 ead and neck cancer, breast cancer, sarcoma, gastrointestinal cancer, genitourinary cancer, gynaecolo
114 us, a high frequency of patients with common gastrointestinal cancers harbor immunogenic mutations th
117 dequate, and associated disorders, including gastrointestinal cancers, have high morbidity and mortal
118 ; 95% CI, 0.39 to 0.84) but a higher risk of gastrointestinal cancer (hazard ratio, 2.70; 95% CI, 1.6
119 itamin E has anticarcinogenic properties for gastrointestinal cancers; however, few studies have exam
120 , NDMA was associated with increased risk of gastrointestinal cancers (HR: 1.13; 95% CI: 1.00, 1.28),
121 l evaluations of these antigens as potential gastrointestinal cancer immunotherapeutic agents have be
122 o assess the ability of ferritin to rule out gastrointestinal cancer in patients with involuntary wei
123 Antioxidants do not aid in the prevention of gastrointestinal cancers in the general population; howe
124 tary NOC (NDMA) was associated with a higher gastrointestinal cancer incidence, specifically of recta
125 n described in renal papillary carcinoma and gastrointestinal cancers including hepatocellular carcin
126 ling has been identified in several types of gastrointestinal cancers, including esophageal, gastric,
127 population-based case-control study of upper gastrointestinal cancers, including gastric cardia (n =
128 9741, a National Cancer Institute-funded and Gastrointestinal Cancer Intergroup-sponsored study coord
131 f Wnt/beta-catenin signaling and its role in gastrointestinal cancers is now emerging as divergent ph
132 isorders, sometimes in association only with gastrointestinal cancer [juvenile polyposis syndrome (JP
133 air defect and are predisposed to developing gastrointestinal cancer, lymphomas and tumors of other o
134 oth alleles of Msh2 gene predisposes mice to gastrointestinal cancer, lymphomas and tumors of the ski
135 en (PSA) and CA 19-9 (a human pancreatic and gastrointestinal cancer marker) ELISAs in serum are enha
137 on and apparent trends in diagnosis of upper gastrointestinal cancers merit further exploration.
139 omly generated networks as well as a 17-gene gastrointestinal cancer network, which, if not reduced,
140 t, although epithelial malignancies (largely gastrointestinal cancers) occur more frequently than exp
142 y at simple repeated sequences characterizes gastrointestinal cancer of the microsatellite mutator ph
143 bility characterizes hereditary and sporadic gastrointestinal cancer of the microsatellite mutator ph
144 ng recurrent missense mutations, not only in gastrointestinal cancer of the MMP but also in gastroint
145 tions in genes that are typically mutated in gastrointestinal cancer of the mutator pathway, includin
146 efects, and it has become apparent that many gastrointestinal cancers originate from a state of chron
147 sing bioelectrical impedance analysis in 128 gastrointestinal cancer patients provided with or withou
148 apy tolerance and prognosis, particularly in gastrointestinal cancer patients with a modified Glasgow
149 a gastric adenocarcinoma but not other upper gastrointestinal cancers, possibly by inducing a hypochl
150 hose receptor is mutated in a rare inherited gastrointestinal cancer predisposition syndrome, was the
151 mall but appreciable proportion of inherited gastrointestinal cancer predisposition syndromes; patien
157 r normal-risk individuals regarding diet and gastrointestinal cancer should probably emphasize the im
158 convened by the National Cancer Institute's Gastrointestinal Cancer Steering Committee to discuss th
159 convened by the National Cancer Institute's Gastrointestinal Cancer Steering Committee to identify t
160 ns are protective against cancer, especially gastrointestinal cancers such as gastric and colon can-c
161 this process usually lead to tissue-specific gastrointestinal cancers such as hepatocellular cancers,
162 as been successful in the treatment of early gastrointestinal cancers, such as oesophageal cancer, an
163 y affected a tenth of patients who underwent gastrointestinal cancer surgery and was associated with
164 enting and controlling human obesity-related gastrointestinal cancers that often exhibit sex differen
165 predictive value of 99% (96-100%), while for gastrointestinal cancer, the sensitivity was lower (89%,
166 es the oncogenic effects of secondary BAs in gastrointestinal cancers, the targeting of which may enh
167 t of the major advances in the screening for gastrointestinal cancers this year were in the area of c
169 associated with family history (FH) of upper gastrointestinal cancer (UGI) cancer in cases with ESCC.
170 inhibits expression of a variety of genes in gastrointestinal cancers, we sought to determine whether
172 f hematopoietic stem cells, 15 patients with gastrointestinal cancers were administered a tracer dose
174 , early stage cancer, and those with lung or gastrointestinal cancers were less likely to be enrolled
176 rgo curative resection for hepatobiliary and gastrointestinal cancers, were English speaking, and wer
178 stinal cause of death and is the most common gastrointestinal cancer, with an incidence of 54 per 100
181 le dietary factors play in the prevention of gastrointestinal cancers, yet evidence regarding the pot
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