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1 n human colonic cells and in mouse models of intestinal cancer.
2 cer and the creation of models of metastatic intestinal cancer.
3     However, aberrant Wnt signaling leads to intestinal cancer.
4 t in diseases such as ulcerative colitis and intestinal cancer.
5 cantly increase risk for both testicular and intestinal cancer.
6 d that cholecystectomy increases the risk of intestinal cancer.
7 oncausal associations between gallstones and intestinal cancer.
8 ight contribute to inflammatory diseases and intestinal cancer.
9 ic epithelial cells in the initial stages of intestinal cancer.
10 h are crucial gatekeepers in common forms of intestinal cancer.
11 iber/whole grains and the incidence of small intestinal cancer.
12 erally associated with a lower risk of small intestinal cancer.
13 ead to aberrant epithelial proliferation and intestinal cancer.
14  is a frequent early event in the genesis of intestinal cancer.
15 r generating PGE(2), in two murine models of intestinal cancer.
16 rences establish SBA as a molecularly unique intestinal cancer.
17 ors of Sphk1 may be useful in the control of intestinal cancer.
18 attenuate tumor burden in a genetic model of intestinal cancer.
19  IBD risk gene Atg16l1 does not induce small intestinal cancer.
20 number of patients with colorectal and other intestinal cancers.
21 hich is highly expressed in murine and human intestinal cancers.
22 signaling mutations drive formation of human intestinal cancers.
23 hrough 2003, 165 individuals developed small intestinal cancers.
24 -catenin signaling is frequently observed in intestinal cancers.
25 ), septicemia (6.8; 95% CI, 2.2-15.8), small intestinal cancer (48.1; 95% CI, 5.8-17.4), respiratory
26  modifier of proapoptotic gene expression in intestinal cancers, acting independently of bile acid me
27 requency questionnaire, in relation to small intestinal cancer among half a million men and women enr
28 or development in mouse models for inherited intestinal cancer, an observation that is reminiscent of
29 al cells, protects mice from colitis-induced intestinal cancer and ApcMin-dependent intestinal tumori
30  activated in Apc(min/+) mice, which develop intestinal cancer and lose weight despite the absence of
31  cue netrin-1, acts as a tumor suppressor in intestinal cancer and lung metastasis by triggering canc
32 eat consumption increases the risk of gastro-intestinal cancers and it is strongly suspected that nit
33 nt glioma, medulloblastoma, prostate cancer, intestinal cancer, and sarcoma from adjacent non-neoplas
34 /+) mice, a recognized mouse model for human intestinal cancer, and to elucidate possible mechanisms
35      We have used a mouse model of inherited intestinal cancer (Apc(Min)/+, Min/+) to analyze the ear
36                                              Intestinal cancers are frequently associated with mutati
37                                              Intestinal cancers are, on occasion, initially misdiagno
38 ly found in preneoplastic lesions, including intestinal cancers arising due to the inactivation of th
39 Min/+) mice, suggesting that Mgmt suppresses intestinal cancer associated with exogenous alkylating a
40 lase SIRT6 regulates tumor initiation during intestinal cancer by controlling glucose metabolism.
41 ncidence, risk factors, and trends for small intestinal cancer by sex, age, and country.
42 that the Apc(Min/+) mouse model for familial intestinal cancer can develop frequent invasive cancers
43                      A total of 64,477 small intestinal cancer cases (age-standardized rate, 0.60 per
44 s p53 in mice) in mouse models of WNT-driven intestinal cancer caused by Csnk1a1 deletion(3,4) or Apc
45  We studied the effects of IL28 on the human intestinal cancer cell line Caco-2 in a wound-healing as
46                                     In human intestinal cancer cells Caco-2/TC7 and SW480 and normal
47 s, we uncover a paracrine mechanism by which intestinal cancer cells reactivate foetal and regenerati
48 y overexpressed in prostate, colorectal, and intestinal cancer cells.
49 of organs and is down-regulated in liver and intestinal cancer cells.
50                                 Thus, common intestinal cancer driven by diet involves mechanisms of
51 rs in genetically engineered mouse models of intestinal cancer (driven by Apc inactivation) or lympho
52 ignaling and loss of PTEN cooperate to drive intestinal cancer formation and progression by suppressi
53               In the Apc(Min) mouse model of intestinal cancer, genetic abrogation of c-Jun N-termina
54 e may be a direct link between inhibition of intestinal cancer growth and selective inhibition of the
55 ults in marked and persistent suppression of intestinal cancer growth by 66%, whereas suppression of
56  of dietary and other risk factors for small intestinal cancer have been sparse and all of a case-con
57 osity was associated with increased risk for intestinal cancer in Apc(min)(/+) mice through a gene-by
58 idylate synthesis modifies susceptibility to intestinal cancer in Apc(min)(/+) mice.
59 pressor gene occurs early in the etiology of intestinal cancer in mammals.
60 inal blockage that has not been reported for intestinal cancer in mouse models.
61 ag, incidence, and frequency reflect >90% of intestinal cancer in Western societies, dietary-induced
62  of dietary-induced sporadic small and large intestinal cancer in WT mice in which tumor etiology, la
63 initiation and progression, respectively, of intestinal cancers in vivo.
64 ere was an overall increasing trend of small intestinal cancer incidence (average annual percent chan
65 estimate the age-standardized rates of small intestinal cancer incidence (International Classificatio
66                                 Higher small intestinal cancer incidence was associated with higher h
67 ere was an overall increasing trend in small intestinal cancer incidence, calling for the development
68 in foods was inversely associated with small intestinal cancer incidence; the RR values were consiste
69 esting its chemopreventive potential against intestinal cancers including CRC.
70 ic colon cancer, and mouse and rat models of intestinal cancer indicate that the majority of early ad
71 ticularly focusing on Th17 cells involved in intestinal cancer initiation.
72                                        Small intestinal cancer is a rare cancer, with limited studies
73 n in this study, between cholecystectomy and intestinal cancer, is very unlikely to be causal.
74                           In mouse models of intestinal cancer, LGR5(+) intestinal stem cells are maj
75 L/6 (B6) Apc(Min/+) mouse model of inherited intestinal cancer, loss of Apc function can occur by los
76  are viable and fertile, their resistance to intestinal cancer may be of therapeutic relevance.
77 stemic colon cancer metastases targeting the intestinal cancer mucosa antigen guanylyl cyclase C (GCC
78 tive reverse transcriptase (RT)-PCR on large intestinal cancers (n=29 cancers, n=16 normals; 10-fold,
79  understanding the greater predisposition to intestinal cancer of Mlh1(-/-) mice.
80  Ikkepsilon in beta-catenin-driven models of intestinal cancer reduced tumor incidence and consequent
81  and, when coexpressed with Lgr5, also marks intestinal cancer stem cells.
82  the JCI, Ragusa and coworkers identified an intestinal cancer subgroup of slow-growing, chemotherapy
83 s hypotheses, Ereg deficiency does not alter intestinal cancer susceptibility, as assayed in the ApcM
84 familial adenomatous polyposis, an autosomal intestinal cancer syndrome.
85 al adenomatous polyposis (FAP), an autosomal intestinal cancer syndrome.
86 reveal a tumor suppressor role for miR-26 in intestinal cancer that overrides putative oncogenic acti
87 gosity, they were less likely to develop the intestinal cancers that normally arise in this tumor-pre
88 cause mutations in Wnt pathway genes lead to intestinal cancer, the role of Wnt signaling in gut epit
89 e ability of CD4+ T cells to protect against intestinal cancer was correlated with their ability to r
90 f inflammatory bowel disease predisposing to intestinal cancer, we analyzed genome-wide DNA methylati
91  cohort of patients with small but not large intestinal cancer, we find a correlation between neutrop
92                   To identify new drivers of intestinal cancer, we performed insertional mutagenesis
93 unction in a well-established mouse model of intestinal cancer, we show that Tgifs promote adenoma gr
94  of Msh2 in the intestinal tract and develop intestinal cancer, we showed vaccination with a combinat
95 , Kras-driven mouse models of pancreatic and intestinal cancers were less responsive to depletion of
96 GPX-DKO mice that have microflora-associated intestinal cancers, which are correlated with increased
97 et gene highly expressed in murine and human intestinal cancers, which indicates that USP28 and c-MYC
98  pathway are associated with the majority of intestinal cancers, while dysregulation of the Hippo/Yes
99  geographic disparity in the burden of small intestinal cancer, with higher incidence observed in cou