コーパス検索結果 (１語後でソート)
通し番号をクリックするとPubMedの該当ページを表示します
1 stinal inflammation and delayed the onset of colitis-associated cancer.
2 and its absence promotes the development of colitis-associated cancer.
3 al epithelial cells (IEC) during colitis and colitis-associated cancer.
4 factor for colorectal cancer, also known as colitis-associated cancer.
5 imed to establish the miRNAs associated with colitis-associated cancer.
6 e (AOM) and dextran sulfate sodium to induce colitis-associated cancer.
7 lates certain proapoptotic RNAs to attenuate colitis-associated cancer.
8 ride (LPS), is over-expressed in humans with colitis-associated cancer.
9 on that may predispose to the development of colitis-associated cancer.
10 ntly upregulated in cohorts of patients with colitis-associated cancer.
11 strongly associated with the development of colitis-associated cancer.
12 olonic mucosa and tumors in a mouse model of colitis-associated cancer.
13 nduced colitis, and severe susceptibility to colitis-associated cancer.
14 ablished a key function for PHB in mediating colitis-associated cancer.
15 mmatory intestinal diseases, such as IBD and colitis-associated cancer.
16 seful therapeutic target in the treatment of colitis-associated cancer.
17 for tr-NK-1R in malignant transformation in colitis-associated cancer.
18 hogenesis of inflammatory bowel diseases and colitis-associated cancer.
19 ell hypothesis has not yet been validated in colitis-associated cancer.
20 es of dextran sodium sulfate (DSS) to induce colitis-associated cancer.
21 ease treatment and define novel mediators of colitis-associated cancer.
22 be useful in the prevention or treatment of colitis-associated cancer.
23 ing through TLR4 may lower the threshold for colitis-associated cancer.
24 nt of intestinal inflammation, infection and colitis-associated cancer.
25 ute colitis, type 2 intestinal infection and colitis-associated cancer.
26 was analyzed in acute colitis, infection and colitis-associated cancer.
27 rget against inflammatory diseases including colitis-associated cancer.
28 20 (CCL20), and increased susceptibility to colitis-associated cancer.
29 lead to new strategies to identify and treat colitis-associated cancers.
30 myeloid cells contributes to development of colitis-associated cancer and Apc(Min)-dependent intesti
31 These mice were bred with Apc(Min/+) mice; colitis-associated cancer and colitis were induced by ad
32 capacity of the test to distinguish between colitis-associated cancer and different ulcerative colit
33 hes to manipulate IDO1 activity in mice with colitis-associated cancer and human colon cancer cell li
34 dence for their roles in the pathogenesis of colitis-associated cancer and sporadic colorectal cancer
35 important insights into the pathogenesis of colitis-associated cancer and suggest that epidermal gro
36 nd germline alterations in 174 patients with colitis-associated cancers and sequenced 29 synchronous
37 of colorectal cancer gave rise to the term "colitis-associated cancer" and the concept that inflamma
38 arthritis, inflammatory intestinal disease, colitis-associated cancer, and lipopolysaccharide (LPS,
39 lammatory signature' genes characteristic of colitis-associated cancer are also upregulated in colore
40 d to exacerbated intestinal inflammation and colitis-associated cancer, but also helped protect again
41 linked to pre-existing inflammation known as colitis-associated cancer, but most develops in patients
42 Here we established a novel mouse model of colitis-associated cancer by genetically inactivating si
43 vation appears to promote the development of colitis-associated cancer by mechanisms including enhanc
44 r findings suggest that PHB protects against colitis-associated cancer by modulating p53- and STAT3-m
45 e intestine, where it helps protects against colitis-associated cancer by regulating HMOX-1 expressio
46 K1) links chronic intestinal inflammation to colitis-associated cancer (CAC) and both are exacerbated
47 myeloid AC protects from tumor incidence in colitis-associated cancer (CAC) and inhibits the expansi
53 fic IKKbeta is involved in the initiation of colitis-associated cancer (CAC), as in its absence mice
54 ling pathway are associated with colitis and colitis-associated cancer (CAC), but how IL-33 modulates
55 trast, MyD88-deficient mice are sensitive to colitis-associated cancer (CAC), since selected cytokine
69 miR-375 was significantly upregulated in the colitis-associated cancer cohort (p=0.0061) compared wit
70 response in sepsis, intestinal colitis, and colitis-associated cancer development through NLRP3-infl
71 mmation and contributes to the prevention of colitis-associated cancer during chronic inflammation th
73 antly attenuated intestinal inflammation and colitis-associated cancer in dextran sodium sulfate mode
85 ions, an early and highly recurrent event in colitis-associated cancers, occur in half of dysplasia,
86 expression was lost in carcinoma tissues of colitis-associated cancer patients, whereas p65 expressi
88 critical role for ITF2 in the repression of colitis-associated cancer progression and ITF2 would be
89 ression of beta-catenin target genes in CUC, colitis-associated cancer, tubular adenomas, and sporadi
90 lear translocation of p65 and thus increased colitis-associated cancer tumorigenesis, which was media
91 dministration of dextran sodium sulfate, and colitis-associated cancer was induced by administration