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1 al epithelial cells (IEC) during colitis and colitis-associated cancer.
2 factor for colorectal cancer, also known as colitis-associated cancer.
3 imed to establish the miRNAs associated with colitis-associated cancer.
4 e (AOM) and dextran sulfate sodium to induce colitis-associated cancer.
5 lates certain proapoptotic RNAs to attenuate colitis-associated cancer.
6 ride (LPS), is over-expressed in humans with colitis-associated cancer.
7 on that may predispose to the development of colitis-associated cancer.
8 ntly upregulated in cohorts of patients with colitis-associated cancer.
9 strongly associated with the development of colitis-associated cancer.
10 olonic mucosa and tumors in a mouse model of colitis-associated cancer.
11 nduced colitis, and severe susceptibility to colitis-associated cancer.
12 ablished a key function for PHB in mediating colitis-associated cancer.
13 mmatory intestinal diseases, such as IBD and colitis-associated cancer.
14 seful therapeutic target in the treatment of colitis-associated cancer.
15 for tr-NK-1R in malignant transformation in colitis-associated cancer.
16 hogenesis of inflammatory bowel diseases and colitis-associated cancer.
17 ell hypothesis has not yet been validated in colitis-associated cancer.
18 es of dextran sodium sulfate (DSS) to induce colitis-associated cancer.
19 ease treatment and define novel mediators of colitis-associated cancer.
20 be useful in the prevention or treatment of colitis-associated cancer.
21 ing through TLR4 may lower the threshold for colitis-associated cancer.
22 and its absence promotes the development of colitis-associated cancer.
23 lead to new strategies to identify and treat colitis-associated cancers.
24 myeloid cells contributes to development of colitis-associated cancer and Apc(Min)-dependent intesti
25 These mice were bred with Apc(Min/+) mice; colitis-associated cancer and colitis were induced by ad
26 capacity of the test to distinguish between colitis-associated cancer and different ulcerative colit
27 hes to manipulate IDO1 activity in mice with colitis-associated cancer and human colon cancer cell li
28 dence for their roles in the pathogenesis of colitis-associated cancer and sporadic colorectal cancer
29 important insights into the pathogenesis of colitis-associated cancer and suggest that epidermal gro
30 of colorectal cancer gave rise to the term "colitis-associated cancer" and the concept that inflamma
31 arthritis, inflammatory intestinal disease, colitis-associated cancer, and lipopolysaccharide (LPS,
32 lammatory signature' genes characteristic of colitis-associated cancer are also upregulated in colore
33 linked to pre-existing inflammation known as colitis-associated cancer, but most develops in patients
34 Here we established a novel mouse model of colitis-associated cancer by genetically inactivating si
35 vation appears to promote the development of colitis-associated cancer by mechanisms including enhanc
36 r findings suggest that PHB protects against colitis-associated cancer by modulating p53- and STAT3-m
37 e intestine, where it helps protects against colitis-associated cancer by regulating HMOX-1 expressio
38 K1) links chronic intestinal inflammation to colitis-associated cancer (CAC) and both are exacerbated
39 myeloid AC protects from tumor incidence in colitis-associated cancer (CAC) and inhibits the expansi
44 fic IKKbeta is involved in the initiation of colitis-associated cancer (CAC), as in its absence mice
45 ling pathway are associated with colitis and colitis-associated cancer (CAC), but how IL-33 modulates
46 trast, MyD88-deficient mice are sensitive to colitis-associated cancer (CAC), since selected cytokine
57 miR-375 was significantly upregulated in the colitis-associated cancer cohort (p=0.0061) compared wit
58 mmation and contributes to the prevention of colitis-associated cancer during chronic inflammation th
60 antly attenuated intestinal inflammation and colitis-associated cancer in dextran sodium sulfate mode
70 ression of beta-catenin target genes in CUC, colitis-associated cancer, tubular adenomas, and sporadi
71 dministration of dextran sodium sulfate, and colitis-associated cancer was induced by administration
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