ライフサイエンスコーパス: intestinal cancer

1 h are crucial gatekeepers in common forms of intestinal cancer.

2 rences establish SBA as a molecularly unique intestinal cancer.

3 cer and the creation of models of metastatic intestinal cancer.

4 However, aberrant Wnt signaling leads to intestinal cancer.

5 t in diseases such as ulcerative colitis and intestinal cancer.

6 cantly increase risk for both testicular and intestinal cancer.

7 d that cholecystectomy increases the risk of intestinal cancer.

8 oncausal associations between gallstones and intestinal cancer.

9 ight contribute to inflammatory diseases and intestinal cancer.

10 ic epithelial cells in the initial stages 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 ors of Sphk1 may be useful in the control of intestinal cancer.

17 n human colonic cells and in mouse models of intestinal cancer.

18 hich is highly expressed in murine and human intestinal cancers.

19 signaling mutations drive formation of human intestinal cancers.

20 hrough 2003, 165 individuals developed small intestinal cancers.

21 number of patients with colorectal and other intestinal cancers.

22 ), septicemia (6.8; 95% CI, 2.2-15.8), small intestinal cancer (48.1; 95% CI, 5.8-17.4), respiratory

23 modifier of proapoptotic gene expression in intestinal cancers, acting independently of bile acid me

24 requency questionnaire, in relation to small intestinal cancer among half a million men and women enr

25 or development in mouse models for inherited intestinal cancer, an observation that is reminiscent of

26 al cells, protects mice from colitis-induced intestinal cancer and ApcMin-dependent intestinal tumori

27 activated in Apc(min/+) mice, which develop intestinal cancer and lose weight despite the absence of

28 eat consumption increases the risk of gastro-intestinal cancers and it is strongly suspected that nit

29 nt glioma, medulloblastoma, prostate cancer, intestinal cancer, and sarcoma from adjacent non-neoplas

30 /+) mice, a recognized mouse model for human intestinal cancer, and to elucidate possible mechanisms

31 We have used a mouse model of inherited intestinal cancer (Apc(Min)/+, Min/+) to analyze the ear

32 Intestinal cancers are frequently associated with mutati

33 Intestinal cancers are, on occasion, initially misdiagno

34 ly found in preneoplastic lesions, including intestinal cancers arising due to the inactivation of th

35 Min/+) mice, suggesting that Mgmt suppresses intestinal cancer associated with exogenous alkylating a

36 that the Apc(Min/+) mouse model for familial intestinal cancer can develop frequent invasive cancers

37 We studied the effects of IL28 on the human intestinal cancer cell line Caco-2 in a wound-healing as

38 In human intestinal cancer cells Caco-2/TC7 and SW480 and normal

39 y overexpressed in prostate, colorectal, and intestinal cancer cells.

40 Thus, common intestinal cancer driven by diet involves mechanisms of

41 rs in genetically engineered mouse models of intestinal cancer (driven by Apc inactivation) or lympho

42 ignaling and loss of PTEN cooperate to drive intestinal cancer formation and progression by suppressi

43 In the Apc(Min) mouse model of intestinal cancer, genetic abrogation of c-Jun N-termina

44 e may be a direct link between inhibition of intestinal cancer growth and selective inhibition of the

45 ults in marked and persistent suppression of intestinal cancer growth by 66%, whereas suppression of

46 of dietary and other risk factors for small intestinal cancer have been sparse and all of a case-con

47 osity was associated with increased risk for intestinal cancer in Apc(min)(/+) mice through a gene-by

48 idylate synthesis modifies susceptibility to intestinal cancer in Apc(min)(/+) mice.

49 pressor gene occurs early in the etiology of intestinal cancer in mammals.

50 inal blockage that has not been reported for intestinal cancer in mouse models.

51 ag, incidence, and frequency reflect >90% of intestinal cancer in Western societies, dietary-induced

52 of dietary-induced sporadic small and large intestinal cancer in WT mice in which tumor etiology, la

53 initiation and progression, respectively, of intestinal cancers in vivo.

54 in foods was inversely associated with small intestinal cancer incidence; the RR values were consiste

55 esting its chemopreventive potential against intestinal cancers including CRC.

56 ic colon cancer, and mouse and rat models of intestinal cancer indicate that the majority of early ad

57 n in this study, between cholecystectomy and intestinal cancer, is very unlikely to be causal.

58 L/6 (B6) Apc(Min/+) mouse model of inherited intestinal cancer, loss of Apc function can occur by los

59 are viable and fertile, their resistance to intestinal cancer may be of therapeutic relevance.

60 stemic colon cancer metastases targeting the intestinal cancer mucosa antigen guanylyl cyclase C (GCC

61 tive reverse transcriptase (RT)-PCR on large intestinal cancers (n=29 cancers, n=16 normals; 10-fold,

62 understanding the greater predisposition to intestinal cancer of Mlh1(-/-) mice.

63 Ikkepsilon in beta-catenin-driven models of intestinal cancer reduced tumor incidence and consequent

64 and, when coexpressed with Lgr5, also marks intestinal cancer stem cells.

65 s hypotheses, Ereg deficiency does not alter intestinal cancer susceptibility, as assayed in the ApcM

66 familial adenomatous polyposis, an autosomal intestinal cancer syndrome.

67 al adenomatous polyposis (FAP), an autosomal intestinal cancer syndrome.

68 reveal a tumor suppressor role for miR-26 in intestinal cancer that overrides putative oncogenic acti

69 gosity, they were less likely to develop the intestinal cancers that normally arise in this tumor-pre

70 cause mutations in Wnt pathway genes lead to intestinal cancer, the role of Wnt signaling in gut epit

71 e ability of CD4+ T cells to protect against intestinal cancer was correlated with their ability to r

72 f inflammatory bowel disease predisposing to intestinal cancer, we analyzed genome-wide DNA methylati

73 cohort of patients with small but not large intestinal cancer, we find a correlation between neutrop

74 To identify new drivers of intestinal cancer, we performed insertional mutagenesis

75 , Kras-driven mouse models of pancreatic and intestinal cancers were less responsive to depletion of

76 GPX-DKO mice that have microflora-associated intestinal cancers, which are correlated with increased

77 et gene highly expressed in murine and human intestinal cancers, which indicates that USP28 and c-MYC

78 pathway are associated with the majority of intestinal cancers, while dysregulation of the Hippo/Yes