ライフサイエンスコーパス: colon adenoma

1 was associated with decreased risk of distal colon adenoma.

2 revent the development of premalignant human colon adenomas.

3 ylation is an early event, detectable in 7/8 colon adenomas.

4 ial activation of an oncogene in established colon adenomas.

5 ALX4 gene methylation was confirmed in colon adenomas (11/13) and more frequently present in pr

6 nomas were missed more often (27%) than left colon adenomas (21%), but the difference was not signifi

7 Most sporadic colon adenomas acquire mutations in the adenomatous poly

8 lyposis coli (APC) gene are thought to cause colon adenoma and carcinoma formation by enhancing colon

9 essor and a candidate therapeutic target for colon adenomas and adenocarcinoma.

10 a gene whose expression is down-regulated in colon adenomas and adenocarcinomas, is a membrane glycop

11 -4 (ALX4) gene that was highly methylated in colon adenomas and cancer was identified.

12 DCA)] are considered to promote formation of colon adenomas and cancer, we have now attempted to find

13 secreted protein that is markedly induced in colon adenomas and cancers, CCSP-2 is a novel candidate

14 (RDH5) and retinol dehydrogenase L (RDHL) in colon adenomas and carcinomas as compared with normal co

15 arian endometrioid adenocarcinomas and mouse colon adenomas and carcinomas carrying gene defects lead

16 Recent studies indicate that human colon adenomas and carcinomas lack retinol dehydrogenase

17 We find that eIF-4E is increased in colon adenomas and carcinomas, and this increase is acco

18 mechanism contributing to the development of colon adenomas and carcinomas.

19 II, III, and IV colon cancers, as well as in colon adenomas and colon cancer cell lines.

20 sociated with 4-HNE-protein adducts in human colon adenomas and CRC.

21 ion of Dnmt3a in murine colon crypts, murine colon adenomas and human colorectal cancer using RNA flu

22 Apart from colon adenomas and primary and metastatic colorectal can

23 R9 protein expression levels were highest in colon adenomas and progressively decreased in invasive a

24 methylation is an early event, detectable in colon adenomas, and in even earlier microscopic colonic

25 um markers of colon cancers and precancerous colon adenomas as potential candidates for noninvasive d

26 ed with familial polyposis and also sporadic colon adenomas, both preconditions to cancer formation.

27 ose expression is absent in normal colon and colon adenomas, but that is commonly induced in malignan

28 utilize polyamine metabolites produced from colon adenomas/carcinomas to build these protective biof

29 ggesting an inhibition in the progression of colon adenoma caused by deletion of GnT-V.

30 istochemically in normal human colon tissue, colon adenomas, colon carcinomas, and normal tissue dist

31 and supplemental calcium were strongest for colon adenoma (descending and sigmoid colon).

32 itors, with potentially significant roles in colon adenoma development and progression.

33 is.Significance: These findings suggest that colon adenomas driven by APC mutations are distinct from

34 was not increased above normal in the three colon adenomas examined.

35 for normal colon and adenomas and found that colon adenomas exhibit a mutator phenotype.

36 through the dysregulated mucosal barrier in colon adenomas, facilitates the adenoma to adenocarcinom

37 ming of ETBF clearance profoundly influences colon adenoma formation, defining a period during which

38 ation of this pathway is thought to initiate colon adenoma formation.

39 polyposis coli (APC) is thought to initiate colon adenoma formation.

40 treatment) and placebo (cervix carcinoma and colon adenoma) groups.

41 ial clusters of colon cancer and early-onset colon adenomas have also been reported.

42 filing in Apc-mutant and Ctnnb1-mutant mouse colon adenomas identified candidate genes for subsequent

43 null Apc(Min)) mice had a 6-fold increase in colon adenoma incidence, and a 50-fold increase in color

44 e observed in human benign neurofibromas and colon adenoma lesions in vivo.

45 itive) in parallel (r = 0.70, P < 0.0001) in colon adenoma (n = 9) as well as primary (n = 46) and me

46 in use was inversely associated with risk of colon adenomas (odds ratio (OR) = 0.71, 95% confidence i

47 esults showed increased Dnmt3a expression in colon adenomas of APC((Min/+)) mice and human colorectal

48 the timing of their onset among 22 MSI human colon adenomas of varying stages.

49 d increase in the number and the diameter of colon adenoma (P<0.0001) compared to ApcMin/+ littermate

50 edly expressed in approximately 60% of human colon adenomas (P < 0.001 versus normal tissues) and in

51 Specifically, in a colon adenoma prevention trial, in all cases tested, ind

52 al loss of 15-PGDH expression in microscopic colon adenomas recovered from patients with familial ade

53 stinal adenomas and four times the number of colon adenomas relative to Min and Pms2+/-;Min mice.

54 he unexpected inverse association of DM with colon adenoma risk among older African American women.

55 uplex-disruptive mutations were absent in 20 colon adenomas, suggesting that these mutations occur la

56 r younger with colon cancer or with advanced colon adenomas that were >1 cm in size or that showed hi

57 olon cancer progression at the transition of colon adenoma to carcinoma in situ.

58 We investigated calcium intake and risk of colon adenoma to evaluate the association of calcium int

59 Guidelines recommend that patients with colon adenomas undergo periodic surveillance colonoscopy

60 Right colon adenomas were missed more often (27%) than left co