ライフサイエンスコーパス: gastric tumor

1 sequenced SMO and PTCH1 genes in a set of 39 gastric tumors.

2 riety of human cancers, including breast and gastric tumors.

3 gen (CEA/Tag) transgenic mice, which develop gastric tumors.

4 rin and p73 transcripts correlate in primary gastric tumors.

5 on is increased in several tumors especially gastric tumors.

6 cer cell lines, 61 colorectal tumors, and 87 gastric tumors.

7 Thirteen novel loci showed FSMs in >20% of gastric tumors.

8 ignificant risk factor in the development of gastric tumors.

9 1 promoter hypermethylation in a total of 65 gastric tumors: 18 with frequent MSI (MSI-H), 8 with inf

10 ned E2F-4 mutations; these comprised 5 of 16 gastric tumors (31%), 4 of 12 ulcerative colitis-associa

11 on, we applied an RNA-sequencing approach to gastric tumor and noncancerous specimens, generating 680

12 o directly track the delivery to the primary gastric tumor and to lung metastatic sites.

13 or point mutations were found in 40 primary gastric tumors and 51 cell lines derived from diverse ty

14 as determined by Western blot in 17 pairs of gastric tumors and corresponding non-neoplastic gastric

15 valuated NPM1 gene and protein expression in gastric tumors and in corresponding non-neoplastic gastr

16 rase chain reaction (RT-qPCR) in 22 pairs of gastric tumors and in matched non-neoplastic gastric tis

17 g for FoxM1b in tumor cell nuclei in various gastric tumors and lymph node metastases.

18 ation Panel I assay on DNA extracted from 60 gastric tumors and matched tumor-adjacent gastric tissue

19 a plays a crucial role in the development of gastric tumors and polymorphisms in the IL-1 gene cluste

20 for tumor EBV status because only 7%-10% of gastric tumors and select NHL subtypes are related to EB

21 requency in different histologic subtypes of gastric tumors and these do not appear to be driver muta

22 at the intestinal lesion is secondary to the gastric tumor, and the mutation patterns in two cases in

23 cifically expressed in embryonic stem cells, gastric tumors, and hepatic stellate cells.

24 Intestinal and diffuse gastric tumors arise rapidly in this model that displays

25 e of RUNX3 protein expression in 86 cases of gastric tumors as compared with that in normal gastric m

26 re found in both intestinal and diffuse type gastric tumors as well as in tumors that exhibit both in

27 cDNA, derived from primary gastric tumors before chemotherapy, was used to determin

28 t reversal of homing receptor profile in the gastric tumor by antigen specific stimulation may be res

29 Gastric tumors can become resistant to gefitinib, an inh

30 In a gastric tumor cell line, neuronostatin induced c-Fos exp

31 Levels of CITED2 in gastric tumors correlate with patients' response to epir

32 Gastric tumors developed in 29% of 80-week-old Villin-Cr

33 cancer is not a common event during sporadic gastric tumor development, at least in patients from Nor

34 In total, 15 of 18 gastric tumors exhibited at least fivefold higher C/EBPb

35 Patients with ovarian or gastric tumors expressing higher levels of HtrA1 showed

36 ibiting Helicobacter infections and blocking gastric tumor formation offer hope that these mechanisms

37 cell lines and tumor samples, as well as in gastric tumors from CEA/Tag mice, compared with non-neop

38 ssion of human gastrokines (GKNs) attenuated gastric tumor growth in gp130F/F mice.

39 Mouse and human gastric tumors had reduced expression of Kruppel-like fa

40 About 5% to 10% of human gastric tumors harbor oncogenic mutations in the KRAS pa

41 Because gastric tumors have been shown to contain a high percent

42 The multiplicity of gastric tumor in carcinogen-treated mice was significant

43 ells in mice and reversed the development of gastric tumors in Tff1(-/-) mice.

44 revealed loss of TFF1 expression in 56 of 59 gastric tumors in which 54 of these tumors exhibited ove

45 COX-2 expression (IHC) in gastric tumors inversely correlated with COX-2 gene meth

46 rstly constructed a carcinogen-induced mouse gastric tumor model combined with H. pylori infection an

47 In a mouse model of gastric tumors (N87), 40 stops tumor growth at 5 mg/kg a

48 Apc(Min/+);Foxl1-/- mice also develop gastric tumors not observed in Apc(Min) mice.

49 The volume of gastric tumors noticeably decreased during the course of

50 h the expression of NPM1 is heterogeneous in gastric tumors, our results suggest that NPM1 down-regul

51 aining showed strong PTGR2 expression in the gastric tumor portion, relative to nearby nontumor porti

52 he inhibition of the Kras gene expression in gastric tumors prevents the occurrence of metastasis to

53 astric carcinogenesis and increased rates of gastric tumor progression than control mice.

54 k of atrophic gastritis, and is considered a gastric tumor promoter.

55 We investigated the role of DARPP-32 in gastric tumor resistance to gefitinib.

56 and TP53 was observed in 45.5% and 21.2% of gastric tumors, respectively.

57 found in intron 8 of the TDG locus to screen gastric tumor samples for loss of heterozygosity.

58 We analyzed gastric tumor samples from patients using immunohistoche

59 Levels of CITED2 were increased in gastric tumor samples from patients who had complete res

60 ively correlated with those of VEGF in human gastric tumor samples.

61 MYC amplification was observed in 51.5% of gastric tumor samples.

62 showed significant CD44v8-10 upregulation in gastric tumor sites.

63 Findings were compared with those from human gastric tumor specimens.

64 with increased C/EBPbeta was observed in the gastric tumors studied.

65 Kruppel-like factor 4 (Klf4) is a putative gastric tumor suppressor gene.

66 he G(1) to S-phase cell cycle transition and gastric tumor suppressor gene.

67 how that H. pylori infection inactivates the gastric tumor suppressor RUNX3 in a CagA-dependent manne

68 s an oncoprotein by blocking the activity of gastric tumor suppressor RUNX3.

69 TFF1 is a gastric tumor suppressor that protects gastric epithelia

70 Trefoil factor family-1 (TFF1) is a key gastric tumor-suppressor gene.

71 Synchronous gastric tumors that consist of both gastrointestinal str

72 aled overexpression of C/EBPbeta in 10 of 13 gastric tumors that exhibited low expression of TFF1 at

73 Resected gastric tumor tissues (n = 102) were analyzed for p-Erk

74 evels were also significantly upregulated in gastric tumor tissues, when compared with paired nontumo

75 o occur at significantly higher frequency in gastric tumor tissues.

76 compared gene expression patterns among 248 gastric tumors; using a robust method of unsupervised cl

77 The neoplastic B cells in the gastric tumor were alpha 4 beta 7-, CD62L+, whereas the

78 ulated in a number of primary colorectal and gastric tumors when compared with matching normal tissue