ライフサイエンスコーパス: colorectal adenocarcinoma

1 to treat patients with pelvic recurrence of colorectal adenocarcinoma.

2 eceptors (TCRs) expressed on TILs from human colorectal adenocarcinoma.

3 ed from whole-genome sequencing of a primary colorectal adenocarcinoma.

4 ioembolization for liver-dominant metastatic colorectal adenocarcinoma.

5 ible to experimental triggers of colitis and colorectal adenocarcinoma.

6 epithelial cell line, SKCO-15, derived from colorectal adenocarcinoma.

7 carcinoma, C33a cervix carcinoma, and LS174T colorectal adenocarcinoma.

8 ype colorectal cancers but down-regulated in colorectal adenocarcinoma.

9 novel target for anti-angiogenic therapy in colorectal adenocarcinoma.

10 erum hypergastrinemia promotes the growth of colorectal adenocarcinoma.

11 sufficient to induce formation of metastatic colorectal adenocarcinomas.

12 clusivity with inactivating APC mutations in colorectal adenocarcinomas.

13 showed frequent overexpression of OATP1B3 in colorectal adenocarcinomas.

14 tatus in patients with Dukes' stage B2 and C colorectal adenocarcinomas.

15 K-ras, and/or p53, occur in the majority of colorectal adenocarcinomas.

16 ontrols in breast, endometrial, pancreas, or colorectal adenocarcinomas.

17 quencies of allelic losses in pancreatic and colorectal adenocarcinomas.

18 , the Smad3 mutant mice become moribund with colorectal adenocarcinomas.

19 in p27 expression in primary and metastatic colorectal adenocarcinomas.

20 Ras mutations are found in 50% of colorectal adenocarcinomas.

21 with a significant risk of gastric, but not colorectal, adenocarcinoma.

22 Among colorectal adenocarcinomas, 10%-15% are mucinous and hav

23 h transmural lesions and a high incidence of colorectal adenocarcinomas (60%) was observed in 6-mo-ol

24 cted with PDGF-BB-bearing tumor cells and in colorectal adenocarcinoma, activated PDGF beta-receptors

25 Caco-2 cells, which are derived from a human colorectal adenocarcinoma and have similar functions to

26 identified recurrent oncogenic mutations in colorectal adenocarcinoma and have surveyed exons of pro

27 by immunohistochemical methods in 30 primary colorectal adenocarcinomas and 24 adenomatous polyps.

28 mmunohistochemical analysis was performed on colorectal adenocarcinomas and adjacent normal mucosa fo

29 rt somatic mutations of RNF43 in over 18% of colorectal adenocarcinomas and endometrial carcinomas.

30 re increased dramatically in 85-90% of human colorectal adenocarcinomas and in 40-50% of colonic aden

31 ation at the EVL/hsa-miR-342 locus in 86% of colorectal adenocarcinomas and in 67% of adenomas, indic

32 2 (colorectal adenocarcinoma), HT29-MTX-E12 (colorectal adenocarcinoma) and HepG2 (hepatocellular car

33 tate cancer, 80% of B-cell lymphomas, 90% of colorectal adenocarcinomas, and many other forms of canc

34 partment, that its expression is elevated in colorectal adenocarcinomas, and that MSI2 loss-of-functi

35 s with locally advanced pelvic recurrence of colorectal adenocarcinoma are described.

36 previously that the pulmonary metastases of colorectal adenocarcinoma are less responsive to therapy

37 Ten to 20% of human colorectal adenocarcinomas are of this histological type

38 Patients with a new diagnosis of colorectal adenocarcinoma at the major hospitals in metr

39 oembolization to treat liver metastases from colorectal adenocarcinoma between July 2002 and December

40 intestinal cells and primary and metastatic colorectal adenocarcinomas but not by extraintestinal ti

41 erved in approximately 25% of stage I/II/III colorectal adenocarcinomas but rarely found in advanced

42 i-ras protooncogene frequently is mutated in colorectal adenocarcinomas, but the etiology of this mol

43 drome (MetS) are differently associated with colorectal adenocarcinoma (CA) by anatomical location is

44 The colorectal adenocarcinoma Caco-2 cell line forms polariz

45 n vitro cell culture model (human epithelial colorectal adenocarcinoma, Caco-2).

46 ctal adenoma cases and 544 controls, and 535 colorectal adenocarcinoma cases and 656 controls) among

47 f follow-up (through February 20, 2004), 220 colorectal adenocarcinoma cases were documented.

48 essed by studying the survival of four human colorectal adenocarcinoma cell cultures after 1 hour of

49 reening phage libraries derived from a human colorectal adenocarcinoma cell line and from noncancerou

50 gallate (ECG, IC50 = 76 microM) against the colorectal adenocarcinoma cell line HCT116.

51 Our studies involving the murine colorectal adenocarcinoma cell line MC38 confirm that IF

52 32H mutation on the metabolism of the HCT116 colorectal adenocarcinoma cell line.

53 rt, placenta, skeletal muscle, kidney, and a colorectal adenocarcinoma cell line.

54 Tumors derived from human colorectal adenocarcinoma cell lines HT29 and HCT-8 rang

55 In human colorectal adenocarcinoma cell lines, we found two major

56 GF and TGFalpha were investigated with human colorectal adenocarcinoma cells (Caco-2).

57 mbled to deliver CO to a suspension of human colorectal adenocarcinoma cells (HT-29) under the contro

58 C3 is expressed in human intestine and LS180 colorectal adenocarcinoma cells and is upregulated by ag

59 In contrast, PD-L1 on MC38 colorectal adenocarcinoma cells is sufficient to suppres

60 ke, and inhibited the proliferation of DLD-1 colorectal adenocarcinoma cells to a greater extent than

61 of lung carcinoma and xenotransplanted human colorectal adenocarcinoma cells was observed after admin

62 Transfection of LS180 human colorectal adenocarcinoma cells with an miR-18a-5p mimic

63 release compounds in Caco-2 human epithelial colorectal adenocarcinoma cells.

64 In the case of colorectal adenocarcinoma (CRA), grading is partly deter

65 ie transformation of colonic epithelium into colorectal adenocarcinoma (CRC) are well described.

66 ase (IBD) and the incidence and mortality of colorectal adenocarcinoma (CRC) has not been evaluated r

67 patients with previously treated metastatic colorectal adenocarcinoma, demonstrating higher response

68 cids (LNA30bcd) in both human IECs and human colorectal adenocarcinoma-derived Caco-2 cells resulted

69 Sinai Hospital between 1960 and 1989 in whom colorectal adenocarcinoma developed.

70 Human colorectal adenocarcinomas exhibited reductions in Rab25

71 Routine molecular screening of patients with colorectal adenocarcinoma for the Lynch syndrome identif

72 -malignant colon tumor sample and late-stage colorectal adenocarcinoma from the same individual.

73 potent cytotoxicity (GI(50) < 1 nM vs human colorectal adenocarcinoma (HCT-116) cells) but did not e

74 As the model system, spheroids of human colorectal adenocarcinoma HT-29 cells are generated by c

75 lines [human breast adenocarcinoma (MCF-7), colorectal adenocarcinoma (HT-29), non-small cell lung c

76 n this study three human cell lines, Caco-2 (colorectal adenocarcinoma), HT29-MTX-E12 (colorectal ade

77 ologic condition of the tumor was metastatic colorectal adenocarcinoma in 18 lesions, primary hepatoc

78 s were found in one-half of the patients and colorectal adenocarcinomas in 14%.

79 follow-up period, we identified 712 interval colorectal adenocarcinomas, including 255 advanced-stage

80 ave analysed specimens from 50 patients with colorectal adenocarcinomas, including cases in which an

81 lded long-lasting growth arrest of the human colorectal adenocarcinoma LS174T grown as s.c. xenograft

82 Athymic mice xenografted with human colorectal adenocarcinoma LS174T were treated intravenou

83 ascl2 as a gene significantly upregulated in colorectal adenocarcinomas (n=36 cancers, n=16 normals;

84 es with at least two siblings diagnosed with colorectal adenocarcinoma or high-grade dysplasia were e

85 To study the regulation of colorectal adenocarcinoma progression by O-GlcNAc, we ha

86 Here, we report that colorectal adenocarcinoma represents one important excep

87 Human tumors, including colorectal adenocarcinoma, secrete angiogenic factors, i

88 g multivariate statistical tools, nine human colorectal adenocarcinoma sections are analyzed with thr

89 ll lines, with the highest levels in Caco-2 (colorectal adenocarcinoma), SKOV3 (ovarian), and HepG2 (

90 DNA methyltransferase genes in 25 individual colorectal adenocarcinoma specimens and matched normal m

91 patients with metastatic breast, ovarian, or colorectal adenocarcinomas that overexpressed HER-2/neu

92 potentially resectable hepatic metastases of colorectal adenocarcinoma, the use of PET-CT compared wi

93 The 30 patients in the series had 33 colorectal adenocarcinomas; three patients (10%) present

94 pound 6 potently inhibits the growth of LoVo colorectal adenocarcinoma tumor cells in vitro and has h

95 ATR mediated phosphorylation of Chk1 in HT29 colorectal adenocarcinoma tumor cells with an IC50 of 50

96 we have found that RREB1 is overexpressed in colorectal adenocarcinoma tumors and cell lines, and the

97 e patients with a diagnosis of nonmetastatic colorectal adenocarcinoma undergoing surgical resection

98 , prospective, cohort study of patients with colorectal adenocarcinoma was performed from August 1, 1

99 alysis of APC, K-ras, and p53 to evaluate 50 colorectal adenocarcinomas, we have shown that mutation

100 in is associated with aggressive behavior in colorectal adenocarcinomas, we used immunohistochemistry

101 h histologically proven pelvic recurrence of colorectal adenocarcinoma were enrolled on a multimodali

102 Mouse xenografts of human primary colorectal adenocarcinomas were found to retain viable F

103 umor microenvironment (B16 melanoma and MC38 colorectal adenocarcinoma), where they contributed to th

104 oma (SRCC) is a rare histological subtype of colorectal adenocarcinoma, which has been associated wit

105 luded one partial response in a patient with colorectal adenocarcinoma with neuroendocrine features,

106 erate antitumor activity against HT-29 human colorectal adenocarcinoma xenograft in mice without over

107 ng the relative change in elastic modulus in colorectal adenocarcinoma xenograft models in vivo and i