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1 ew cancer cell lines from four patients with gastrointestinal tumors.
2 AKT pathway activation, commonly observed in gastrointestinal tumors.
3 d expression of 14-3-3sigma and p21 in human gastrointestinal tumors.
4 lications in the mutations observed in human gastrointestinal tumors.
5 both Xist-deleted and wild-type mice develop gastrointestinal tumors.
6  be an important etiological agent for human gastrointestinal tumors.
7 e is an important target in the treatment of gastrointestinal tumors.
8  a valuable diagnostic/prognostic marker for gastrointestinal tumors.
9 articular emphasis on lymphoma, melanoma and gastrointestinal tumors.
10                These criteria do not include gastrointestinal tumors.
11  less frequently mutated in near-diploid MMP gastrointestinal tumors.
12 portant role for SMAD4 in the development of gastrointestinal tumors.
13 the Min mice, but no control mice, developed gastrointestinal tumors.
14 ging may have potential for local staging of gastrointestinal tumors.
15 allelic deletion and aberrant transcripts in gastrointestinal tumors.
16 s, gene expression patterns were examined in gastrointestinal tumors.
17                             Twenty-two of 59 gastrointestinal tumors (37%) contained E2F-4 mutations;
18 f tumors, the most predominant of which were gastrointestinal tumors and B- as well as T-cell lymphom
19 tumor cell-endothelial cell communication in gastrointestinal tumors and glioblastomas, but its mecha
20 e examined apobec-1 gene expression in human gastrointestinal tumors and in colon cancer-derived cell
21 e similarity in p53 mutations found in human gastrointestinal tumors and in shuttle vector studies, w
22 nd in the p53 tumor suppressor gene in human gastrointestinal tumors and in shuttle vector studies.
23  mechanism for activation of beta-catenin in gastrointestinal tumors and support the concept that ove
24 icacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569
25 s) and about 15% of nonselected ("sporadic") gastrointestinal tumors belong to the MMP pathway of tum
26 ation is an important treatment modality for gastrointestinal tumors, but intestinal injury is a comm
27 lasms account for only a small percentage of gastrointestinal tumors, but their prognosis is one of t
28 pecies (ROS), Ca(2+), and ceramide levels in gastrointestinal tumor cells.
29 essible chromatin using sequencing data from gastrointestinal tumors, Clonalscope successfully labele
30 ifts in the microbiomes of patients with non-gastrointestinal tumors compared with healthy donors.
31 ter, an important target in the treatment of gastrointestinal tumors, contains two such stretches of
32 lyposis coli (APC) gene are common events in gastrointestinal tumor development, we sought to investi
33 rmine if aspirin would significantly inhibit gastrointestinal tumor formation in a mouse model of fam
34  Wnt pathway, via Apc/APC mutation, leads to gastrointestinal tumor formation in both the mouse and h
35 d closely with those reported previously for gastrointestinal tumors from a PET/5-[(18)F]FU + enilura
36 ver the past decade, the microenvironment of gastrointestinal tumors has gained increasing attention
37 iology, their involvements in progression of gastrointestinal tumor have not been explored.
38 lignancy was poor in patients with leukemia, gastrointestinal tumors, lung cancer, and sarcoma.
39 iew the different cellular components of the gastrointestinal tumor microenvironment and their functi
40 tocellular carcinoma (n = 10) and metastatic gastrointestinal tumors (n = 28) for phosphoprotein IHC
41  of cancer, including lung cancer (n = 113), gastrointestinal tumors (n = 84), hematological malignan
42                                     Numerous gastrointestinal tumors, notably sporadic and ulcerative
43 s, such as TGFbetaRII and BAX, are common in gastrointestinal tumors of the microsatellite mutator ph
44 rapy for treatment of small and medium sized gastrointestinal tumors originating from the muscularis
45 asia, spastic esophageal disorders and upper gastrointestinal tumors originating from the muscularis
46 vomiting > or = 3 d/mo; previous surgery for gastrointestinal tumor; self-reported heart failure; rec
47 ered in any patient presenting with multiple gastrointestinal tumors, since our patient could not be
48               Based on limited data from the Gastrointestinal Tumor Study Group, adjuvant chemoradiat
49 based studies in esophageal cancer and other gastrointestinal tumors, suggesting that a higher nodal
50         Patients with known CEACAM5-positive gastrointestinal tumors suggestive of lung metastasis we
51  impaired DNA-damage response, and increased gastrointestinal tumor susceptibility.
52 found significant overexpression of AURKA in gastrointestinal tumor tissues compared with non-tumor t
53 rization of a large series of SBAs and other gastrointestinal tumors to draw comparisons and identify
54                           Overall, all major gastrointestinal tumors were associated with increased r
55  that inhibit AURKA might slow the growth of gastrointestinal tumors with activation of KRAS.