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1 d expression of 14-3-3sigma and p21 in human gastrointestinal tumors.
2 lications in the mutations observed in human gastrointestinal tumors.
3 be an important etiological agent for human gastrointestinal tumors.
4 e is an important target in the treatment of gastrointestinal tumors.
5 a valuable diagnostic/prognostic marker for gastrointestinal tumors.
6 articular emphasis on lymphoma, melanoma and gastrointestinal tumors.
7 less frequently mutated in near-diploid MMP gastrointestinal tumors.
8 portant role for SMAD4 in the development of gastrointestinal tumors.
9 the Min mice, but no control mice, developed gastrointestinal tumors.
10 ging may have potential for local staging of gastrointestinal tumors.
11 allelic deletion and aberrant transcripts in gastrointestinal tumors.
12 s, gene expression patterns were examined in gastrointestinal tumors.
13 AKT pathway activation, commonly observed in gastrointestinal tumors.
15 f tumors, the most predominant of which were gastrointestinal tumors and B- as well as T-cell lymphom
16 tumor cell-endothelial cell communication in gastrointestinal tumors and glioblastomas, but its mecha
17 e examined apobec-1 gene expression in human gastrointestinal tumors and in colon cancer-derived cell
18 e similarity in p53 mutations found in human gastrointestinal tumors and in shuttle vector studies, w
19 nd in the p53 tumor suppressor gene in human gastrointestinal tumors and in shuttle vector studies.
20 mechanism for activation of beta-catenin in gastrointestinal tumors and support the concept that ove
21 icacy of SU-11248 against imatinib-resistant gastrointestinal tumors, and the EGFR inhibitors EKB-569
22 s) and about 15% of nonselected ("sporadic") gastrointestinal tumors belong to the MMP pathway of tum
23 ation is an important treatment modality for gastrointestinal tumors, but intestinal injury is a comm
24 lasms account for only a small percentage of gastrointestinal tumors, but their prognosis is one of t
26 ter, an important target in the treatment of gastrointestinal tumors, contains two such stretches of
27 lyposis coli (APC) gene are common events in gastrointestinal tumor development, we sought to investi
28 rmine if aspirin would significantly inhibit gastrointestinal tumor formation in a mouse model of fam
29 Wnt pathway, via Apc/APC mutation, leads to gastrointestinal tumor formation in both the mouse and h
30 d closely with those reported previously for gastrointestinal tumors from a PET/5-[(18)F]FU + enilura
31 ver the past decade, the microenvironment of gastrointestinal tumors has gained increasing attention
33 iew the different cellular components of the gastrointestinal tumor microenvironment and their functi
35 s, such as TGFbetaRII and BAX, are common in gastrointestinal tumors of the microsatellite mutator ph
36 asia, spastic esophageal disorders and upper gastrointestinal tumors originating from the muscularis
37 rapy for treatment of small and medium sized gastrointestinal tumors originating from the muscularis
38 vomiting > or = 3 d/mo; previous surgery for gastrointestinal tumor; self-reported heart failure; rec
39 ered in any patient presenting with multiple gastrointestinal tumors, since our patient could not be
41 based studies in esophageal cancer and other gastrointestinal tumors, suggesting that a higher nodal
43 rization of a large series of SBAs and other gastrointestinal tumors to draw comparisons and identify
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