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1 erium that can infect hypoxic regions within experimental tumors.
2  tension) is a hallmark feature of human and experimental tumors.
3 be deregulated in several forms of human and experimental tumors.
4 ependent development of lymphatic vessels in experimental tumors.
5 IP for bioactivity and its ability to detect experimental tumors.
6 vaccines, we used lacZ-transduced CT26 as an experimental tumor and beta-galactosidase (beta-gal) as
7 e immune response against a weakly antigenic experimental tumor and therefore has potential as a nove
8  histopathological finding in many human and experimental tumors and is thought to be of importance i
9 asis of their efficacy profile in additional experimental tumors and lack of cardiotoxicity in precli
10 ysiological characteristic of most human and experimental tumors and may be responsible, in part, for
11  associated with a variety of both human and experimental tumors, and cooperation of other oncogenes
12 ention has been given to situations in which experimental tumors are induced by multiple cooperating
13  we have showed targeted drug activity in an experimental tumor-bearing mouse model.
14 rus sT oncoproteins have been found to cause experimental tumors by blocking the activities of a grou
15 s depleted of CD8(+) T cells at the onset of experimental tumor cell challenge developed lung tumor f
16                                        In an experimental tumor construct, MCF7 and MDA-MB-231 breast
17 pproach, and show how it could be applied to experimental tumor data to study clonal selection and in
18  (PV) have been historically associated with experimental tumor development and recently described in
19 mids and effectively treated mice bearing an experimental tumor expressing the model antigen.
20 n to investigate the contribution of AMPK to experimental tumor growth and core glucose metabolism.
21 e in urothelial carcinoma and contributes to experimental tumor growth and metastasis.
22 man pituitary tumors in vitro and suppressed experimental tumor growth in vivo, concomitantly with re
23 e, our previous studies showed that although experimental tumor growth is enhanced by low levels of c
24  level of inhibition of Lewis lung carcinoma experimental tumor growth.
25 m patients at baseline and was essential for experimental tumor growth.
26 ribution of AMPK to the growth of aggressive experimental tumors has a critical microenvironmental co
27                Numerous studies in human and experimental tumors have demonstrated low p27(Kip1) leve
28  blocks the growth of primary and metastatic experimental tumors Here we report that VEGF expression
29 e successful at controlling the growth of an experimental tumor in rabbits appreciably better than do
30 mice, a high-salt diet reduced the growth of experimental tumors in a CD8(+) T cell-dependent manner
31 itro and showed an increased accumulation in experimental tumors in mice when compared with nontarget
32 eit poorly defined, role in the formation of experimental tumors in mice.
33 vivo via immunofluorescent image analysis of experimental tumors in mice.
34                   Furthermore, the growth of experimental tumors is not increased.
35 ect of anti-vascular agents on the growth of experimental tumors is well studied.
36           The suppression of spontaneous and experimental tumor metastases and methylcholanthrene (MC
37 Le(X) by the 4'-deoxy analog also diminished experimental tumor metastasis by Lewis lung carcinoma in
38                            Here, by using an experimental tumor metastasis model and in vitro studies
39 inished metastatic potential in a setting of experimental tumor metastasis to the lung.
40 using them to inhibit carbohydrate-dependent experimental tumor metastasis.
41 nd its constituent silibinin in a variety of experimental tumor models and cell culture systems.
42 iness of tumor vessels is well documented in experimental tumor models and in human cancer, but the m
43 is in human tumors may serve to substantiate experimental tumor models and thus increase our understa
44 ck into the cell cycle, both in vitro and in experimental tumor models in vivo Mechanistically, we fo
45 the effects of anti-VEGF therapy in multiple experimental tumor models that differ in their glycolyti
46                  The limited availability of experimental tumor models that faithfully mimic the prog
47 IL-12), is clinically significant in certain experimental tumor models, in that a number of well-esta
48 specific protective immunity in a variety of experimental tumor models.
49 ible and correlate with angiogenic burden in experimental tumor models.
50 us mediated HSV-tk/GCV gene therapy in these experimental tumor models.
51 ted the importance of AMPK for the growth of experimental tumors prepared from HRAS-transformed mouse
52                                           In experimental tumors, reducing mitochondrial metabolism t
53  universal Ras-GEF in various KRAS-dependent experimental tumor settings.
54 luate relationships between study design and experimental tumor volume effect sizes.
55    In contrast, pathological angiogenesis in experimental tumors was altered, resulting in smaller tu
56 blish a novel therapy for solid tumors in an experimental tumor xenograft model.