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1 ependent development of lymphatic vessels in experimental tumors.
2 erium that can infect hypoxic regions within experimental tumors.
3 tension) is a hallmark feature of human and experimental tumors.
4 be deregulated in several forms of human and 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
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
17 (PV) have been historically associated with experimental tumor development and recently described in
19 n to investigate the contribution of AMPK to experimental tumor growth and core glucose metabolism.
21 man pituitary tumors in vitro and suppressed experimental tumor growth in vivo, concomitantly with re
22 e, our previous studies showed that although experimental tumor growth is enhanced by low levels of c
24 ribution of AMPK to the growth of aggressive experimental tumors has a critical microenvironmental co
26 blocks the growth of primary and metastatic experimental tumors Here we report that VEGF expression
27 e successful at controlling the growth of an experimental tumor in rabbits appreciably better than do
28 itro and showed an increased accumulation in experimental tumors in mice when compared with nontarget
34 Le(X) by the 4'-deoxy analog also diminished experimental tumor metastasis by Lewis lung carcinoma in
39 iness of tumor vessels is well documented in experimental tumor models and in human cancer, but the m
40 is in human tumors may serve to substantiate experimental tumor models and thus increase our understa
41 ck into the cell cycle, both in vitro and in experimental tumor models in vivo Mechanistically, we fo
42 the effects of anti-VEGF therapy in multiple experimental tumor models that differ in their glycolyti
44 IL-12), is clinically significant in certain experimental tumor models, in that a number of well-esta
48 ted the importance of AMPK for the growth of experimental tumors prepared from HRAS-transformed mouse
50 In contrast, pathological angiogenesis in experimental tumors was altered, resulting in smaller tu
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