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1 tment to the bone marrow, a key location for hematopoietic tumors.
2  the highly sensitive and readily accessible hematopoietic tumors.
3 helial carcinomas, soft tissue sarcomas, and hematopoietic tumors.
4 g pathway play an important role in lymphoid/hematopoietic tumors.
5 elial cancers, but has not been described in hematopoietic tumors.
6 in the cell lines derived from solid as from hematopoietic tumors.
7 earrangements are found in a large number of hematopoietic tumors.
8 tatic tumor growth in a variety of solid and hematopoietic tumors.
9 ted equivalent immunity against A20 and P815 hematopoietic tumors.
10 ontaneous aneuploidy and a predisposition to hematopoietic tumors.
11 pectral karyotypic analysis that MYC-induced hematopoietic tumors are highly genetically complex and
12  chemotherapy for the treatment of solid and hematopoietic tumors are underway.
13 three genes are almost universal in lymphoid/hematopoietic tumors but the patterns of gene methylated
14                         Mutation analysis of hematopoietic tumor cell lines and B-CLL tumor samples r
15                                      In some hematopoietic tumor cell lines having altered c-myc gene
16 d by multiple genotoxic stress agents in all hematopoietic tumor cell lines we have examined.
17 ion of mRNA and protein for VEGF in 12 human hematopoietic tumor cell lines, representing multiple li
18                                           In hematopoietic tumor cell lines, the association of p18-c
19 f TME-mediated drug resistance that protects hematopoietic tumor cells from the initial effect of div
20                    Earlier we showed that in hematopoietic tumor cells, caspase-mediated cleavage of
21 eavage of Cyclin E generates p18-Cyclin E in hematopoietic tumor cells.
22 ent proteolysis of cyclin E for apoptosis of hematopoietic tumor cells.
23 tions reveal that Cdk4 and Cdk6 cooperate in hematopoietic tumor development and suggest a role for C
24 , or DNA agarose gels in xenografts of human hematopoietic tumors HL-60, SUDHL-4, and Nalm/6.
25 d, or constitutively activated in many human hematopoietic tumors; however, the molecular mechanisms
26                                              Hematopoietic tumors in both humans and mice frequently
27 sufficient to induce sustained regression of hematopoietic tumors in transgenic mice, except in tumor
28 ene is aberrantly methylated in 86% of human hematopoietic tumors, including 8 of 9 pediatric acute l
29  Whereas H-Ras(G12V) elicited papillomas and hematopoietic tumors, K-Ras(G12V) induced lung tumors an
30    We show here in a Drosophila melanogaster hematopoietic tumor model, however, that JAK overactivat
31 ccine approach was assessed in several other hematopoietic tumor models and was also therapeutically
32                     We examined 150 lymphoid/hematopoietic tumors or potential premalignant specimens
33  Retroviral insertional mutagenesis in mouse hematopoietic tumors provides a potent cancer gene disco
34  Retroviral insertional mutagenesis in mouse hematopoietic tumors provides a powerful cancer gene dis
35                               Analysis of 63 hematopoietic tumors revealed that PiggyBac is capable o
36 ubiquitin ligase Fbw7, a recently identified hematopoietic tumor suppressor that can target for degra
37 sm leading to inactivation of this important hematopoietic tumor suppressor.
38 itutive activation of Rel/NF-kappaB in human hematopoietic tumors, the v-Rel oncoprotein induces aggr
39  because bfl-1 is up-regulated in many human hematopoietic tumors, this finding suggests that strateg
40             Furthermore, a host of solid and hematopoietic tumor types exhibit constitutive activatio

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