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1  may not be appropriate for the treatment of plasma cell tumors.
2 le in the development of a broad spectrum of plasma cell tumors.
3 tively or IGF-I-dependently activated in all plasma cell tumors.
4 ned the mechanism of CD23 down-regulation by plasma cell tumors.
5 ose Ig and Myc-family genes in AID-deficient plasma cell tumors.
6 m for the derivation of cytokine-independent plasma cell tumors and suggest that both IL-6-dependent
7 tible to the development of pristane-induced plasma cell tumors, and have a rare allelic variant in t
8                                IgM-secreting plasma cell tumors are rare variants of typical isotype-
9 e previously found that splenic B cells from plasma cell tumor-bearing mice exhibit decreased CD23 ex
10 reased CD23 expression on B cells induced by plasma cell tumors because 1) Abs to IL-10 prevent the l
11 to IL-10 prevent the loss of CD23 induced by plasma cell tumors both in vitro and in vivo; 2) enginee
12  repressed class II transactivator gene in a plasma cell tumor but, in several other tumor cell lines
13 6K and Akt may be differentially used by the plasma cell tumors derived from mice and humans, respect
14                                              Plasma cell tumors display a wide spectrum of clinical p
15 Collectively, these results demonstrate that plasma cell tumors down-regulate CD23 expression on B ce
16          The failure of rapamycin to inhibit plasma cell tumor growth suggests that FRAP antagonists
17 combinations with c-myc in t(12;15)-positive plasma cell tumors in BALB/c mice.
18 tions between Ig switch regions and c-Myc in plasma cell tumors in mice.
19 gineered Vk*MYC mice is sufficient to induce plasma cell tumors in which a variety of secondary mutat
20 tion into Igh predictably induces B-cell and plasma-cell tumors in mice, providing a valuable mouse m
21                    The development of murine plasma cell tumors induced by raf/myc containing retrovi
22                                              Plasma cell tumor induction in mice by pristane is under
23 osteolytic lesions were observed adjacent to plasma cell tumor masses in the bone marrow, indicating
24 the setting of a genetic disease, the B-cell/plasma cell tumor microenvironment (TME) contributes sig
25  been eliminated, developed pristane-induced plasma cell tumors over a shorter latency period than th
26                                        Mouse plasma cell tumor (PCT) and human multiple myeloma (MM)
27                         We extracted nascent plasma cell tumor (PCT) cells from within inflammatory o
28                           In contrast, mouse plasma cell tumor (PCT) lines, expressing wild type PTEN
29 within the cell, we studied pristane-induced plasma cell tumors (PCTs).
30                          Mice susceptible to plasma cell tumors provide a useful model for human mult
31                                       Murine plasma cell tumors share a number of common features wit
32 pecially broad and high expression levels in plasma cell tumors such as multiple myeloma (MM).
33                                           In plasma cell tumors such as multiple myeloma the repressi
34 ouble-transgenic Myc/Bcl-X(L) mice developed plasma cell tumors with short onset (135 days on average