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1 OR ranged from 2.07 for lymphoma to 7.25 for lymphoid leukemia).
2            As expected, these mice developed lymphoid leukemia.
3  infected WT animals developed predominantly lymphoid leukemia.
4 r cells, including those in acute myeloid or lymphoid leukemia.
5 ia, myelodysplastic syndrome (MDS) and acute lymphoid leukemia.
6  drive the pathogenesis of acute myeloid and lymphoid leukemia.
7  CBFB-MYH11 association with myeloid but not lymphoid leukemia.
8 slocations associated with acute myeloid and lymphoid leukemia.
9  approved to treat relapsed/refractory acute lymphoid leukemia.
10 emia (CML) and in some patients with acute B-lymphoid leukemia.
11 loperoxidase or an antigen consistent with a lymphoid leukemia.
12 o distinguish megakaryoblastic leukemia from lymphoid leukemia.
13 lly promote the development of an aggressive lymphoid leukemia.
14 healthy mice treated with ATC also developed lymphoid leukemia.
15 ronic myeloid leukemia and a subset of acute lymphoid leukemias.
16 combination for the treatment of myeloid and lymphoid leukemias.
17  60 (0.1%) Hodgkin lymphomas, and 126 (0.2%) lymphoid leukemias.
18 ator in the pathogenesis of myeloid and some lymphoid leukemias.
19 lead to dysregulated splicing in myeloid and lymphoid leukemias.
20 iant forms of MTHFR have a decreased risk of lymphoid leukemias.
21 ates were 36% in CLL and 60% in other B-cell lymphoid leukemias.
22 ion of malignant clones in acute myeloid and lymphoid leukemias.
23 o a selective GVL effect against myeloid and lymphoid leukemias after F-->M HSCT.
24 Analyses were performed separately for acute lymphoid leukemia (ALL) and acute nonlymphoid leukemia (
25 nitor cells of sensitized mice induced acute lymphoid leukemia (ALL) of B-1 progenitor phenotype, whi
26 id leukemia (AML) and BCR/ABL-positive acute lymphoid leukemia (ALL), and inhibits leukemic colony fo
27 imary acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL), as well as normal hematopoietic
28 is of acute myeloid leukemia (AML) and acute lymphoid leukemia (ALL).
29 te megakaryocytic leukemia (AMKL), and acute lymphoid leukemia (ALL).
30 requently in primary colon cancers and acute lymphoid leukemias (ALL), respectively, and methylation
31 oid leukemias (AMLs) and 8 (6%) of 131 acute lymphoid leukemias (ALLs), but not in other tumor types.
32 induced a mixture of acute myeloid and acute lymphoid leukemias (AML+ALL).
33        A total of 10 720 patients with acute lymphoid leukemia and 1323 patients with acute myeloid l
34 s to the development of a well-characterized lymphoid leukemia and a less well-defined non lymphoid d
35 sed in numerous tumor types, including acute lymphoid leukemia and acute myeloid leukemia (AML).
36 d with both acute myeloid leukemia and acute lymphoid leukemia and are usually associated with a rela
37 urately models human Philadelphia-positive B-lymphoid leukemia and chronic myeloid leukemia (CML).
38 as of diverse lineages ensued, most commonly lymphoid leukemia and erythroleukemia.
39  that is aberrantly expressed in myeloid and lymphoid leukemia and in this issue of Blood, Doubrovina
40                                          The lymphoid leukemias and macrophage tumors had provirus in
41 d wild-type bone marrow nucleated cells into lymphoid leukemia, and healthy mice treated with ATC als
42  of primary human LSCs from both myeloid and lymphoid leukemias, and is also highly cytotoxic to bulk
43 s involved the pathogenesis of lymphomas and lymphoid leukemias are often based on the physiology of
44 uent targets of genetic alterations in human lymphoid leukemias are transcription factor genes with e
45 athogenesis of BCR-ABL1-positive myeloid and lymphoid leukemias are unknown.
46 ng, leukemia-initiating cells to result in B-lymphoid leukemia (B-ALL) in vivo.
47 en challenged with primary acute myeloid and lymphoid leukemia blasts; and (5) Vdelta2 cells are expa
48 pression induces the development of not only lymphoid leukemia but also erythro-megakaryocytic leukem
49 ifically, we determined that KDM2B maintains lymphoid leukemias, but restrains RAS-driven myeloid tra
50 sk of breast, prostate, kidney, bladder, and lymphoid leukemia cancer.
51 alent cytotoxicity found between myeloid and lymphoid leukemia cell lines.
52               Using a combination of human B lymphoid leukemia cells and mouse models, we now show th
53 mpare the deformability of human myeloid and lymphoid leukemia cells and neutrophils at low deformati
54                     These data indicate that lymphoid leukemia cells of different molecular subtypes
55 which adaphostin can damage both myeloid and lymphoid leukemia cells, but also indicate that this nov
56                     In patients with chronic lymphoid leukemia (CLL) or small lymphocytic lymphoma (S
57                        Patients with chronic lymphoid leukemia (CLL), even in the Omicron era and aft
58                            The human myeloid-lymphoid leukemia gene, MLL (also called ALL-1, Htrx, or
59 human MLL (mixed-lineage leukemia or myeloid-lymphoid leukemia) gene belongs to the trithorax gene fa
60 slocations associated with acute myeloid and lymphoid leukemia, has >50 known partner genes with whic
61 5% CI 1.8-12.9; P = 0.002), as well as acute lymphoid leukemia (HR 2.4, 95% CI 1.3-4.4; P = 0.003) an
62 2 domain was not required for induction of B-lymphoid leukemia in mice by BCR/ABL.
63 1, which can induce both acute myeloid and T-lymphoid leukemia in mice.
64          Thus far, reports of engraftment of lymphoid leukemia in SCID mice have mainly been from pat
65 nct roles in the pathogenesis of myeloid and lymphoid leukemias induced by BCR-ABL1, validating NF-ka
66 increased expression, as seen in a subset of lymphoid leukemia, inhibits myeloid cell proliferation a
67 delay, with other recipients succumbing to B-lymphoid leukemia instead.
68 us genetic mechanisms of tumor initiation in lymphoid leukemias (LL) will lead to improvements in pro
69 is gene was recently identified as a myeloid/lymphoid leukemia (MLL) fusion protein partner in acute
70  BCR-ABL cases, de novo e13-e14a2/p210 Ph(+) lymphoid leukemia more frequently showed CML-type backgr
71 nts with CLL (n = 40) or other mature B-cell lymphoid leukemias (n = 10) were treated with four weekl
72 ts (12%) (smoldering myeloma, n = 2; chronic lymphoid leukemia, n = 1; and refractory cytopenia with
73       In contrast, among patients with acute lymphoid leukemia, no differences in cell depth were obs
74 ed by BCR/ABL, with mice developing B- and T-lymphoid leukemias of longer latency.
75                            Acute myeloid and lymphoid leukemias often harbor chromosomal translocatio
76 nts were children with newly diagnosed acute lymphoid leukemia or acute myeloid leukemia.
77 1.17-2.31], respectively) cancers as well as lymphoid leukemia (OR, 2.08 [95% CI, 1.17-3.69]; OR, 2.2
78 tudy, TP53-mutated or -deficient myeloid and lymphoid leukemias outcompeted isogenic controls with in
79 logic schemes used to classify lymphomas and lymphoid leukemias over the last several decades.
80 logic neoplasms, including lymphoma, chronic lymphoid leukemias, plasma cell neoplasms, acute leukemi
81 s involved dozens of genes involved in human lymphoid leukemia, such as Notch1, Pten, Pax5, Trp53, an
82 event-free survival of pediatric pre-B acute lymphoid leukemia, suggesting that SHOC2 could be a pote
83 cription factors are frequently mutated in B-lymphoid leukemias, suggesting a close link between norm
84  to play a role in the pathogenesis of human lymphoid leukemias through downregulation of the INK4A-A
85  histone methyltransferases Set1 and myeloid/lymphoid leukemia to these promoters, which was unaffect
86 likely explains the increased sensitivity of lymphoid leukemias to short-term exposure of MTX as comp
87 tic factors of myeloma, Hodgkin disease, and lymphoid leukemia using the United States Renal Data Sys
88                   In patient 2, B cell acute lymphoid leukemia was diagnosed 10 months after liver tr
89 th a myeloproliferative disorder (MPD) and B-lymphoid leukemia, whereas BCR-ABL(P210)-transformed old
90 ET analysis linked prior TB DNAm patterns to lymphoid leukemia, while dbGaP analysis identified assoc
91                         P190 BCR/ABL induced lymphoid leukemia with shorter latency than P210 or P230
92 n utilized in the treatment of lymphomas and lymphoid leukemias with impressive results.
93 emia (MLL) gene is described in B-cell acute lymphoid leukemia without structural cytogenetic abnorma