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1 MALT) lymphoma is the most common extranodal lymphoid neoplasm.
2  homeobox transcription factor TLX3 to cause lymphoid neoplasms.
3 ctations, and therapeutic strategies for the lymphoid neoplasms.
4 oietic progenitors contribute to some mature lymphoid neoplasms.
5  that lineage plasticity may occur in mature lymphoid neoplasms.
6 al for elucidating etiologies of the various lymphoid neoplasms.
7  heterogeneity among the various subtypes of lymphoid neoplasms.
8  HIP1 was associated with the development of lymphoid neoplasms.
9  been observed, particularly with regards to lymphoid neoplasms.
10 ptosis-regulatory genes of hematopoietic and lymphoid neoplasms.
11 identification of a tumor-specific marker in lymphoid neoplasms.
12 tribute to development and/or progression of lymphoid neoplasms.
13 national Lymphoma Study Group, to categorize lymphoid neoplasms.
14 e outside its previously recognized realm of lymphoid neoplasms.
15 t of B-cell lymphoma and other CD20-positive lymphoid neoplasms.
16 l involvement of PTEN in the pathogenesis of lymphoid neoplasms.
17 in the innate and adaptive immune system and lymphoid neoplasms.
18 ion signatures in a broad set of myeloid and lymphoid neoplasms.
19  HCV eradication can reduce the incidence of lymphoid-neoplasms.
20 lymphoid cells of only 24 of 156 (15%) other lymphoid neoplasms (127 B cell, 27 T cell, and two null
21 ly diagnosed mature lymphomas, 321 precursor lymphoid neoplasms, 314 myeloid disorders, and 200 nonhe
22 consensus system for classification of mouse lymphoid neoplasms according to their histopathologic an
23 cal and critical role for CXCR4 oligomers in lymphoid neoplasms and demonstrated that their selective
24 may be associated with a high-risk subset of lymphoid neoplasms and may further support the potential
25            CD52 is expressed by a variety of lymphoid neoplasms and most human mononuclear cell subse
26 r epigenetic changes influence risk of adult lymphoid neoplasms and suggest a difference in this asso
27  that there is etiologic heterogeneity among lymphoid neoplasms and support the pursuit of epidemiolo
28 ld Health Organization classification of the lymphoid neoplasms and the accompanying monograph is bei
29  World Health Organization classification of lymphoid neoplasms and the International Classification
30 ding genetic/molecular landscape of numerous lymphoid neoplasms and their clinical correlates, and re
31                   The incidence rates of any lymphoid-neoplasms and NHL were significantly greater in
32 r, the identity of the cells in which mature lymphoid neoplasms are initiated remains unclear.
33 environment; however, their contributions to lymphoid neoplasms are less clear.
34 deletions associated with certain aggressive lymphoid neoplasms are not required for the genesis of l
35 in chronic lymphocytic leukemia and in other lymphoid neoplasms, as well as activity against acute my
36                                  Myeloid and lymphoid neoplasm associated with FGFR1 is an aggressive
37 are active in mantle cell lymphoma and other lymphoid neoplasms, but responses are usually partial an
38 ed the impact of parental age on the risk of lymphoid neoplasms by subtype.
39             Adult T-cell leukemia (ATL) is a lymphoid neoplasm caused by human T-cell leukemia virus
40      Waldenstrom macroglobulinemia (WM) is a lymphoid neoplasm characterised by a monoclonal lymphopl
41  was observed among patients with aggressive lymphoid neoplasms compared with patients with indolent
42 ely, both P < 0.001), even after we excluded lymphoid-neoplasms developed within the first year of fo
43 ducted a comprehensive assessment of 114,548 lymphoid neoplasms diagnosed during 1992-2001 in 12 Surv
44 ol study, we identified 32,000 patients with lymphoid neoplasms, diagnosed at ages 0-79 years during
45 associated with a two-fold increased risk of lymphoid-neoplasms, especially NHL, in Asian patients; a
46 genes, which have applications as markers of lymphoid neoplasms for tracing the success of therapy.
47 mplification and/or overexpression to T-cell lymphoid neoplasms has only of late been established wit
48 ization classification for hematopoietic and lymphoid neoplasms has provided a framework for defining
49 on (WHO) classification of hematopoietic and lymphoid neoplasms has recently been published.
50                                           No lymphoid neoplasms have been identified in transgenic an
51 with a 3% increase in incidence of offspring lymphoid neoplasms (hazard ratio = 1.03, 95% confidence
52 ociated with an increased risk of either any lymphoid-neoplasms (hazard ratio = 2.30, 95% confidence
53  World Health Organization Classification of Lymphoid Neoplasms identifies Burkitt lymphoma/leukemia
54 imental evidence that UV irradiation induces lymphoid neoplasms in genetically susceptible mice and s
55                           Ten EBV-associated lymphoid neoplasms in patients with rheumatoid arthritis
56 ates the discovery of the molecular basis of lymphoid neoplasms in the basic science laboratory.
57 f these two abl oncogenes for myeloid versus lymphoid neoplasms is due to specific intrinsic properti
58                           Pleiotropy between lymphoid neoplasms (LNs) has been suggested in family hi
59 tly present at chromosomal translocations in lymphoid neoplasms, may promote genomic instability by a
60 ation (ICC) both include a category "myeloid/lymphoid neoplasms (MLN) with eosinophilia (eo) and tyro
61 inally until 2009 for a new diagnosis of any lymphoid-neoplasms or NHL.
62  World Health Organization classification of lymphoid neoplasms recently acknowledged the complexity
63     In the Revised European-American list of lymphoid neoplasms recently proposed by the hematopathol
64 he restricted expression of pRB in low-grade lymphoid neoplasms remain to be determined.
65                   Because the causes of most lymphoid neoplasms remain unknown, comparison of inciden
66 k estimates, and association between HCV and lymphoid-neoplasms remain unclear.
67  role of hormonal factors in the etiology of lymphoid neoplasms remains unclear.
68 cidence patterns and trends were observed by lymphoid neoplasm subtype and population.
69 hoid neoplasms to facilitate the analysis of lymphoid neoplasm subtypes in epidemiologic research.
70 s bear the highest incidence burden for most lymphoid neoplasm subtypes, most notably for hairy cell
71 imab may have activity in a variety of other lymphoid neoplasms, such as chronic lymphocytic leukemia
72 lucocorticoids are used for the treatment of lymphoid neoplasms, taking advantage of the well-known a
73 ferative disorders (PTLD) are EBV-associated lymphoid neoplasms that are caused by the uncontrolled g
74 erative disorders are a family of extranodal lymphoid neoplasms that arise from mature postthymic T c
75                                      For the lymphoid neoplasms, this classification provides a refin
76  present a proposed nested classification of lymphoid neoplasms to facilitate the analysis of lymphoi
77 poral relationship between HCV infection and lymphoid-neoplasms using a nationwide population-based c
78                             The incidence of lymphoid neoplasms was significantly higher than expecte
79 rin, not previously known to be expressed in lymphoid neoplasms, was specifically found in all 4 anap
80 es of CD95 and Bcl-2 in growth regulation of lymphoid neoplasms, we studied by immunohistochemistry t
81    They concluded that clinical groupings of lymphoid neoplasms were neither necessary nor desirable.
82  Revised European-American Classification of Lymphoid Neoplasms, WHO).
83 lymphoma (MCL) is one of the most aggressive lymphoid neoplasms whose pathogenesis is not fully under
84 , not otherwise specified (CEL-NOS), myeloid/lymphoid neoplasm with eosinophilia and tyrosine kinase
85 l lymphoma (DLBCL) is a highly heterogeneous lymphoid neoplasm with variations in gene expression pro
86 nizes both molecularly defined ('myeloid and lymphoid neoplasms with eosinophilia and abnormalities o
87 Health Organization (WHO) category, "Myeloid/lymphoid neoplasms with eosinophilia and rearrangement o
88 ar disease detection in selected myeloid and lymphoid neoplasms, with a focus on the current and futu
89  overexpressed in approximately 25% of human lymphoid neoplasms, with increased frequencies in T-cell