ライフサイエンスコーパス: lymphoid neoplasm

1 MALT) lymphoma is the most common extranodal lymphoid neoplasm.

2 oietic progenitors contribute to some mature lymphoid neoplasms.

3 that lineage plasticity may occur in mature lymphoid neoplasms.

4 al for elucidating etiologies of the various lymphoid neoplasms.

5 heterogeneity among the various subtypes of lymphoid neoplasms.

6 HIP1 was associated with the development of lymphoid neoplasms.

7 been observed, particularly with regards to lymphoid neoplasms.

8 ptosis-regulatory genes of hematopoietic and lymphoid neoplasms.

9 identification of a tumor-specific marker in lymphoid neoplasms.

10 tribute to development and/or progression of lymphoid neoplasms.

11 national Lymphoma Study Group, to categorize lymphoid neoplasms.

12 e outside its previously recognized realm of lymphoid neoplasms.

13 t of B-cell lymphoma and other CD20-positive lymphoid neoplasms.

14 l involvement of PTEN in the pathogenesis of lymphoid neoplasms.

15 ctations, and therapeutic strategies for the lymphoid neoplasms.

16 HCV eradication can reduce the incidence of lymphoid-neoplasms.

17 lymphoid cells of only 24 of 156 (15%) other lymphoid neoplasms (127 B cell, 27 T cell, and two null

18 ly diagnosed mature lymphomas, 321 precursor lymphoid neoplasms, 314 myeloid disorders, and 200 nonhe

19 consensus system for classification of mouse lymphoid neoplasms according to their histopathologic an

20 may be associated with a high-risk subset of lymphoid neoplasms and may further support the potential

21 CD52 is expressed by a variety of lymphoid neoplasms and most human mononuclear cell subse

22 r epigenetic changes influence risk of adult lymphoid neoplasms and suggest a difference in this asso

23 that there is etiologic heterogeneity among lymphoid neoplasms and support the pursuit of epidemiolo

24 ld Health Organization classification of the lymphoid neoplasms and the accompanying monograph is bei

25 World Health Organization classification of lymphoid neoplasms and the International Classification

26 ding genetic/molecular landscape of numerous lymphoid neoplasms and their clinical correlates, and re

27 The incidence rates of any lymphoid-neoplasms and NHL were significantly greater in

28 r, the identity of the cells in which mature lymphoid neoplasms are initiated remains unclear.

29 environment; however, their contributions to lymphoid neoplasms are less clear.

30 deletions associated with certain aggressive lymphoid neoplasms are not required for the genesis of l

31 Myeloid and lymphoid neoplasm associated with FGFR1 is an aggressive

32 are active in mantle cell lymphoma and other lymphoid neoplasms, but responses are usually partial an

33 ed the impact of parental age on the risk of lymphoid neoplasms by subtype.

34 Waldenstrom macroglobulinemia (WM) is a lymphoid neoplasm characterised by a monoclonal lymphopl

35 ely, both P < 0.001), even after we excluded lymphoid-neoplasms developed within the first year of fo

36 ducted a comprehensive assessment of 114,548 lymphoid neoplasms diagnosed during 1992-2001 in 12 Surv

37 ol study, we identified 32,000 patients with lymphoid neoplasms, diagnosed at ages 0-79 years during

38 associated with a two-fold increased risk of lymphoid-neoplasms, especially NHL, in Asian patients; a

39 genes, which have applications as markers of lymphoid neoplasms for tracing the success of therapy.

40 mplification and/or overexpression to T-cell lymphoid neoplasms has only of late been established wit

41 ization classification for hematopoietic and lymphoid neoplasms has provided a framework for defining

42 on (WHO) classification of hematopoietic and lymphoid neoplasms has recently been published.

43 No lymphoid neoplasms have been identified in transgenic an

44 with a 3% increase in incidence of offspring lymphoid neoplasms (hazard ratio = 1.03, 95% confidence

45 ociated with an increased risk of either any lymphoid-neoplasms (hazard ratio = 2.30, 95% confidence

46 World Health Organization Classification of Lymphoid Neoplasms identifies Burkitt lymphoma/leukemia

47 imental evidence that UV irradiation induces lymphoid neoplasms in genetically susceptible mice and s

48 Ten EBV-associated lymphoid neoplasms in patients with rheumatoid arthritis

49 ates the discovery of the molecular basis of lymphoid neoplasms in the basic science laboratory.

50 f these two abl oncogenes for myeloid versus lymphoid neoplasms is due to specific intrinsic properti

51 tly present at chromosomal translocations in lymphoid neoplasms, may promote genomic instability by a

52 inally until 2009 for a new diagnosis of any lymphoid-neoplasms or NHL.

53 World Health Organization classification of lymphoid neoplasms recently acknowledged the complexity

54 In the Revised European-American list of lymphoid neoplasms recently proposed by the hematopathol

55 he restricted expression of pRB in low-grade lymphoid neoplasms remain to be determined.

56 Because the causes of most lymphoid neoplasms remain unknown, comparison of inciden

57 k estimates, and association between HCV and lymphoid-neoplasms remain unclear.

58 cidence patterns and trends were observed by lymphoid neoplasm subtype and population.

59 hoid neoplasms to facilitate the analysis of lymphoid neoplasm subtypes in epidemiologic research.

60 s bear the highest incidence burden for most lymphoid neoplasm subtypes, most notably for hairy cell

61 imab may have activity in a variety of other lymphoid neoplasms, such as chronic lymphocytic leukemia

62 lucocorticoids are used for the treatment of lymphoid neoplasms, taking advantage of the well-known a

63 ferative disorders (PTLD) are EBV-associated lymphoid neoplasms that are caused by the uncontrolled g

64 For the lymphoid neoplasms, this classification provides a refin

65 present a proposed nested classification of lymphoid neoplasms to facilitate the analysis of lymphoi

66 poral relationship between HCV infection and lymphoid-neoplasms using a nationwide population-based c

67 The incidence of lymphoid neoplasms was significantly higher than expecte

68 rin, not previously known to be expressed in lymphoid neoplasms, was specifically found in all 4 anap

69 es of CD95 and Bcl-2 in growth regulation of lymphoid neoplasms, we studied by immunohistochemistry t

70 They concluded that clinical groupings of lymphoid neoplasms were neither necessary nor desirable.

71 Revised European-American Classification of Lymphoid Neoplasms, WHO).

72 lymphoma (MCL) is one of the most aggressive lymphoid neoplasms whose pathogenesis is not fully under

73 nizes both molecularly defined ('myeloid and lymphoid neoplasms with eosinophilia and abnormalities o

74 Health Organization (WHO) category, "Myeloid/lymphoid neoplasms with eosinophilia and rearrangement o

75 ar disease detection in selected myeloid and lymphoid neoplasms, with a focus on the current and futu

76 overexpressed in approximately 25% of human lymphoid neoplasms, with increased frequencies in T-cell