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1                            Cancer is a hyper-proliferative disease.
2 ting future therapeutic targets for vascular proliferative disease.
3 oma viral nephropathy, and no posttransplant proliferative disease.
4 of Ldha, Mct1, and Mct4 as well as with more proliferative disease.
5 s relevant to the onset and progression of a proliferative disease.
6 therapeutic significance in the treatment of proliferative disease.
7 the molecular mechanisms underlying vascular proliferative disease.
8 itute an effective intervention for arterial proliferative disease.
9 es of neovascularization and corneal surface proliferative disease.
10 issue injury and the progression of vascular-proliferative disease.
11 and loss-to-follow-up in intervals of active proliferative disease.
12 temic survey to exclude systemic plasma cell proliferative diseases.
13 presenting a therapeutic target for vascular proliferative diseases.
14 activity, particularly in patients with less proliferative diseases.
15 MCs may be beneficial in preventing vascular proliferative diseases.
16  repair, as well as pathogenesis of vascular proliferative diseases.
17 le cells (SMCs) plays a key role in vascular proliferative diseases.
18 and a therapeutic target in the treatment of proliferative diseases.
19 P) and that human PNP is a target for T-cell proliferative diseases.
20 nt wound healing process or to treat various proliferative diseases.
21 ular events important in the pathogenesis of proliferative diseases.
22 t may contribute to the pathogenesis of some proliferative diseases.
23  in the treatment of ocular inflammatory and proliferative diseases.
24 elopment of reagents for treating immune and proliferative diseases.
25  cycle is considered a key event in vascular proliferative diseases.
26 e in the pathogenesis of leukemias and other proliferative diseases.
27 hat may regulate the progression of vascular proliferative diseases.
28 peutic target for the prevention of vascular proliferative diseases.
29 tic effects of retinoids in inflammatory and proliferative diseases.
30 ations for the treatment of inflammatory and proliferative diseases.
31 constitute a possible treatment for vascular proliferative diseases.
32 teristic phenomenon of glomerular epithelial proliferative diseases.
33 d have therapeutic utility for metabolic and proliferative diseases.
34 hway that act as growth suppressors in adult proliferative diseases.
35 and unifying driver of glomerular epithelial proliferative diseases.
36 he mammary gland leads to the development of proliferative disease and cancer.
37 xpression reflects disease biology of highly proliferative disease and distinct IP but does not appea
38  appointment, interval between conversion to proliferative disease and panretinal photocoagulation or
39 able safety profile in patients with rapidly proliferative disease and very poor prognosis.
40 is thus a therapeutic candidate for vascular proliferative diseases and cancer.
41 rstanding of the pathophysiology of vascular proliferative diseases and for the development of molecu
42 rus (EBV) is often present in EBV-associated proliferative diseases and is critical for the immortali
43 ld-type Flt3 characterize many hematopoietic proliferative diseases and neoplasms, providing a potent
44                                     Vascular proliferative diseases are characterized by VSMC prolife
45                                              Proliferative disease developed in 4 patients, which was
46                      Keloid, a chronic fibro-proliferative disease, exhibits distinctive histological
47  play a major role in the etiology of benign proliferative disease in the context of an aging tissue
48        In one the cells were consistent with proliferative disease, in three there was atypical epith
49 is implicated in the development of numerous proliferative diseases, in particular cancer.
50 prevention and treatment of asbestos-induced proliferative diseases including lung cancers, mesotheli
51 ne proteins associated with degenerative and proliferative disease, including lung fibrosis (surfacta
52 re implicated in the pathogenesis of several proliferative diseases, including atherosclerosis and ca
53 c strategy to reduce progression of vascular proliferative diseases, including atherosclerosis and re
54 inflammatory responses that lead to vascular proliferative diseases, including atherosclerosis and re
55 emotherapeutics for the treatment of various proliferative diseases, including breast cancer.
56 gets for therapeutic intervention in various proliferative diseases, including cancer.
57 mportant role in the development of vascular proliferative diseases, including restenosis and atheros
58 f loss-to-follow-up for patients with active proliferative disease increased odds of vitrectomy by 10
59 cell lymphoma (CTCL) constitutes a malignant proliferative disease involving mostly CD4(+) T cells ar
60                                     X-linked proliferative disease is a monogenic disorder that is as
61           The role of AIP1 in VSMCs and VSMC proliferative disease is not known.
62 treatment and maintain critical follow-up in proliferative disease may reduce vision-threatening comp
63  growth in BaF3 cells, and induces a myeloid proliferative disease (MPD) with features of megakaryobl
64 anular lymphocyte (LGL) leukemia is a clonal proliferative disease of T and natural killer (NK) cells
65                           The diagnosis of a proliferative disease of the cerebellum was established
66   Pulmonary arterial hypertension (PAH) is a proliferative disease of the pulmonary vasculature that
67 usly known as histiocytosis X, is a reactive proliferative disease of unknown pathogenesis.
68 t has been implicated in the pathogenesis of proliferative diseases of lymphocytes and tumors of epit
69                                              Proliferative diseases of the endometrium such as endome
70 ic fungal infections in patients treated for proliferative diseases of the hematopoietic system are c
71 s been implicated in regenerative growth and proliferative diseases of the human bladder epithelium (
72 n humans for the treatment of this and other proliferative diseases of the retina involving fibrosis
73 % CI 1.25 to 4.27, p = 0.008), with existing proliferative disease (OR 2.12, 95% CI 1.11 to 4.04, p =
74 ecurrence of primary disease, sepsis, lympho-proliferative disease, or vascular or biliary complicati
75 aglobulinemia in a subset of X-linked lympho-proliferative disease patients without involvement of Ep
76 ients were excluded if they had a history of proliferative disease (proliferative diabetic retinopath
77 tinuing search for medicinal agents to treat proliferative diseases, quinazoline derivatives were syn
78 uman herpesvirus 8, is associated with three proliferative diseases ranging from viral cytokine-induc
79 n ACCORD-Eye as >/= 3 steps (ETDRS scale) or proliferative disease requiring laser or vitrectomy trea
80  that bacterial components can contribute to proliferative disease states in squamous epithelium thro
81                                     Vascular proliferative diseases such as atherosclerosis and coron
82 constitute a new therapeutic target for cell proliferative diseases such as atherosclerosis.
83 eral signal transduction pathways related to proliferative diseases such as cancer, atherosclerosis,
84 ide an effective method for the treatment of proliferative diseases such as cancer.
85 hanges in lncRNA-regulatory networks lead to proliferative diseases such as cancer.
86               This may have implications for proliferative diseases such as proliferative vitreoretin
87 ytostatic gene therapy in models of vascular proliferative disease using antisense oligodeoxynucleoti
88 ing our search for medicinal agents to treat proliferative diseases, we have discovered 2-substituted
89 therapeutic intervention against a number of proliferative diseases, we have discovered the 2-aminopy
90 e than half of patients with X-linked lympho-proliferative disease, which is caused by a defect in th
91 pecimens diagnosed as nonproliferative (NP), proliferative disease without atypia (PDWA), or atypical
92                          Among women who had proliferative disease without atypia as compared with wo
93 treatment or prevention of immunological and proliferative diseases without gastrointestinal or hemat
94 eutic equivalent for ASA in inflammatory and proliferative diseases without the deleterious effects o