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1 focus on striking a balance between cure and long term toxicity.
2 aft acceptance without significant short- or long-term toxicity.
3 ous administration of these drugs may elicit long-term toxicity.
4 preferred in patients with IGHV-UM, to limit long-term toxicity.
5 served breast-without increasing the risk of long-term toxicity.
6  to control the inflammation while incurring long-term toxicity.
7 ted therapies with acceptable short-term and long-term toxicity.
8 s immunologic response did not result in any long-term toxicity.
9 phasing-out stavudine because of its risk of long-term toxicity.
10 ould be to minimize the risk for relapse and long-term toxicity.
11  as surrogate measures for treatment-related long-term toxicity.
12 ellent survival but often confer significant long-term toxicity.
13 resholds usually associated with significant long-term toxicity.
14 uses), and deliver immunosuppression without long-term toxicity.
15 s and may spontaneously reverse with minimal long-term toxicity.
16 s in diagnosis, treatment, and prevention of long-term toxicity.
17 ce, survival (disease-free and overall), and long-term toxicity.
18 ials using cisplatin-based therapy with less long-term toxicity.
19 s is not optimal due to emerging evidence of long-term toxicities.
20                   Survivors have significant long-term toxicities.
21 ssues and the corresponding lack of short or long-term toxicities.
22 adly, and the therapy carries short-term and long-term toxicities.
23            The continuous treatment leads to long-term toxicities and can profoundly suppress protect
24 mphoblastic leukemia (B-ALL), short-term and long-term toxicities and chemoresistance are shortcoming
25 owever, further studies are needed to assess long-term toxicity and clinical efficacy.
26                   Significant short-term and long-term toxicity and increases in fluconazole-resistan
27 iation results in high cure rates but causes long-term toxicity and may represent overtreatment of so
28 on, residual concerns about costs, potential long-term toxicities, and behavioral disinhibition.
29 red to assess the character and frequency of long-term toxicities, and to provide insights into the b
30 heir susceptibilities to drug resistance and long term toxicity are serious impediments to their use,
31                                    Acute and long-term toxicities are acceptable.
32 nt trials that attempt to decrease acute and long-term toxicity are reviewed.
33 ace of scarce organ supply, or prevention of long-term toxicity associated with immunosuppression.
34 ntation in young adults means that issues of long-term toxicity become especially important in judgin
35 -Pro-labeled cells demonstrated no short- or long-term toxicity, changes in differentiation capacity
36 oice for patients with CML in chronic phase; long-term toxicity continues to be assessed, and data su
37   The administered activities were high, and long-term toxicity effects (</=60 wk) were clear.
38 ed 5-year follow-up sensitivity analysis and long-term toxicity findings.
39 revention of chronic diseases, assessment of long-term toxicity from HAART, and surveillance for addi
40 nal cancer, in an effort to reduce acute and long-term toxicity from radiotherapy.
41 nal radiation is associated with significant long-term toxicities has led to the development of novel
42 iosafety profiles should be used to decrease long-term toxicity in cases where systemic exposure occu
43 fe-threatening acute toxicities, and serious long-term toxicities, including cardiomyopathy, pulmonar
44 l ganglia-mediated learning and suggest that long-term toxicity induced by METH alters the cognitive
45                                    The major long-term toxicity is chronic graft-versus-host disease
46 imens devised for Hodgkin disease in adults, long-term toxicity is enhanced in the developing individ
47          There is no evidence that short- or long-term toxicity is increased among obese patients rec
48 therapy in patients with LPL, but short- and long-term toxicities need to be carefully weighed agains
49 are highly active in WM, although short- and long-term toxicities need to be carefully weighed agains
50                                              Long-term toxicities occurred in 2 patients: hypokalemia
51 ilure, and discusses emerging concerns about long term toxicity of these factors.
52                        Given the substantial long-term toxicities of current combination therapy regi
53 germ cell tumors need to be developed, while long-term toxicities of therapies need to be further mod
54 uidelines to reduce the risk of sex-specific long-term toxicities of therapy.
55 prove our ability to identify short-term and long-term toxicities of these new agents.
56 rrent progressive disease, and the acute and long-term toxicities of this option should be carefully
57 ion tomography may reduce the short-term and long-term toxicities of treatment of early-stage nonbulk
58 ort a 15-month toxicity study that showed no long-term toxicity of AuNRs in vivo.
59                                     However, long-term toxicity of SiNPs remains unknown.
60                                              Long-term toxicity of therapy also remains significant.
61 iotherapy and to describe the short-term and long-term toxicity of therapy.
62                 A major concern has been the long-term toxicity of treatment, most of which is attrib
63             No evidence of increased risk of long-term toxicity or long-term adverse consequences of
64  in cure but may increase risk for acute and long-term toxicities, particularly in children.
65 Study results show that TACE has a favorable long-term toxicity profile in patients with HCC.
66  has high efficacy and a favorable acute and long-term toxicity profile when administered to patients
67 ucing durable responses and with a favorable long-term toxicity profile.
68 phrotoxicity, highlighting the importance of long-term toxicity studies and microscale dosimetry.
69                                              Long-term toxicity studies confirmed that the dose-limit
70 inical toxicities, 1843U89 may present fewer long-term toxicities than D1694.
71 DNA damage at low L1:iron ratios may lead to long-term toxicities that might preclude administration
72 de-effects often lead to secondary short and long-term toxicities that negatively impact patient's qu
73          To increase cure rates and decrease long-term toxicity, there is great interest in incorpora
74 oid non-specific background fluorescence and long-term toxicity, they need to be cleared from the bod
75 e optimized for efficacy and minimization of long-term toxicity, through dosimetry, and adapted to ea
76                       Methamphetamine causes long-term toxicity to dopamine nerve endings of the stri
77 eptor radionuclide therapy (PRRT) may induce long-term toxicity to the bone marrow (BM).
78 all survival were calculated, and short- and long-term toxicity was assessed according to National Ca
79                                              Long-term toxicity was assessed in mice for 12 mo.
80                               Short-term and long-term toxicities were similar to historical control
81 lls along with cell viability and short- and long-term toxicity were evaluated.
82 uestion is whether the risk of immediate and long-term toxicity with use of busulfan is justified, pa

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