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1 These findings could benefit anticancer treatment.
2 tion of dTDP from dTMP is a new strategy for anticancer treatment.
3 in (18)F-FDG uptake may predict response to anticancer treatment.
4 age, CVD risk factors, menopausal status, or anticancer treatment.
5 anoids as an ex vivo platform to personalize anticancer treatment.
6 oysite nanotubes is a promising platform for anticancer treatment.
7 oxicity without compromising the efficacy of anticancer treatment.
8 and mitosis, offering attractive targets for anticancer treatment.
9 e development of intracellular protein-based anticancer treatment.
10 g chemotherapy, supporting the use of CQ for anticancer treatment.
11 e, and health service outcomes during active anticancer treatment.
12 monitor the patient's individual response to anticancer treatment.
13 ides proof of concept of this approach as an anticancer treatment.
14 e in various afucosylated therapeutic Abs in anticancer treatment.
15 ad cancer cells with calcium as an efficient anticancer treatment.
16 at can successfully be combined with current anticancer treatment.
17 thus being considered for use as a potential anticancer treatment.
18 ing tumor development, tumor progression and anticancer treatment.
19 imuli, including genotoxic stress induced by anticancer treatment.
20 ise the overall efficacy of chemotherapeutic anticancer treatment.
21 herefore lead to development of an effective anticancer treatment.
22 wn to influence the toxicity and efficacy of anticancer treatment.
23 se activity may have therapeutic value as an anticancer treatment.
24 tion of CAR T-cell therapy into conventional anticancer treatments.
25 tic brain cancer, resistant to many existing anticancer treatments.
26 ggressiveness and resistance to conventional anticancer treatments.
27 is a major obstacle for developing effective anticancer treatments.
28 arget for countering multidrug resistance in anticancer treatments.
29 nt cancer cells can often be resensitized to anticancer treatments.
30 cells and reduce cancer cell sensitivity to anticancer treatments.
31 ors against these receptors are now used for anticancer treatments.
32 for tumour relapse after seemingly effective anticancer treatments.
33 l system and suggesting possible targets for anticancer treatments.
34 ne)--are becoming a significant component of anticancer treatments.
35 exploited to identify novel mechanism-based anticancer treatments.
36 lity of new strategies in the development of anticancer treatments.
37 growth and counteracts apoptosis induced by anticancer treatments.
38 rgeted therapies have been widely applied in anticancer treatment and have given oncologists a promis
39 argely due to the resistance to conventional anticancer treatments and high metastatic potential.
40 r are known to mediate resistance to several anticancer treatments and to promote cancer relapse.
41 ed on whether to designate unlabeled uses of anticancer treatments as experimental and thus outside t
42 of prostate carcinoma cells to a variety of anticancer treatments, as well as reduction of the cell'
43 e translocations can be present early during anticancer treatment at low cumulative doses of DNA topo
45 ogeneity hampers the success of marker-based anticancer treatment because the targeted therapy may el
46 rostate cancer is refractory to conventional anticancer treatments because of frequent overexpression
47 are censored for initiation of an effective anticancer treatment before the protocol-defined progres
48 ation therapy is a primary form of cytotoxic anticancer treatment, but agents that successfully modif
50 of avoidable harm to patients from systemic anticancer treatments, but data for this indicator are l
54 te the identification and diversification of anticancer treatment for aggressive subtypes of pediatri
56 reated with potentially cardiovascular toxic anticancer treatment (ie, anthracyclines, platinum, and/
57 NF-kappaB, they show an enhanced response to anticancer treatment in an in vivo xenograft tumour mode
58 The ability to monitor the efficacy of an anticancer treatment in real time can have a critical ef
60 hat checkpoint status affects sensitivity to anticancer treatments in vivo, and these findings have i
61 Wip1 and RUNX2 that resulted, in response to anticancer treatment, in RUNX2-dependent transcriptional
63 se is highly responsive to a wide variety of anticancer treatments including conventional cytotoxic c
68 Information about symptomatic toxicities of anticancer treatments is not based on direct report by p
71 nce is lacking to determine whether changing anticancer treatment on the basis of change in receptor
72 ntrolled trials of patients receiving active anticancer treatment or supportive care irrespective of
73 se levels in patients taking rapamycin as an anticancer treatment, particularly those with preexistin
75 e results support the idea that conventional anticancer treatments rely on stimulation of anticancer
76 identifying patients likely to benefit from anticancer treatments, selecting dose, and understanding
77 Immunomodulation is a promising strategy in anticancer treatment, so this novel mode of action of do
78 ovide prototypical targets for testing novel anticancer treatment strategies within the newer paradig
85 ay increase the negative effects of specific anticancer treatments such as androgen suppression thera
89 ligand (TRAIL) has attracted interest as an anticancer treatment, when used in conjunction with stan
91 the lethal genotoxic stress associated with anticancer treatment without promoting the formation of
92 blockade has shown significant promise as an anticancer treatment, yet the determinants of response a
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