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1 ries suggest novel RNA-based therapeutics in anticancer treatment.
2 imuli, including genotoxic stress induced by anticancer treatment.
3 ise the overall efficacy of chemotherapeutic anticancer treatment.
4 herefore lead to development of an effective anticancer treatment.
5 wn to influence the toxicity and efficacy of anticancer treatment.
6 se activity may have therapeutic value as an anticancer treatment.
7 ys after the last dose and before subsequent anticancer treatment.
8 ficacy of the vaccine with regard to type of anticancer treatment.
9 it cancer cell apoptosis, independently from anticancer treatment.
10 dicine in the era of tissue regeneration and anticancer treatment.
11 ocatalysts can be applied for photocatalytic anticancer treatment.
12 at a fast pace under expedited programs for anticancer treatment.
13 omising target for the future development of anticancer treatment.
14 y good clinical condition to receive optimal anticancer treatment.
15 eresting platform for synergistic therapy in anticancer treatment.
16 ovided a PROTAC-based pyroptosis inducer for anticancer treatment.
17 le of neutrophils and NETs in the outcome of anticancer treatment.
18 microtubule depolymerizing drug relevant to anticancer treatment.
19 immune engineering as a powerful modality in anticancer treatment.
20 cancer and may represent a novel target for anticancer treatment.
21 These findings could benefit anticancer treatment.
22 monitor the patient's individual response to anticancer treatment.
23 e in various afucosylated therapeutic Abs in anticancer treatment.
24 tion of dTDP from dTMP is a new strategy for anticancer treatment.
25 in (18)F-FDG uptake may predict response to anticancer treatment.
26 age, CVD risk factors, menopausal status, or anticancer treatment.
27 anoids as an ex vivo platform to personalize anticancer treatment.
28 oysite nanotubes is a promising platform for anticancer treatment.
29 oxicity without compromising the efficacy of anticancer treatment.
30 and mitosis, offering attractive targets for anticancer treatment.
31 e development of intracellular protein-based anticancer treatment.
32 g chemotherapy, supporting the use of CQ for anticancer treatment.
33 e, and health service outcomes during active anticancer treatment.
34 ides proof of concept of this approach as an anticancer treatment.
35 ad cancer cells with calcium as an efficient anticancer treatment.
36 at can successfully be combined with current anticancer treatment.
37 thus being considered for use as a potential anticancer treatment.
38 ing tumor development, tumor progression and anticancer treatment.
39 nisms of oncogenesis and for individualizing anticancer treatments.
40 ne)--are becoming a significant component of anticancer treatments.
41 exploited to identify novel mechanism-based anticancer treatments.
42 lity of new strategies in the development of anticancer treatments.
43 growth and counteracts apoptosis induced by anticancer treatments.
44 roenvironment including exposure to targeted anticancer treatments.
45 hrough the mitigation of the side-effects of anticancer treatments.
46 hy (CIPN) is a substantial adverse effect of anticancer treatments.
47 y with agents that induce ER stress as novel anticancer treatments.
48 central position in the development of novel anticancer treatments.
49 ition, the results are not impacted by other anticancer treatments.
50 ly enhances our ability to develop effective anticancer treatments.
51 orn outcomes compared with exposure to other anticancer treatments.
52 and/or newborn outcomes compared with other anticancer treatments.
53 cell death represents a primary goal of most anticancer treatments.
54 orbidity and mortality associated with these anticancer treatments.
55 ogy, prognosis and responsiveness to various anticancer treatments.
56 ity but can also provoke neurotoxicity after anticancer treatments.
57 tion of CAR T-cell therapy into conventional anticancer treatments.
58 ggressiveness and resistance to conventional anticancer treatments.
59 immunity and to hinder the effectiveness of anticancer treatments.
60 tic brain cancer, resistant to many existing anticancer treatments.
61 is a major obstacle for developing effective anticancer treatments.
62 arget for countering multidrug resistance in anticancer treatments.
63 e implications for regenerative medicine and anticancer treatments.
64 nt cancer cells can often be resensitized to anticancer treatments.
65 cells and reduce cancer cell sensitivity to anticancer treatments.
66 ors against these receptors are now used for anticancer treatments.
67 for tumour relapse after seemingly effective anticancer treatments.
68 l system and suggesting possible targets for anticancer treatments.
69 proving persistence of and adherence to oral anticancer treatment among patients with early breast ca
70 mong 22 101 patients with NSCLC who received anticancer treatment analyzed in this study, 17 350 pati
71 h solid tumors undergoing active intravenous anticancer treatment and 78 controls who received the se
72 rgeted therapies have been widely applied in anticancer treatment and have given oncologists a promis
73 5 lines and mean medical costs of documented anticancer treatment and supportive care drugs per patie
74 number of patients who received second-line anticancer treatment and the occurrence of other maligna
75 argely due to the resistance to conventional anticancer treatments and high metastatic potential.
76 of 2 or less, with no more than two previous anticancer treatments and no more than one previous chem
78 ploited to increase the therapeutic index of anticancer treatments and thereby improve patient outcom
79 r are known to mediate resistance to several anticancer treatments and to promote cancer relapse.
80 ge selection in early clinical trials of new anticancer treatments and ultimately, outcomes for patie
82 no metastatic disease, no previous systemic anticancer treatment, and an Eastern Cooperative Oncolog
84 register intention to start all new systemic anticancer treatments approved for use in England since
85 patients on cytotoxic chemotherapy or other anticancer treatment are at an increased risk of mortali
87 ed on whether to designate unlabeled uses of anticancer treatments as experimental and thus outside t
88 of prostate carcinoma cells to a variety of anticancer treatments, as well as reduction of the cell'
89 e translocations can be present early during anticancer treatment at low cumulative doses of DNA topo
91 ogression has helped guide efforts to design anticancer treatments based on inhibition or promotion o
92 ld lead to the development of more effective anticancer treatments based on maintaining, increasing,
93 ogeneity hampers the success of marker-based anticancer treatment because the targeted therapy may el
94 rostate cancer is refractory to conventional anticancer treatments because of frequent overexpression
96 are censored for initiation of an effective anticancer treatment before the protocol-defined progres
97 he challenge of resistance entails extending anticancer treatments beyond targeting cancer cells by a
98 ation therapy is a primary form of cytotoxic anticancer treatment, but agents that successfully modif
100 of avoidable harm to patients from systemic anticancer treatments, but data for this indicator are l
101 of novel targeted CAFs-PIT with conventional anticancer treatments can be expected to provide a more
104 e (12.4 of 36 months) not receiving systemic anticancer treatments compared with 30.8% (11.1 of 36 mo
105 tic strategies which, combined with existing anticancer treatments, could lead to deeper and longer-l
107 ombination therapies are becoming widespread anticancer treatments, dual catalysis by ArMs has not ye
108 ed patients aged 18 to 64 years who received anticancer treatment during the 6 months after a new bre
109 te the identification and diversification of anticancer treatment for aggressive subtypes of pediatri
110 pharmacies from 2011 to 2019, including oral anticancer treatments (from 10% to 34%), antivirals (fro
112 articularly those who are receiving systemic anticancer treatments, have been postulated to be at inc
113 reated with potentially cardiovascular toxic anticancer treatment (ie, anthracyclines, platinum, and/
114 6.6%) of the patients were undergoing active anticancer treatment in a neoadjuvant/adjuvant and 560 o
115 NF-kappaB, they show an enhanced response to anticancer treatment in an in vivo xenograft tumour mode
116 t of COVID-19 on the prescribing of systemic anticancer treatment in England, immediately after lockd
117 The ability to monitor the efficacy of an anticancer treatment in real time can have a critical ef
118 nd that 43% of randomized clinical trials of anticancer treatment in the adjuvant or neoadjuvant cont
120 hat checkpoint status affects sensitivity to anticancer treatments in vivo, and these findings have i
121 Wip1 and RUNX2 that resulted, in response to anticancer treatment, in RUNX2-dependent transcriptional
123 se is highly responsive to a wide variety of anticancer treatments including conventional cytotoxic c
129 Information about symptomatic toxicities of anticancer treatments is not based on direct report by p
131 titumor immunity and is a promising clinical anticancer treatment modality in several tumor types, bu
132 ance of considering the off-target impact of anticancer treatment on normal cells to improve drug dev
134 nce is lacking to determine whether changing anticancer treatment on the basis of change in receptor
135 e for many years through the use of systemic anticancer treatments on a background of multidisciplina
136 r radionuclide therapy is a relatively novel anticancer treatment option using radiolabeled, tumor-sp
138 ntrolled trials of patients receiving active anticancer treatment or supportive care irrespective of
139 has failed to deliver clinically significant anticancer treatment, owing in part to low selectivity,
140 se levels in patients taking rapamycin as an anticancer treatment, particularly those with preexistin
141 g an antagonist of a necrotic signal with an anticancer treatment potentiates the prolonged therapeut
143 consequences regarding the effectiveness of anticancer treatment regimens when TOP2-targeting drugs
145 e results support the idea that conventional anticancer treatments rely on stimulation of anticancer
146 This work holds the potential to affect anticancer treatment research, by offering a label-free,
148 identifying patients likely to benefit from anticancer treatments, selecting dose, and understanding
149 rs and has emerged as a promising target for anticancer treatment, so that several LSD1 inhibitors ar
150 Immunomodulation is a promising strategy in anticancer treatment, so this novel mode of action of do
151 ovide prototypical targets for testing novel anticancer treatment strategies within the newer paradig
157 ascertain whether targeting HAT1 is a viable anticancer treatment strategy, we sought to identify sma
161 ay increase the negative effects of specific anticancer treatments such as androgen suppression thera
162 Radiotherapy (RT) is a highly effective anticancer treatment that is delivered to more than half
163 ve been developed to enhance the efficacy of anticancer treatments that induce DNA damage in cancer c
164 vents associated with chemotherapy and other anticancer treatments that pose major threats in terms o
168 autophagy have failed to produce successful anticancer treatments using currently available inhibito
170 patients age 75 years and older under active anticancer treatment were consecutively recruited in six
172 reby enhancing therapeutic responses towards anticancer treatment when used in conjunction with conve
173 ligand (TRAIL) has attracted interest as an anticancer treatment, when used in conjunction with stan
174 his localization can enhance the efficacy of anticancer treatment while minimizing off-target effects
177 evaluable (ie, had progression, began a new anticancer treatment, withdrew consent, died, had stable
178 the lethal genotoxic stress associated with anticancer treatment without promoting the formation of
179 blockade has shown significant promise as an anticancer treatment, yet the determinants of response a
180 ed therapy resistance is a major problem for anticancer treatment, yet the underlying molecular mecha