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1 tate the optimization and personalization of cancer therapy.
2 CC for drugs recently approved for precision cancer therapy.
3 , mutp53 has become an attractive target for cancer therapy.
4 ggest that lipin-1 is a potential target for cancer therapy.
5 considerably affect the outcome of prostate cancer therapy.
6 le oncogenic pathways is a desirable goal in cancer therapy.
7 or in vitro diagnosis and its implication in cancer therapy.
8 ll combinations can be used for personalised cancer therapy.
9 g-resistant CSCs and improve the efficacy of cancer therapy.
10 tivation that bears important implication in cancer therapy.
11 ve wide-spectrum and cost-effective drugs in cancer therapy.
12 d photonic micelles for effectively trimodal cancer therapy.
13 bitors, which are frequently used for breast cancer therapy.
14 and this property can be exploited for anti-cancer therapy.
15 Proteolytic enzymes have shown efficacy in cancer therapy.
16 metastasis and a druggable target for breast cancer therapy.
17 em provides a new platform for high fidelity cancer therapy.
18 merases (PARPs) elicits clinical benefits in cancer therapy.
19 elivery of photosensitizers for photodynamic cancer therapy.
20 have advocated the role of glutamic acid in cancer therapy.
21 insertion may be a viable genotype-specific cancer therapy.
22 es as an indirect MYC-targeting approach for cancer therapy.
23 tion factors, represent a major challenge in cancer therapy.
24 herapeutic option for triple negative breast cancer therapy.
25 herapeutic target to affect Th9 responses in cancer therapy.
26 mor immune response promise to revolutionize cancer therapy.
27 dergoing clinical evaluation as a target for cancer therapy.
28 viruses pose many questions in their use in cancer therapy.
29 c micelles show great promise for multimodal cancer therapy.
30 ing these mutants appealing targets for lung cancer therapy.
31 rs provides great potential for personalized cancer therapy.
32 response in tumor cells and CQ resistance in cancer therapy.
33 PDZ1i hold promise to advance targeted brain cancer therapy.
34 ents with heart problems caused by cancer or cancer therapy.
35 hil tumor infiltration enhances nanoparticle cancer therapy.
36 ly used to detect early treatment changes in cancer therapy.
37 evelopment of BET bromodomain degradation as cancer therapy.
38 being engineered as vectors for vaccines and cancer therapy.
39 ene fusions can offer actionable targets for cancer therapy.
40 elf-reinforcing characteristic of PLT-PTT in cancer therapy.
41 ABBV-075 and other BET family inhibitors for cancer therapy.
42 g cell division and is a putative target for cancer therapy.
43 tive and versatile nanocarriers for targeted cancer therapy.
44 sible of resistance to a particular targeted cancer therapy.
45 cally inducing cell death in vivo, e.g., for cancer therapy.
46 ce and for targeting glutamine metabolism in cancer therapy.
47 based immunotherapeutics a real prospect for cancer therapy.
48 this pathway are being increasingly used as cancer therapy.
49 i-tumour potential of macrophages to enhance cancer therapy.
50 ed into a practical anti-IGF-1R strategy for cancer therapy.
51 ed great interest in targeting autophagy for cancer therapy.
52 l cues-a mechanism that may be exploited for cancer therapy.
53 pressor function that could be harnessed for cancer therapy.
54 rent approaches aimed at PLK1 inhibition for cancer therapy.
55 ilization could be exploited to help improve cancer therapy.
56 s survival, and whether they are affected by cancer therapy.
57 or the more common late effects of childhood cancer therapy.
58 er driver genes that may serve as targets of cancer therapy.
59 apoptosis is a widely practiced strategy for cancer therapy.
60 of synthetic lethal interactions relevant to cancer therapy.
61 esents an attractive approach to develop new cancer therapy.
62 edicine of synergistic drug combinations for cancer therapy.
63 implementation of IL-15 in adoptive NK-cell cancer therapy.
64 e (DUB) activity is a promising strategy for cancer therapy.
65 in the use of high dose vitamin C (VC) as a cancer therapy.
66 cancer biomarkers and potential targets for cancer therapy.
67 otential to improve outcomes associated with cancer therapy.
68 tantial attention for their potential use in cancer therapy.
69 ould pave the way to precision materials for cancer therapy.
70 er especially attractive vaccine targets for cancer therapy.
71 eutic delivery system -'nanosomes'- for lung cancer therapy.
72 an cancers and has profound implications for cancer therapy.
73 o TNKS inhibition as a potential Wnt pathway cancer therapy.
74 l subsets, making them attractive for use in cancer therapy.
75 cule inhibitors to target glutaminolysis for cancer therapy.
76 n of Hv1 could be an innovative approach for cancer therapy.
77 en receptor (CAR) has emerged as a promising cancer therapy.
78 rticles for their potential for photothermal cancer therapy.
79 a co-receptor, HER2, have been approved for cancer therapy.
80 FR could potentially offer an effective oral cancer therapy.
81 lications to broadly improve the efficacy of cancer therapy.
82 onate crosslinked micelles (BCM) for ovarian cancer therapy.
83 of other strategies to downregulate PD-1 for cancer therapy.
84 and how they may be used to better optimize cancer therapy.
85 in various biomedical applications including cancer therapy.
86 d have been considered potential targets for cancer therapy.
87 iew the state-of-the-art of macrophage-based cancer therapy.
88 oncogenic PTPs as compelling candidates for cancer therapy.
89 (PET) multimodal imaging-guided combination cancer therapy.
90 nce is one of the major problems in targeted cancer therapy.
91 ction, and have been effectively targeted in cancer therapy.
92 se systems, holding great promise for future cancer therapy.
93 likely result in both effective and specific cancer therapy.
94 itizing cancer cells to DR5 activation-based cancer therapy.
95 utologous T cells has shown great promise in cancer therapy.
96 bitors of this histone demethylase family in cancer therapy.
97 ns in tumor cells remains an elusive goal in cancer therapy.
98 dentifying novel, more effective targets for cancer therapy.
99 nown about HSP90 inhibition-mediated bladder cancer therapy.
100 suppressor complex that could be targeted in cancer therapy.
101 ement of the cardiovascular complications of cancer therapy.
102 y and used to engineer examples of bsAbs for cancer therapy.
103 metastasis making it an important target for cancer therapy.
104 py (PTT) has shown significant potential for cancer therapy.
105 ria targeted PDT applications in deep tissue cancer therapy.
106 layer in oncogenesis and a viable target for cancer therapy.
107 entation with citrate may be beneficial as a cancer therapy.
108 ntal importance and carries implications for cancer therapy.
109 guidance in the design of novel or existing cancer therapies.
110 preserve neural stem cells during cytostatic cancer therapies.
111 yet there are still no approved Ras-targeted cancer therapies.
112 eukemia and new, more specific NK cell-based cancer therapies.
113 tegy to actively deliver nanotherapeutics in cancer therapies.
114 tual framework for developing more effective cancer therapies.
115 tool for the timely development of targeted cancer therapies.
116 strategy to enhance the outcome of anti-VEGF cancer therapies.
117 fying drugs for use as adjuvants to existing cancer therapies.
118 ver new opportunities to refine personalized cancer therapies.
119 that microbes can influence the efficacy of cancer therapies.
120 opment of highly selective broad-acting anti-cancer therapies.
121 to RTKs represents a key element in targeted cancer therapies.
122 ttractive targets for the development of new cancer therapies.
123 elp to prevent or reverse resistance to some cancer therapies.
124 ed molecular mechanisms and to develop novel cancer therapies.
125 apoptosis, and they are proposed targets for cancer therapies.
126 on therapy (ADT), after adjustment for other cancer therapies.
127 apeutic target that may complement cytotoxic cancer therapies.
128 nd quality of life to assess the benefits of cancer therapies.
129 have not been actively explored for targeted cancer therapies.
130 mising treatment of side effects of prostate cancer therapies.
131 of Rho GTPase targeting strategies in future cancer therapies.
132 ising drug target for the development of new cancer therapies.
133 ral to the advancement of new antibody-based cancer therapies.
134 efficacy and reduce adverse side effects of cancer therapies.
135 proved drugs can be repurposed as novel anti-cancer therapies.
136 the development and implementation of novel cancer therapies.
137 phenotypes can translate into effective anti-cancer therapies.
138 nale for upregulating IFNAR1 to improve anti-cancer therapies.
139 in enhancement of immunomodulatory and anti-cancer therapies.
140 (SC) subpopulations to molecularly targeted cancer therapies.
141 offer potential novel targets in future anti-cancer therapies.
142 nt of translational, carrier-free RNAi-based cancer therapies.
143 pite the availability of PARP inhibitors for cancer therapy, a biomarker to clearly stratify patients
144 he growing availability of nanomaterials for cancer therapy, a material that responds to each patient
148 about the metabolic reprogramming induced by cancer therapies and how this contributes to therapeutic
149 wever, after analysis was adjusted for other cancer therapies and other covariates, patients with ADT
150 llenge as they are resistant to conventional cancer therapies and play essential roles in metastasis
151 ndels that are associated with resistance to cancer therapies and provide patients personalized treat
152 an important concern for patients undergoing cancer therapy and astronauts on long missions in deep s
154 gates have emerged as a powerful strategy in cancer therapy and combine the ability of monoclonal ant
155 couplings can be used as a reliable guide to cancer therapy and expand our understanding of the effec
156 ments illustrate the importance of stroma in cancer therapy and how its impact on treatment resistanc
157 that HCV infection should not contraindicate cancer therapy and infected patients should have access
158 Ionizing radiation (IR) is commonly used in cancer therapy and is a main source of DNA double-strand
159 eceptor (EGFR) is a breakthrough in targeted cancer therapy and marks a drastic change in the treatme
162 tus to the practical improvement of ion-beam cancer therapy and the development of more efficient tre
163 l diversity of core components of front-line cancer therapy and the potential benefits of applying a
164 sporters can mediate multidrug resistance in cancer therapy and their dysfunction is linked to variou
165 tance is an almost inevitable consequence of cancer therapy and ultimately proves fatal for the major
166 activity is a suggested predictive marker in cancer therapy and, consequently, the described highly s
167 Mps1 has emerged as a potential target for cancer therapy, and a variety of compounds have been dev
168 of exploiting the tumor microenvironment in cancer therapy, and how this could be translated to clin
169 hese findings have profound implications for cancer therapy, and provide new mechanistic insights int
170 LIM kinases (LIMK) are emerging targets for cancer therapy, and they function as network hubs to coo
171 degree of symptom-related suffering early in cancer therapy, and very few patients or parents in this
172 es according to the Functional Assessment of Cancer Therapy-Anemia (FACT-An) and the Euro Qol 5 Dimen
174 predicting the risk for long-term effects of cancer therapy are well known, the impact of genetic ris
175 assist endoscopic and surgical guidance for cancer therapy as well as create opportunities to direct
176 a molecular dynamic continuum for potential cancer therapy, as well as understanding the cytotoxicit
177 of a 2-part review, we will review cancer or cancer therapy-associated systemic and pulmonary hyperte
178 seline screening and had not received active cancer therapy at least 6 months prior to screening.
179 cer cells will be crucial for advancement of cancer therapies based on the cell's metabolic state.
180 therapy (PIT) is an emerging low side effect cancer therapy based on a monoclonal antibody (mAb) conj
181 discuss some new applications for plasma in cancer therapy based on plasma self-organization, which
182 ific singlet oxygen ((1) O2 ) generation for cancer therapy, based on a Fenton-like reaction between
183 ong been considered a tantalizing target for cancer therapy because it mediates activation of the ext
184 epresent promising targets in the context of cancer therapy because they are an innate immune cell po
186 s assessed by using Functional Assessment of Cancer Therapy-Bone Pain (FACT-BP) scores (scale, 0-60 p
187 ant drug that is used in transplantation and cancer therapy but which causes a number of side effects
188 of defined structure hold great promise for cancer therapies, but further advances are constrained b
190 ong been considered an attractive target for cancer therapy, but few specific inhibitors have been fo
191 NA (siRNA) is a promising molecular tool for cancer therapy, but its clinical success is limited by t
192 odies have made significant contributions to cancer therapy, but suffer from several limitations that
193 mours, and fibrosis is a promising target in cancer therapy, but tools for its non-invasive quantific
194 le nanocarriers offer remarkable promise for cancer therapy by discriminating against devastating cyt
195 int inhibitors, have set off a revolution in cancer therapy by releasing the power of the immune syst
197 linicians soon after completion of childhood cancer therapy can predict individual risk for subsequen
198 cognitive function (Functional Assessment of Cancer Therapy Cognitive Function [FACT-COG] perceived c
199 trols completed the Functional Assessment of Cancer Therapy-Cognitive Function (FACT-Cog) at prechemo
200 on of intracellular hydrogen peroxide during cancer therapy constitutes an unexplored and fascinating
203 ery vehicle can have a significant impact on cancer therapy due to the potential for overcoming issue
204 otoxins (RIT) have been highly successful in cancer therapy due, in part, to the high cancer-specific
206 life (QOL) via the Functional Assessment of Cancer Therapy (FACT)-Lung Cancer Subscale (LCS) in the
209 tment data on Taxol-based neoadjuvant breast cancer therapy from multiple sources, we demonstrate tha
210 s assessed with the Functional Assessment of Cancer Therapy-General (FACT-G) questionnaire at baselin
212 (Brief COPE), QOL (Functional Assessment of Cancer Therapy-General), and mood (Hospital Anxiety and
213 assessments of QOL (Functional Assessment of Cancer Therapy-General), depressive symptoms (Patient He
214 s of resistance to conventional and targeted cancer therapies has focused on cell intrinsic pathways
217 nd patients using a proteasome inhibitor for cancer therapy have a higher incidence of heart failure.
220 sferase 1 (CARM1) is a propitious target for cancer therapy; however, few CARM1 substrates are known,
221 o describe the cumulative burden of curative cancer therapy in a clinically assessed ageing populatio
225 yet identification of plausible targets for cancer therapy in the microenvironment has proven elusiv
227 ade reactions, has potential applications in cancer therapy, including targeted approaches as in anti
228 irst part of a 2-part review, we will review cancer therapy-induced cardiomyopathy and ischemia.
229 tter prevention, diagnosis, and treatment of cancer therapy-induced cardiovascular complications.
230 with cancer specialists to prevent and treat cancer therapy-induced cardiovascular complications.
231 ervous system injury is a frequent result of cancer therapy involving cranial irradiation, leaving pa
232 Plasmonic nanoparticle-based photothermal cancer therapy is a promising new tool to inflict locali
234 inical efficacy of immune cytokines used for cancer therapy is hampered by elements of the immunosupp
237 l challenge in the development of epigenetic cancer therapy is the ability to direct selectivity in m
239 ammatory gene expression following genotoxic cancer therapy is well documented, yet the events underl
241 s assessed with the Functional Assessment of Cancer Therapy-Kidney Symptom Index-Disease Related Symp
242 ate that DNA-damaging modalities used during cancer therapy lead to the release of ssDNA fragments fr
243 action and solid rationale for their use in cancer therapy, mTORis have met only modest success rate
244 the following symptoms in the first month of cancer therapy: nausea (n = 109; 84.5%), loss of appetit
247 g normal tissues would significantly enhance cancer therapy outcomes and reduce cancer-related mortal
248 tentially provide a broad-based strategy for cancer therapy owing to frequent p53 inactivation in hum
250 rug resistance remains an elusive problem in cancer therapy, particularly for novel targeted therapie
252 ed for response to anti-PD1, suggesting that cancer therapies promoting Treg fragility may be efficac
255 n from a cardiovascular perspective develops cancer therapy-related cardiac dysfunction or a high-ris
256 both prevention and treatment of cancer and cancer therapy-related complications, and the first clin
257 o received trastuzumab and protected against cancer therapy-related declines in LVEF; however, trastu
259 ted significance for five frontline prostate cancer therapies, representing a significant enrichment
261 neoadjuvant therapy were compared to breast cancer therapy response, as determined by residual tumor
262 a-lactamase (P99betaL), a component of ADEPT cancer therapies, revealed that the population possessed
266 overing opportunities to refine personalized cancer therapies.Significance: Systematic analysis of tr
267 Our important findings could provide a novel cancer therapy strategy by blocking either Ser-176 or Se
272 decisions can be pursued in order to provide cancer therapy that is personalized to the patient and h
273 tosis-inducing ligand (TRAIL) is a potential cancer therapy that selectively targets cancer cell deat
274 b by Tg analogues is considered for prostate cancer therapy, the inhibition of SPCA1a by Tg might rep
275 a high-risk cardiovascular patient requires cancer therapy, the team of oncologists and cardiologist
278 d to drive resistance to multiple classes of cancer therapies, thereby limiting their effectiveness.
280 therapy (SDT) has become a new modality for cancer therapy through activating certain chemical sensi
281 ession can enhance CD8(+) T-cell function in cancer therapy to a similar degree as PD-1 blocking anti
282 ession can enhance CD8(+) T-cell function in cancer therapy to a similar degree as PD-1-blocking anti
283 GFR small-molecule inhibitor used for breast cancer therapy, upregulated Perp in ErbB2-positive human
285 re planned to test new immune modulators for cancer therapy using a variety of modified response crit
286 es and opportunities employed in combination cancer therapy using nucleic acids therapeutics for succ
288 information by perturbing-for example, with cancer therapies-viable primary tumor cells from patient
289 potent cytotoxic agents to cancer cells for cancer therapy, we here report the synthesis of antisens
290 been implicated to be a potential target for cancer therapy, we selected this protein for further inv
294 mune mechanisms of conventional and targeted cancer therapies will lead toward novel combinatorial an
295 eted in ongoing clinical trials that combine cancer therapies with antimalarial drugs for the treatme
297 , have limited effectiveness as single agent cancer therapies, with feedback mechanisms inherent to t
298 tably, ERK1/2 pathway inhibitors are used in cancer therapy, with severe and noncharacterized ocular
299 xtraterminal inhibitors (BETi) are promising cancer therapies, yet prominent side effects of BETi at
300 the most commonly used therapeutic drugs for cancer therapy, yet prolonged cisplatin treatment freque
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