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1 e diverse pharmacological effects, including anticancer.
2 in clinical research and their mechanisms of anticancer action have been reported in large volumes ov
3                 Specifically, their combined anticancer activities and selective visual signal respon
4                        In summary, GE exerts anticancer activities by inducing apoptosis and suppress
5 eveloping therapeutic drugs that exert their anticancer activities by producing massive chromosome an
6 platform through the identification of novel anticancer activities for cycloviolacins by their cytoto
7 ysates or peptides with immunomodulatory and anticancer activities have been reported from a variety
8                     The immunomodulatory and anticancer activities of food derived protein hydrolysat
9 al constituents that are responsible for the anticancer activities of propolis were analyzed.
10 mistry of their tetrapeptidic backbones, the anticancer activities of these precursors largely match
11 same seeds, has been shown to have potential anticancer activities.
12                           Vitamin D may have anticancer activities.
13    Entire compounds were evaluated for their anticancer activity against HeLa (cervical cancer), MCF-
14  its parent drug, P-SMART showed significant anticancer activity against melanoma cells in cytotoxici
15 g combinations of approved drugs with potent anticancer activity for further mechanistic study and tr
16  a safe therapy with encouraging and durable anticancer activity in patients with R/R NHL.
17 a poly(ADP-ribose) polymerase inhibitor, has anticancer activity in recurrent ovarian carcinoma harbo
18 /IL-24 (mda-7/IL-24) displays broad-spectrum anticancer activity in vitro, in vivo in preclinical ani
19 ling ability of small molecules controls the anticancer activity of EISA.
20                                          The anticancer activity of papaya pectin is dependent on the
21                                          The anticancer activity of some of the obtained compounds ag
22          This synergistic improvement in the anticancer activity was apoptosis-dependent that was con
23                      In particular, enhanced anticancer activity was demonstrated in acute myeloid le
24         When the first titanium complex with anticancer activity was identified in the 1970s, it was
25 gate in vitro the health-promoting benefits (anticancer activity, alpha-amylase and alpha-glucosidase
26  analyzed for sensitivity patterns, synergy, anticancer activity, and were validated in low-throughpu
27  human breast cancer cell line MCF7 in vitro anticancer activity, which defines the molecular level u
28 ponent of saffron spice, is known to have an anticancer activity.
29 prepared and evaluated for hypoxia-selective anticancer activity.
30 under NIR irradiation, resulting in enhanced anticancer activity.
31 reparing stable nanoformulations with potent anticancer activity.
32 m is an aryl sulfonamide drug with selective anticancer activity.
33                  HuR inhibition has profound anticancer activity.
34  conjugation platform for the preparation of anticancer ADCs.
35            Doxorubicin is a highly effective anticancer agent but causes cardiotoxicity in many patie
36 ze isoanabasine, preclamol, and niraparib-an anticancer agent in several clinical trials.
37                           CPI-613 is a novel anticancer agent that selectively targets the altered fo
38 of specialized metabolites that includes the anticancer agent vincristine, antimalarial quinine and n
39 any alternate oral, injectable, or infusible anticancer agent within 90 days.
40 ones with camptothecin (CPT), a largely used anticancer agent, KuQs have been tested against Cisplati
41  days after adjudication) for the index oral anticancer agent.
42  explored the potential of stauprimide as an anticancer agent.
43  they characterize DOT1L inhibitors as novel anticancer agents against MYCN-amplified neuroblastoma.
44 -directed intraperitoneal targeting of other anticancer agents and nanoparticles using peptides and o
45 ween the mechanisms of action of these novel anticancer agents and the imaging appearance of tumor re
46 e syntheses of tetrasubstituted olefin-based anticancer agents are described.
47  Moreover, because the latest generations of anticancer agents are founded on biological mechanisms,
48                           The platinum-based anticancer agents cisplatin, carboplatin, and oxaliplati
49 ltransferase Porcupine (Porcn) are candidate anticancer agents in clinical testing.
50             Purpose The number of novel oral anticancer agents is increasing, but financial barriers
51 of HOTAIR in pancreatic cancer resistance to anticancer agents is unknown.
52 re is a steady increase in costs of patented anticancer agents over time.
53 ted their potential as promising theranostic anticancer agents that can circumvent cisplatin resistan
54  a possible new route for the development of anticancer agents that could suppress KRAS expression.
55                                      Several anticancer agents that form DNA adducts in the minor gro
56 cs have facilitated the development of novel anticancer agents that have decreased side effects and i
57 nia is a major side effect of a new class of anticancer agents that target histone deacetylase (HDAC)
58 ese cells, for the first time, two different anticancer agents were synthesized simultaneously intrac
59 g conjugates (ADCs) are a promising class of anticancer agents which have undergone substantial devel
60  and complications associated with the novel anticancer agents will be summarized, since these are fr
61     Acylfulvenes are a class of experimental anticancer agents with a unique repair profile suggestin
62  have demonstrated or predicted potential as anticancer agents, but a detailed structural basis for t
63 enium complexes are promising candidates for anticancer agents, especially NKP-1339 (sodium trans-[te
64 tion of Rac hyperactivation to resistance to anticancer agents, including targeted therapies, as well
65 ring resistance to many structurally diverse anticancer agents, leading to the phenomenon called mult
66           For two thirds of FDA approvals of anticancer agents, the requirement for predictive biomar
67 ng pursuit of CXCR4 antagonists as potential anticancer agents, we recently developed a potent, selec
68  of alternate oral, injectable, or infusible anticancer agents.
69 spliceosome-modulating activity as potential anticancer agents.
70 ms of RCC provide specific targets for novel anticancer agents.
71     Autophagy mediates resistance to various anticancer agents.
72 compounds represent a new potential class of anticancer agents.
73 soform, and this may limit their efficacy as anticancer agents.
74 eudolaric acid B (PAB) holds promise for new anticancer agents.
75 erable interest as potential chemopreventive anticancer agents.
76 cting compounds may represent novel powerful anticancer agents.
77  adjudicated prescription for any of 38 oral anticancer agents.
78 have elucidated the binding mechanism of the anticancer alkaloid berberine to the human telomeric G4
79 d due to its antioxidant, anti-inflammatory, anticancer and anti-aging properties.
80 soybean proteins asa source of peptides with anticancer and anti-inflammatory activities produced aft
81 cs for type 2 diabetes mellitus and also has anticancer and antiaging properties.
82 hat squalamine, a natural product with known anticancer and antiviral activity, dramatically affects
83                    These results demonstrate anticancer and apoptosis-inducing potentials of 9f in MC
84 but can be used as a bioengineering tool for anticancer and gene therapies.
85 tion of several antibacterial, antimalarial, anticancer, and immunomodulatory agents.
86 the Basidiomycota taxon possess antioxidant, anticancer, and most significantly, anti-inflammatory pr
87 ns beyond its antimalarial activity, such as anticancer, antiviral, and anti-inflammatory effects.
88  regulate motility and appetite, and produce anticancer, anxiolytic, and neuroprotective efficacies v
89 MPORTANCE Oncolytic virus (OV) therapy is an anticancer approach that uses viruses that selectively i
90 CC-specific suppressor and uncover its novel anticancer-associated functions.
91                                        It is anticancer because of its cytotoxicity.
92 he development of ruthenium(ii) complexes as anticancer candidates and biocatalysts, including arene
93 have also attracted significant attention as anticancer candidates; however, only a few of them have
94 tabilizers are an established opportunity in anticancer chemotherapy.
95 activatable dopamine-conjugated platinum(IV) anticancer complex (Pt-DA) has been incorporated into G-
96 profiling conducted after treatment with the anticancer compound Minnelide revealed deregulation of t
97  the EGFR kinase inhibitor lapatinib and the anticancer compound YM155 that is preserved across sever
98  route to potent epipolythiodiketopiperazine anticancer compounds.
99 ha (IFNalpha) is important for antiviral and anticancer defenses.
100 mor multidrug resistance (MDR) is to deliver anticancer drug along with P-glycoprotein (P-gp) inhibit
101  Moreover, camptothecin (CPT) is used as the anticancer drug and modified into a dimer (CPT)2 -ss-Mal
102      Mutants sensitive to 5-fluorouracil, an anticancer drug are under-represented within the 305 pos
103 odytes nimmoniana is a rich source of potent anticancer drug camptothecin (CPT) whose biosynthetic pa
104                         Among them, Ru-based anticancer drug candidates have become a central subject
105                                   Conclusion Anticancer drug costs may change substantially after lau
106 lso compromised the inhibitory effect of the anticancer drug dasatinib on Src kinase oncogenic potent
107 y, protected delivery of bioactive moieties, anticancer drug delivery systems, and theranostics (i.e.
108 g in vitro and potentially also for specific anticancer drug delivery.
109 on as important tools in cancer research and anticancer drug development.
110 lls, endorsing their further exploration for anticancer drug discovery.
111 the cell cycle and are validated targets for anticancer drug discovery.
112 ap the hydrophobic dye Nile Red (NR) and the anticancer drug doxorubicin (DOX).
113                                              Anticancer drug efficacy has been tested on circulating
114          Cisplatin is the most commonly used anticancer drug for the treatment of testicular germ cel
115                               When given the anticancer drug gefitinib or the retroviral drug atazana
116 sor has been tested for immobilization of an anticancer drug gemcitabine (2',2'-difluoro-2'-deoxycyti
117           Our previous study showed that the anticancer drug Gleevec lowers Abeta levels through indi
118 ll culture results indicative of synergistic anticancer drug interactions rarely translate clinically
119 veloped algorithm are capable of binding the anticancer drug irinotecan (CPT-11) with micromolar affi
120 uccessfully detected the abundance change of anticancer drug irinotecan and its metabolites inside sp
121 o papers in Cell exploit C. elegans to infer anticancer drug mechanisms.
122 trial importance as the active moiety of the anticancer drug mipsagargin, currently in clinical trial
123                                 The Ru-based anticancer drug NKP-1339 was studied applying XANES (Cl
124 oids upon treatment with the clinically used anticancer drug oxaliplatin.
125                                          The anticancer drug paclitaxel (Taxol) exhibits paradoxical
126      In silico analysis identified 390 novel anticancer drug pairs belonging to 10 drug classes that
127  Smo inhibitor vismodegib, a clinically used anticancer drug reported to distort smell perception in
128  and further characterized tumorigenesis and anticancer drug responses.
129 ell DNA-damage response and is an attractive anticancer drug target.
130 ng cell division, and as such, it is a broad anticancer drug target.
131       Cancer cell mitochondria are promising anticancer drug targets because they control cell death
132 process and its application in delivering an anticancer drug to treat cancer cells are also successfu
133 he feasibility and benefits of delivering an anticancer drug using a carrier-free nanoparticle formul
134 ted by coencapsulating doxorubicin (DOX) (an anticancer drug) and IR780 iodide (IR780) (an NIR-absorb
135 resence of chlorambucil as a model template (anticancer drug).
136       We found that the binding of candidate anticancer drug, curaxin, to cellular DNA results in unc
137 onitoring of biointeraction occurred between anticancer drug, Daunorubicin (DNR), and DNA.
138 ggressive CIPN model utilizing the frontline anticancer drug, paclitaxel (PTX).
139  new therapeutic strategy to protect against anticancer drug-induced peripheral neurotoxicity.
140 i warrants further evaluation as a potential anticancer drug.
141 nificantly improves the effectiveness of the anticancer drug.
142 stance calls for continuously developing new anticancer drugs and combination chemotherapy regimens.
143  transporter that confers resistance to many anticancer drugs and plays a role in the disposition and
144  mechanisms of action of ruthenium(ii)-based anticancer drugs and the relationship between their chem
145                     Most of the FDA approved anticancer drugs are organic molecules, while metallodru
146                               Activity of IP anticancer drugs can be further potentiated by encapsula
147 ophobic and amphipathic compounds, including anticancer drugs from cells.
148  of action (MoA) for new and uncharacterized anticancer drugs is important for optimization of treatm
149   Limiting out-of-pocket costs for expensive anticancer drugs like the IMiDs may improve access to or
150  Food and Drug Administration (FDA)-approved anticancer drugs or compounds currently in clinical deve
151 of AH-7614 containing features found in many anticancer drugs suggests that a novel close chemical an
152 tment with sunitinib and erlotinib, approved anticancer drugs that inhibit AAK1 or GAK activity, or w
153 osts for a cohort of 24 patented, injectable anticancer drugs that were approved by the US Food and D
154            Nanoparticles are used to deliver anticancer drugs to solid tumors.
155 BCB1 and ABCG2 limit the exposure of several anticancer drugs to the brain, leading to suboptimal tre
156  can be used to improve therapeutic index of anticancer drugs used for PC treatment.
157                               Combination of anticancer drugs with therapeutic microRNA (miRNA) has e
158    TOP2 poisons are valuable and widely used anticancer drugs, but they are associated with the occur
159 some, has been associated with resistance to anticancer drugs, leading autophagy inhibition to be wid
160 nducive for the efficient delivery of NO and anticancer drugs, simultaneously.
161 trast to cisplatin or the progenitor RAPTA-C anticancer drugs, the binuclear agents neither arrest sp
162 emonstrate that both types of Top2-targeting anticancer drugs, the catalytic inhibitor dexrazoxane (I
163                               Using 5 common anticancer drugs, we exemplified detection of differenti
164 target for the development of several useful anticancer drugs, which compromise rapidly dividing cell
165 elopment and may represent novel targets for anticancer drugs.
166  a promising lead for the development of new anticancer drugs.
167 lating compounds that represent the earliest anticancer drugs.
168 large storage space and release channels for anticancer drugs.
169 ibodies, an increasingly successful class of anticancer drugs.
170 ance and serves as a major target of several anticancer drugs.
171 ging evidence in favor of SMAPs as potential anticancer drugs.
172 ic load should make tumors more sensitive to anticancer drugs.
173 es together with their response to 24 common anticancer drugs.
174 or inevitably acquire such when treated with anticancer drugs.
175 d numerous TFs whose activity interacts with anticancer drugs.
176 ination resulted in a remarkable synergistic anticancer effect on intracranial human and murine gliob
177 erior in their selective apoptosis-mediating anticancer effect than free form of these proteins and 5
178 ch yields a remarkable H2 O2 -NO cooperative anticancer effect with minimal adverse effect.
179                                 However, its anticancer effects and mechanisms on prostate cancer hav
180 ynchronized delivery system elicits enhanced anticancer effects and merits further development in the
181  inhibition of cyclooxygenase-1, whereas its anticancer effects may be due to inhibition of cyclooxyg
182                                  Synergistic anticancer effects of combined bortezomib and doxorubici
183 ic ultrasound pulses as well as the improved anticancer effects under hypoxic conditions.
184 bitors Physcion and its derivative S3, shows anticancer effects.
185                 The library was screened for anticancer efficacy in established and stem cell-like gl
186 re, PFT-mu administration did not impair the anticancer efficacy of cisplatin and radiotherapy in tum
187 n vivo, coadministration of tPA improved the anticancer efficacy of nanoparticle-encapsulated paclita
188 , and targeting this pathway may improve the anticancer efficacy of platinum-based chemotherapy.
189 n be targeted and inactivated to improve the anticancer efficacy of PLN-delivered drugs.
190                                              Anticancer efficacy of TLR5 agonists stems from TLR5-dep
191 able highly effective X-PDT to afford superb anticancer efficacy.
192 w agelastatin alkaloid derivatives and their anticancer evaluation in the context of the breast cance
193 mprehensive overview of immunomodulatory and anticancer food derived protein hydrolysates or peptides
194                    Most immunomodulatory and anticancer food protein hydrolysates or peptides were te
195 s for the production of immunomodulatory and anticancer food protein hydrolysates.
196 n apoptosis and cell cycle arrest, and these anticancer functions are inhibited by AKT-induced phosph
197  the blockade of autophagy enhances TH9 cell anticancer functions in vivo, and mice with T cell-speci
198 in epidermal terminal differentiation and of anticancer genes such as Cgref1, Brsk1, Basp1, Dusp5, Bt
199 or by acting as a chemoattractant to recruit anticancer immune cells expressing its receptor, the che
200 e tolerance, defense against infections, and anticancer immune responses.
201 ineering biomaterials for the enhancement of anticancer immunity is given, including the perspectives
202  PD-L1 and B7-1 interactions, reinvigorating anticancer immunity.
203  mechanisms and may contribute to protective anticancer immunity.
204  miR-155 expression could be used to improve anticancer immunotherapies.
205       To extend application of TLR5-targeted anticancer immunotherapy to tumors that do not naturally
206 TLR5) is considered an attractive target for anticancer immunotherapy.
207 files, while repurposing known drugs for new anticancer indications has become a viable alternative.
208                                          The anticancer mechanism seems to be tightly linked to the r
209 ied drivers of price growth of targeted oral anticancer medications (TOAMs) in private insurance plan
210                                              Anticancer modalities based on oxygen free radicals, inc
211 tency factors in breast cancer and effective anticancer modulation of this axis with HNK treatment.
212 ously untested synergy predictions involving anticancer molecules.
213 y for improving therapeutic effectiveness of anticancer nanomedicine.
214  actively exploited for targeted delivery of anticancer nanomedicines resulting in numerous pharmaceu
215          As such, it represents a target for anticancer or antidiabetic drug development.
216                           When resistance to anticancer or antimicrobial drugs evolves in a patient,
217 antioxidant peptides, peptide affinity tags, anticancer peptides, and others.
218 ge to peripheral afferent sensory neurons by anticancer pharmacotherapy, leading to debilitating neur
219 these clinical observations, we examined the anticancer potential of combined treatment with 6PGD inh
220                                To assess the anticancer potential of inhibitors targeting DYRK kinase
221  developed resistances to TRAIL which limits anticancer potential.
222 on blue emission in the system activates the anticancer prodrug molecules and shows effective tumor g
223 core, and amphiphilic polymers encapsulating anticancer prodrug molecules as the shell.
224 c][1,2,4]triazin-3-yl]ace tate (ETTA), a new anticancer prodrug, using adsorptive stripping voltammet
225  in vivo titration of the photorelease of an anticancer prodrug.
226 A1 to obtain the selective release of potent anticancer products within cancer tissues is a promising
227         Our results demonstrate the enhanced anticancer properties along with gastroprotective effect
228 eclinical studies have shown aspirin to have anticancer properties and epidemiologic studies have ass
229          Ferrociphenols are known to display anticancer properties by original mechanisms dependent o
230 light the enhanced Hh pathway inhibition and anticancer properties of MDB5 leaving a platform for mon
231  vivo evidence highlighted its potential for anticancer properties.
232                           Despite the potent anticancer property, there is still no proper method to
233 fects are observed in combination with other anticancer regimens or in the presence of cancer.
234 s that govern the strength and timing of the anticancer response.
235 erapies will lead toward novel combinatorial anticancer strategies with improved clinical benefit.
236  being devoted to the investigation of novel anticancer strategies.
237 hus, inhibition of Clks might become a novel anticancer strategy, leading to a selective depletion of
238  microRNA (miRNA) has emerged as a promising anticancer strategy.
239 he proapoptotic Bcl2 family member Bax as an anticancer strategy.
240  genetic analysis has identified MAT2A as an anticancer target in tumor cells lacking expression of 5
241                We apply this approach to the anticancer target PD-1 and its ligands PD-L1 and PD-L2.
242 ene promoters are considered to be promising anticancer targets.
243 damage is key to our ability to devise novel anticancer therapeutic strategies.
244 small molecules has been a long sought-after anticancer therapeutic strategy.
245                          Encapsulation of an anticancer therapeutic, alpha-cyano-4-hydroxycinnamic ac
246   Moreover, EVs take part in the response to anticancer therapeutics not least by promoting drug resi
247 that the bone marrow niche can be altered by anticancer therapeutics, resulting in drug resistance th
248 g lead compound for the development of novel anticancer therapeutics.
249 ecules, especially for molecular imaging and anticancer therapeutics.
250 and cytosol and is an established target for anticancer therapeutics.
251 g point for the development of protein-based anticancer therapeutics.
252 mportant enzyme that is an active target for anticancer therapeutics.
253 or implications for the development of novel anticancer therapeutics.
254 cations of 17e in both vaccine adjuvants and anticancer therapies based on multi-TLR activation.
255 l studies suggest that statins combined with anticancer therapies delay relapse and prolong life in s
256              While rare outlier responses to anticancer therapies exist, barriers limit our understan
257 ce of the tumor microenvironment in targeted anticancer therapies has been well recognized.
258 chanisms and potential utility with targeted anticancer therapies remain unknown.
259            However, in the current armory of anticancer therapies, a specific category of anti-invasi
260 electively enriched in residual tumors after anticancer therapies, which may account for tumor recurr
261  in cancer patients before the initiation of anticancer therapies.
262 present a novel target for glutamine-related anticancer therapies.
263 -limiting side effect of all the most common anticancer therapies.
264 P39-targeting strategies as the basis of new anticancer therapies.
265 protein inhibitors are emerging as promising anticancer therapies.
266 tral nervous system metastases, had received anticancer therapy 14 days or fewer before starting the
267 provide evidence for synergy of conventional anticancer therapy and CAR T cells and heralds future st
268  signaling sensitized breast cancer cells to anticancer therapy and strengthened immune responses by
269 preclinical evidence for targeting RPS19 for anticancer therapy enhancing antitumor T cell responses.
270 atients were ineligible if they had received anticancer therapy or surgery (except colostomy or ileos
271 and disease progression following first-line anticancer therapy tested for a KRAS mutation, 866 were
272 d the approval of methylation inhibitors for anticancer therapy were discussed.
273 drugs have made significant contributions to anticancer therapy, along with other therapeutic methods
274 t therapies, radiotherapy, surgery, systemic anticancer therapy, and referral to supportive care and
275 eived up to three previous lines of systemic anticancer therapy, had at least one measurable lesion a
276 ial barrier to accessing orally administered anticancer therapy, warranting urgent attention from pol
277 ists could provide an efficient nongenotoxic anticancer therapy.
278  proceeded to observation without additional anticancer therapy.
279 ates that may find promising applications in anticancer therapy.
280 mission without consolidative SCT or any new anticancer therapy.
281 long been recognised as important targets of anticancer therapy.
282 y in tumor cells often confers resistance to anticancer therapy.
283 l, and has emerged as a candidate target for anticancer therapy.
284 own as tools for gene delivery and oncolytic anticancer therapy.
285 tabolism could potentially be targeted as an anticancer therapy.
286 poration may offer a simple general tool for anticancer therapy.
287 ate that is vulnerable to trapping by potent anticancer TOP2 drugs.
288                          Following cytotoxic anticancer treatment, tumor-derived DAMPs (damage-associ
289 12 weeks, and having recovered from previous anticancer treatment-related toxicities.
290 monitor the patient's individual response to anticancer treatment.
291 e in various afucosylated therapeutic Abs in anticancer treatment.
292                 These findings could benefit anticancer treatment.
293                                 Whereas many anticancer treatments induce apoptosis, others induce ce
294 tion of CAR T-cell therapy into conventional anticancer treatments.
295 ggressiveness and resistance to conventional anticancer treatments.
296 us opening access to potential self-adjuvant anticancer vaccine candidates.
297 fabrication of a biomimetic, nanoparticulate anticancer vaccine that is capable of delivering autolog
298 onfer long-term immunity against tumors, and anticancer vaccines therefore should maximize their gene
299                                              Anticancer vaccines train the body's own immune system t
300 ture development of personalized, autologous anticancer vaccines with broad applicability.

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