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1 genome (e.g., by irradiation or radiomimetic chemotherapeutics).
2  patient samples (16 untreated, 3 treated by chemotherapeutics).
3 luding both targeted as well as conventional chemotherapeutics.
4 w bacteria affect the C. elegans response to chemotherapeutics.
5 S-driven cancers are infamously resistant to chemotherapeutics.
6 res in response to metabolic inhibitors, and chemotherapeutics.
7 pecific effects regulating the resistance to chemotherapeutics.
8 e rational design of alpha-tubulin targeting chemotherapeutics.
9 tance (MDR), being capable of effluxing many chemotherapeutics.
10 astasis and to increase tumor sensitivity to chemotherapeutics.
11 f unique molecules including highly valuable chemotherapeutics.
12 meter-sized particle that can be loaded with chemotherapeutics.
13 nge of clinical and preclinical stage cancer chemotherapeutics.
14 increases tumour sensitivity to conventional chemotherapeutics.
15 nd following treatment with mitosis-blocking chemotherapeutics.
16 tment to improve the efficacy of traditional chemotherapeutics.
17  potential adjuvants for DNA-damaging cancer chemotherapeutics.
18 ions and metabolites to siRNA, peptides, and chemotherapeutics.
19 e strategy for the development of anticancer chemotherapeutics.
20  apoptosis in breast cancer cells exposed to chemotherapeutics.
21 logy research tools and clinically as cancer chemotherapeutics.
22 signaling and open the door to new selective chemotherapeutics.
23 rs can enhance the efficacy of common cancer chemotherapeutics.
24 pt host-parasite interactions, or to deliver chemotherapeutics.
25 so the cellular target of camptothecin (CPT) chemotherapeutics.
26 eration and a target of commonly used cancer chemotherapeutics.
27 isease progression and resistance to current chemotherapeutics.
28 anslates into an enhanced ability to deliver chemotherapeutics.
29 epresent candidate molecular targets for new chemotherapeutics.
30 sistant to a variety of chemically unrelated chemotherapeutics.
31 ity and are garnering increasing interest as chemotherapeutics.
32 ide range of imidazole-based antibiotics and chemotherapeutics.
33 methyltransferases (KMTs) being developed as chemotherapeutics.
34  and are resistant to conventional cytotoxic chemotherapeutics.
35  as well as an increasing variety of anionic chemotherapeutics.
36 -based antiretroviral medications and cancer chemotherapeutics.
37  the delivery of HSP targeted macromolecular chemotherapeutics.
38 y and repopulate the tumor after exposure to chemotherapeutics.
39 er, immunosuppressant, and anti-inflammatory chemotherapeutics.
40  breast cancers, which are resistant to many chemotherapeutics.
41 vances and the development of more effective chemotherapeutics.
42 umor penetration and therapeutic efficacy of chemotherapeutics.
43 ionizing radiation as well as treatment with chemotherapeutics.
44 cers, as well as resistance to commonly used chemotherapeutics.
45 tumors while minimizing systemic exposure to chemotherapeutics.
46 harnessed extensively as carriers for cancer chemotherapeutics.
47 ptosis and enhances the potency of cytotoxic chemotherapeutics.
48 allows cell survival, even against cytotoxic chemotherapeutics.
49 CITED2), a gene that mediates sensitivity to chemotherapeutics.
50 the tumor, is also resistant to conventional chemotherapeutics.
51 reme resistance to conventional DNA-damaging chemotherapeutics.
52 overcoming major drawbacks of currently used chemotherapeutics.
53 esidues associated with resistance to cancer chemotherapeutics.
54 and bound to the three structurally distinct chemotherapeutics.
55 hat they have emerged as excellent potential chemotherapeutics.
56 ion of IL-8 pathway to the class of platinum chemotherapeutics.
57  in tumor, can evaluate the effectiveness of chemotherapeutics.
58 ia in order to increase the effectiveness of chemotherapeutics.
59 ntifolates that could potentially be used as chemotherapeutics.
60 s can potentially improve the selectivity of chemotherapeutics.
61 eric radiation, environmental chemicals, and chemotherapeutics.
62 ies and DNA-damaging agents that are used as chemotherapeutics.
63 latinum drugs, which are among the most used chemotherapeutics.
64 sistance and rapidly identifying combination chemotherapeutics.
65         ICD can be induced by treatment with chemotherapeutics.
66 es the anticancer efficacy of platinum-based chemotherapeutics.
67 ng TLS is an attractive avenue for improving chemotherapeutics.
68 e panel of DNA-damaging agents, enriched for chemotherapeutics.
69 the role of bacteria in the host response to chemotherapeutics.
70 l line exacerbated DNA damage in response to chemotherapeutics.
71 ncer that resists efforts to identify better chemotherapeutics.
72 e-of-day may alter inflammatory responses to chemotherapeutics.
73 atory axis, conferring resistance to various chemotherapeutics.
74  resistance to a broad range of DNA-damaging chemotherapeutics.
75 tin, are some of the most widely used cancer chemotherapeutics.
76 ent blood-brain barrier (BBB) penetration of chemotherapeutics.
77 revealing a broad window for PfCRK4-targeted chemotherapeutics.
78 minent carcinogens(1,2) and important cancer chemotherapeutics(3,4).
79 will respond positively or negatively to two chemotherapeutics: 5-Fluorouracil and Gemcitabine.
80 for arsenic toxicity and for arsenic-focused chemotherapeutics across human populations.
81 poor and nonselective penetration of current chemotherapeutics across the plasma membranes of cancer
82                                      As most chemotherapeutics act on intracellular targets, this pre
83  potential mechanism by which p53-activating chemotherapeutics, acting upon p53-sufficient macrophage
84 , F. evanescens, and U. pinnatifida as novel chemotherapeutics against different types of cancer.
85 us for future structure-based drug design of chemotherapeutics against malaria.
86                       The range of available chemotherapeutics against Trypanosoma is limited, and th
87  an attractive target for the development of chemotherapeutics against tuberculosis.
88 DE cultures were exposed to standard-of-care chemotherapeutics agents for 2 weeks, attesting the abil
89                         Targeted delivery of chemotherapeutics aims to increase efficacy and lower to
90 e encapsulating ATP-responsive elements with chemotherapeutics and a liposome containing ATP was deve
91 r pathological role in neoplastic evasion of chemotherapeutics and antibiotics.
92 apies, including multiple chemotherapeutics, chemotherapeutics and biologics, chemotherapeutics and p
93  were treated with varying concentrations of chemotherapeutics and corresponding miRNAs.
94 ologically inhibit GATA2 in concert with AML chemotherapeutics and found this augmented cell killing
95 /AEG-1 mice displayed profound resistance to chemotherapeutics and growth factor deprivation with act
96 ess the spatial distribution of administered chemotherapeutics and metabolites with MALDI-imaging mas
97 le disease, but the combination of optimized chemotherapeutics and molecularly targeted agents holds
98 c cancer cell lines with clinically relevant chemotherapeutics and monitored proteolytic fragments re
99 concerning the sensitivity towards different chemotherapeutics and moreover, can obtain resistance, t
100 erapeutics, chemotherapeutics and biologics, chemotherapeutics and photodynamic therapy, and chemothe
101 associated with resistance to platinum-based chemotherapeutics and poly(ADP ribose) polymerase (PARP)
102 ns with standard-of-care treatments (such as chemotherapeutics and radiation), novel molecularly targ
103 motherapeutics and photodynamic therapy, and chemotherapeutics and radiotherapy.
104 on, increase accessibility for DNA targeting chemotherapeutics and reduce cytotoxic drug resistance.N
105 e-negative breast cancer xenograft tumors to chemotherapeutics and reduces metastasis.
106 izes KRAS-mutated leukemic cells to standard chemotherapeutics and represents a promising approach fo
107  cancer stem cells (CSCs), more resistant to chemotherapeutics and responsible of GBM recurrence; (iv
108 e platform vehicle that can encapsulate both chemotherapeutics and siRNA to achieve maximal efficacy
109 n and survival in response to UVB stress and chemotherapeutics and suggest that Sesn2 is oncogenic in
110                     With the advent of novel chemotherapeutics and targeted molecular, cellular, and
111 emically modified liposomes for loading with chemotherapeutics and targeting them for the transporter
112 ancer specificity of prodrugs from classical chemotherapeutics and the potency of mitotic kinase inhi
113 opulation of supportive BMDCs in response to chemotherapeutics and uncovered a new potential strategy
114 treated with rituximab, 34.5% with different chemotherapeutics, and 13.8% with corticosteroids only f
115 lonal antibodies, small molecule inhibitors, chemotherapeutics, and cell-based treatment strategies h
116 induced by environmental methylating agents, chemotherapeutics, and natural cellular methyl donors.
117 45 muM), the standard metallodrug used in CC chemotherapeutics, and our leading compound 14Ru was sho
118 CLs) are generated by endogenous sources and chemotherapeutics, and pose a threat to genome stability
119  responding to the threat; new knowledge and chemotherapeutics are being created to safeguard our fut
120                      Often the toxicities of chemotherapeutics are due to the induction of significan
121 ny human diseases, including cancer, wherein chemotherapeutics are exported from target cells by memb
122 esectable disease, locoregional and systemic chemotherapeutics are primary treatment options.
123         Single-nanoparticle (NP) combination chemotherapeutics are quickly emerging as attractive alt
124                                 DNA-damaging chemotherapeutics are widely used in cancer treatments,
125             Cisplatin and other DNA-damaging chemotherapeutics are widely used to treat a broad spect
126  inhibitors of sirtuins for potential use as chemotherapeutics as well as tools to modulate sirtuin a
127 A lesions caused by reactive metabolites and chemotherapeutics, as well as stable nucleoprotein compl
128 argeted herein for the controlled release of chemotherapeutics at the tumour site, while sparing heal
129 re are currently no effective antiflaviviral chemotherapeutics available for human use.
130  used for development of novel DNA-targeting chemotherapeutics based on benzo[c]quinolizinium derivat
131 stemic toxicities associated with modern day chemotherapeutics but also address resistance issues tha
132 TCF3-HLF ALL with resistance to conventional chemotherapeutics but sensitivity to glucocorticoids, an
133   Other options include observation or novel chemotherapeutics, but little guidance exists on selecti
134 er cells to PARP inhibitors and DNA-damaging chemotherapeutics by reducing expression of the genes in
135  cells, combining immunotherapy with certain chemotherapeutics can lead to increased efficacy compare
136                           Several front-line chemotherapeutics cause mitochondria-derived, oxidative
137    Acute treatment with replication-stalling chemotherapeutics causes reversal of replication forks.
138 of combination therapies, including multiple chemotherapeutics, chemotherapeutics and biologics, chem
139 ead to increased resistance to the frontline chemotherapeutics cisplatin and paclitaxel.
140 These NCP particles contain high payloads of chemotherapeutics cisplatin or cisplatin plus gemcitabin
141  presence of nontargeted chemicals including chemotherapeutics consistent with a local hospital waste
142 CAR inhibitors, in combination with existing chemotherapeutics, could therefore be used to attenuate
143                            Many antibiotics, chemotherapeutics, crop protection agents and food prese
144 c options that moves away from the expensive chemotherapeutics currently dominating the research clim
145                                    Aging and chemotherapeutics damage hematopoietic stem cells (HSCs)
146 l compound camptothecin (CPT) and the cancer chemotherapeutics derived from it, irinotecan and topote
147              To date, there are no effective chemotherapeutics despite a myriad of clinical trials.
148     Interestingly, radiation and antimitotic chemotherapeutics did not increase overall tumor burden
149                   Moreover, the investigated chemotherapeutics dose dependently induced vessel format
150 The change in impedance magnitude on flowing chemotherapeutics drugs measured at 12h for drug-suscept
151       Resistance to anthracyclines and other chemotherapeutics due to P-glycoprotein (pgp)-mediated e
152 drug resistance via lysosomes, the cytotoxic chemotherapeutics (e.g. DOX, daunorubicin, or vinblastin
153 into the organelle, thereby trapping certain chemotherapeutics (e.g. doxorubicin; DOX).
154                               Many cytotoxic chemotherapeutics elicit a proinflammatory response whic
155 he SK1-specific inhibitor SK1-I and standard chemotherapeutics, expression of CIB2 also sensitized ov
156                                              Chemotherapeutics fail to effectively treat tumors becau
157                               Many potential chemotherapeutics fail to reach patients.
158 stent with these observations, IFN-gamma and chemotherapeutics failed to activate autophagy in CLL pa
159 re are five clinically approved nanoparticle chemotherapeutics for cancer and many more under clinica
160 anomaterials show great potential to deliver chemotherapeutics for cancer treatment.
161 xifen and fulvestrant have been evaluated as chemotherapeutics for ovarian cancer, particularly in ca
162 ynamic abilities of porphyrinoids, can carry chemotherapeutics for synergistic modalities, and can be
163 of using truncated latrunculins as potential chemotherapeutics for the treatment of malaria.
164 model, with values similar to currently used chemotherapeutics for the treatment of solid tumors.
165 itargeted approaches rather than traditional chemotherapeutics for this disease.
166 ng strategy to increase the effectiveness of chemotherapeutics for treatment of solid tumors.
167       Furthermore, given that platinum-based chemotherapeutics form the frontline therapy for a broad
168 cause these membrane transporters remove the chemotherapeutics from the targeted cells.
169 administration of UPI peptide with cytotoxic chemotherapeutics further sustained tumor inhibition.
170 ing both naked and nanoparticle-encapsulated chemotherapeutics, genes, and radioisotopes.
171                  Use of traditional adjuvant chemotherapeutics has been challenged in clinical trials
172                                 Conventional chemotherapeutics have been developed into clinically us
173       Genotoxic agents such as radiation and chemotherapeutics have been shown to activate the Wnt/be
174           Short-chain fatty acids or certain chemotherapeutics have been used to induce EBV lytic-pha
175 s and resistances of kinases to DNA-damaging chemotherapeutics have not been possible, partially due
176            Nitrogen mustards, widely used as chemotherapeutics, have limited safety and efficacy.
177      Despite the broad use of platinum-based chemotherapeutics, identification of their full range of
178 t potent additivity or synergy with existing chemotherapeutics in animal models of cancer and may red
179            To investigate the enhancement of chemotherapeutics in cancer cells, high MGMT expressing
180                 We also sought regulation of chemotherapeutics in cancer microenvironment towards phe
181  they are ideally suited for the delivery of chemotherapeutics in cancer treatment.
182  B, and Janus kinase, which are activated by chemotherapeutics in epithelial cell-transitioned prosta
183 and reduced sensitivity to antiestrogens and chemotherapeutics in estrogen receptor alpha (ERalpha)-p
184  optimizing chemotherapeutic combinations or chemotherapeutics in novel delivery systems.
185          We conclude that the repurposing of chemotherapeutics in osteosarcoma by using an in vitro s
186 he immunostimulatory effects of conventional chemotherapeutics in the context of ICI-based immunother
187 loped for screening compounds for use as gut chemotherapeutics in the future.
188 in development in rats caused by widely used chemotherapeutics in the taxane (paclitaxel), platinum-c
189  a useful strategy for rescuing DNA-damaging chemotherapeutics in TP53-mutant cancers.
190  to predict cytotoxic response of cancers to chemotherapeutics in vivo.
191                Melanomas resist conventional chemotherapeutics, in part, through intrinsic disrespect
192  single agents and in combination with other chemotherapeutics, in several subtypes of breast cancer
193 shed targets of some of the most widely used chemotherapeutics, including dihydrofolate reductase, th
194 s induced synthetic lethality with genotoxic chemotherapeutics, including PARP inhibitors, and nongen
195      In response to the challenges of cancer chemotherapeutics, including poor physicochemical proper
196  protection against the cytotoxic actions of chemotherapeutics, including reductions in oxidative str
197                        It is known that many chemotherapeutics induce cellular apoptosis over hours t
198 tically, we observe that mTOR inhibitors and chemotherapeutics induce translational activation of a s
199 cytes mediate the resistance to DNA-damaging chemotherapeutics induced by two platinum-induced fatty
200 sm constitutes a rich source of antibiotics, chemotherapeutics, insecticides and other high-value che
201        Unfortunately, the development of new chemotherapeutics is a long and costly process.
202 a induced by inflammation, nerve injury, and chemotherapeutics is abolished in mice lacking the neuro
203                                              Chemotherapeutics is available; however, rapid emergence
204              Although their translation into chemotherapeutics is complex, collaborative programs con
205                Although a vast repertoire of chemotherapeutics is currently available for treating ca
206 e clinical use of multiple classes of cancer chemotherapeutics is limited by irreversible, dose-depen
207 r challenge in the clinical use of cytotoxic chemotherapeutics is maximizing efficacy in tumors while
208 fective and safer treatments, especially non-chemotherapeutics, is needed for patients with Waldenstr
209 here Pgp-mediated lysosomal sequestration of chemotherapeutics leads to MDR that is amenable to thera
210               However, drawbacks for current chemotherapeutics lie in the fact that they develop resi
211                           The pitfall of all chemotherapeutics lies in drug resistance and the severe
212 activity when combined with non-ICD inducing chemotherapeutics like cisplatin.
213 e bladder condition associated with systemic chemotherapeutics, like cyclophosphomide.
214 ations, including the mitochondria-targeting chemotherapeutics lonidamine and alpha-tocopheryl succin
215                   These results suggest that chemotherapeutics may be stimulative to cancer stem cell
216  is considered a crucial target for platinum chemotherapeutics, metallodrug-DNA binding studies domin
217  (CLL) involve a combination of conventional chemotherapeutics, monoclonal antibodies, and targeted s
218                                 Conventional chemotherapeutics nonselectively kill all rapidly dividi
219                                       Cancer chemotherapeutics often fail to reach all diseased cells
220       Ototoxic drugs, such as platinum-based chemotherapeutics, often lead to permanent hearing loss
221 e storm or through direct effects of certain chemotherapeutics on stromal and/or immune cells, the mo
222     Combination therapy can include multiple chemotherapeutics or combinations of chemotherapeutics w
223 plementary immunotherapeutic strategies with chemotherapeutics or other oncogenic pathway inhibitors.
224 ingle-agent or in combination therapies with chemotherapeutics or radiotherapy.
225  drug allergies to two common platinum-based chemotherapeutics, oxaliplatin and carboplatin.
226 r-1 (NCP-1) for simultaneous delivery of two chemotherapeutics, oxaliplatin and gemcitabine monophosp
227 rs for encapsulating 17-AAG along with other chemotherapeutics, providing an opportunity to overcome
228 pressive cancer microenvironment and include chemotherapeutics, radiation, indoleamine 2,3-dioxygenas
229          The efficient delivery of liposomal chemotherapeutics relies, however, on the enhanced perme
230            Targeted and on-demand release of chemotherapeutics remains a challenge.
231 in synergistic combination with conventional chemotherapeutics, represents an alternative approach to
232 eatment of tumor-bearing mice with different chemotherapeutics resulted in a three- to 10-fold increa
233                             While all tested chemotherapeutics revealed high potency for apoptosis in
234 ered in combination with existing first-line chemotherapeutics rifampicin and isoniazid.
235 ge of cellular interactions of Pt(II) -based chemotherapeutics, robust and efficient methods to track
236                          Unlike conventional chemotherapeutics, SCNPs cause immunogenic cell death or
237 oside levels, and co-treatment with standard chemotherapeutics sensitized cells to mitochondrial memb
238  intervention studies using standard-of-care chemotherapeutics showed the value of this model in dete
239 t in response to UV irradiation or genotoxic chemotherapeutics, SOX9 is actively degraded in various
240 e show that DNA double strand break-inducing chemotherapeutics stimulate CycG2 expression and correla
241 erful platform for the development of cancer chemotherapeutics, stimulated by the Hoffmann-La Roche d
242 nd is differentiated from other DNA-targeted chemotherapeutics such as cisplatin by its potency, cell
243 e that is resistant to many standard of care chemotherapeutics such as cisplatin.
244 ingly, these cells are not only resistant to chemotherapeutics such as doxorubicin, but also are stim
245 rse range of substrates includes many common chemotherapeutics such as imatinib, doxorubicin, and mit
246                                 In contrast, chemotherapeutics such as paclitaxel and cisplatin were
247 e oleandrin as a coadjuvant drug to standard chemotherapeutics such as temozolomide.
248            Topo II can be poisoned by common chemotherapeutics (such as doxorubicin and etoposide), l
249 lexes as viable alternatives to conventional chemotherapeutics, such as cisplatin.
250                     Background Anthracycline chemotherapeutics, such as doxorubicin, are used widely
251 perature-sensitive liposomal formulations of chemotherapeutics, such as doxorubicin, can achieve loca
252                    At odds with conventional chemotherapeutics, targeted anticancer agents are design
253                  Drug resistance to platinum chemotherapeutics targeting DNA often involves abrogatio
254 e-clinical rapid in vivo validation of novel chemotherapeutics targeting early lesions in patients fo
255 rom a drug screen consisting of conventional chemotherapeutics tested on patient-derived cell lines.
256 set were more resistant than non-SP cells to chemotherapeutics that are effluxed by MDR1.
257 t some Food and Drug Administration-approved chemotherapeutics that can inhibit the growth of Drosoph
258 late BRCA2-deficient cancer cell response to chemotherapeutics that cause fork degradation.BRCA prote
259 novel nanocarrier for the co-delivery of two chemotherapeutics that have distinctive mechanisms of ac
260 hat can be exploited for design of potential chemotherapeutics that specifically inhibit CatD and rel
261 tes and provide the rationale for developing chemotherapeutics that stabilize the covalent Tdp1-DNA i
262                                              Chemotherapeutics that target influenza virus are availa
263  concerns about potential cardiotoxicity for chemotherapeutics that target MCL-1.
264 stic insights could aid development of novel chemotherapeutics that target pathological changes in th
265 le for RNF168 in the response to anti-cancer chemotherapeutics that target TOP2.
266 eatment for childhood leukemia, but like all chemotherapeutics, their use is limited by inherent or a
267                                        Among chemotherapeutics, thiopurines are key drugs in ALL comb
268                Tumours develop resistance to chemotherapeutics through a variety of mechanisms, with
269 f chikungunya, supporting the development of chemotherapeutics through drug discovery and design targ
270 fficult to achieve efficient distribution of chemotherapeutics throughout the tumor.
271  concept for a method to enhance delivery of chemotherapeutics to breast cancer cells within the bone
272 l approach to selectively target and deliver chemotherapeutics to CTCs in the bloodstream.
273 e the tendency of topoisomerase II-targeting chemotherapeutics to generate secondary malignancies.
274 rapy or combination therapy with established chemotherapeutics to improve treatment outcomes in CRC p
275 igate the potential clinical use of low dose chemotherapeutics to induce differentiation instead of c
276 at limit the access of potentially effective chemotherapeutics to metastatic lesions.
277 tumour burden after the targeted delivery of chemotherapeutics to the tumours.
278 practical method for delivering both RNA and chemotherapeutics to tumor cells and expands existing na
279 ive vaccines, more reliable diagnostics, and chemotherapeutics, tuberculosis remains a threat to glob
280                  After exposure to cytotoxic chemotherapeutics, tumor cells alter their translatome t
281  poisons are one of the most common class of chemotherapeutics used in cancer.
282  drugs constitute a major class of cytotoxic chemotherapeutics used in the clinic, killing cancer cel
283 nhibitors can (re)sensitize cancer cells for chemotherapeutics via "epigenetic priming".
284 enoid indole alkaloids (TIAs), including the chemotherapeutics, vincristine and vinblastine.
285                 Efficacy of standard-of-care chemotherapeutics was assessed by measuring cell viabili
286  form an integrated detoxification unit with chemotherapeutics, we assessed whether these proteins co
287 c bifunctional silyl ether (ABS) prodrugs of chemotherapeutics were synthesized and incorporated with
288 NA damage induction by ionizing radiation or chemotherapeutics, whereas cancer cells typically remain
289 re, therefore, critical for developing novel chemotherapeutics, which are currently limited because o
290 o the resistance of melanoma to DNA-damaging chemotherapeutics, which is one of the major obstacles t
291  sensitivity of cancer cells to DNA-damaging chemotherapeutics, which may induce certain repair genes
292  the effectiveness of existing drugs such as chemotherapeutics, while simultaneously enabling the del
293  obtain resistance, the development of novel chemotherapeutics with a broad activity spectrum, high e
294 r findings is that supplementing traditional chemotherapeutics with anti-inflammatories may reduce tu
295 to improve the delivery and effectiveness of chemotherapeutics with low molecular weights, but it rem
296 ultiple chemotherapeutics or combinations of chemotherapeutics with other treatment modalities like s
297  carboxylated gallium corroles are promising chemotherapeutics with the advantage that they also can
298 pies involving various oncolytic viruses and chemotherapeutics, with the goal of inducing tumor-speci
299  and eradicated, at which point conventional chemotherapeutics would be sufficient to eliminate the r
300  agents as diagnostic probes mirrors that of chemotherapeutics; yet despite an increasing number of P

 
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