ライフサイエンスコーパス: chemotherapeutic

1 genome (e.g., by irradiation or radiomimetic chemotherapeutics).

2 lve the co-delivery of a Pgp inhibitor and a chemotherapeutic.

3 l concentration and sustained release of the chemotherapeutic.

4 umor penetration and therapeutic efficacy of chemotherapeutics.

5 hat they have emerged as excellent potential chemotherapeutics.

6 and bound to the three structurally distinct chemotherapeutics.

7 ion of IL-8 pathway to the class of platinum chemotherapeutics.

8 in tumor, can evaluate the effectiveness of chemotherapeutics.

9 ntifolates that could potentially be used as chemotherapeutics.

10 ia in order to increase the effectiveness of chemotherapeutics.

11 s can potentially improve the selectivity of chemotherapeutics.

12 eric radiation, environmental chemicals, and chemotherapeutics.

13 ICD can be induced by treatment with chemotherapeutics.

14 ies and DNA-damaging agents that are used as chemotherapeutics.

15 latinum drugs, which are among the most used chemotherapeutics.

16 signaling and open the door to new selective chemotherapeutics.

17 pt host-parasite interactions, or to deliver chemotherapeutics.

18 ide range of imidazole-based antibiotics and chemotherapeutics.

19 will respond positively or negatively to two chemotherapeutics: 5-Fluorouracil and Gemcitabine.

20 for arsenic toxicity and for arsenic-focused chemotherapeutics across human populations.

21 poor and nonselective penetration of current chemotherapeutics across the plasma membranes of cancer

22 As most chemotherapeutics act on intracellular targets, this pre

23 adiation but also specifically activates its chemotherapeutic action in hypoxic tumor microenvironmen

24 The chemotherapeutic action of AraC derives from its ability

25 nds are known to exhibit chemopreventive and chemotherapeutic activity; moreover, these compounds are

26 herapy priming preceded a single activatable chemotherapeutic administration.

27 Despite surgical and chemotherapeutic advances over the past few decades, the

28 has the potential to serve as an anticancer chemotherapeutic against several Hh-dependent malignanci

29 The range of available chemotherapeutics against Trypanosoma is limited, and th

30 Furthermore, antitumor activity of a chemotherapeutic agent (doxorubicin) and immune checkpoi

31 Blocking cell proliferation via a chemotherapeutic agent 5-fluorouracil (5-Fu) eliminated

32 osphorylation of its subunit p65/RelA by the chemotherapeutic agent adriamycin (ADR), but not NF-kapp

33 the promising potential of this complex as a chemotherapeutic agent against cancer.

34 al foundation to establish it as a promising chemotherapeutic agent against cancer.

35 tion of the Notch inhibitor GSI-XII with the chemotherapeutic agent Ara-C lowered bone marrow leukemi

36 hich is highly expressed in tumours, and the chemotherapeutic agent camptothecin) that self-assemble

37 The chemotherapeutic agent cisplatin is renowned for its oto

38 air the interstrand crosslinks caused by the chemotherapeutic agent cisplatin.

39 f chemotherapy when it was combined with the chemotherapeutic agent Doxil, resulting in some longer-t

40 .05) and exhibited decreased response to the chemotherapeutic agent doxorubicin (DOX) (P < 0.01).

41 n be stabilized by TOP2 poisons, such as the chemotherapeutic agent etoposide (ETO).

42 e glucocorticoid dexamethasone (DEX) and the chemotherapeutic agent etoposide.

43 h gemcitabine (Gem), a first- or second-line chemotherapeutic agent for PDAC treatment.

44 Doxorubicin is a widely used chemotherapeutic agent that causes dose-dependent cardio

45 cancer cells more sensitive to paclitaxel, a chemotherapeutic agent that induces ER stress-mediated c

46 smart prodrug, delivering a highly cytotoxic chemotherapeutic agent to cancer tumors.

47 Doxorubicin, a brain-impermeable chemotherapeutic agent, is also readily and selectively

48 The platinum-based chemotherapeutic agent, oxaliplatin, is used to treat ad

49 Vincristine, a widely used chemotherapeutic agent, produces painful peripheral neur

50 B-IL-17RB axis protected leukemic cells from chemotherapeutic agent-induced apoptotic effects.

51 Cs to cisplatin, a prototypic platinum-based chemotherapeutic agent.

52 e before and 48 hours after treatment with a chemotherapeutic agent.

53 vely resensitized the p53-null cells to this chemotherapeutic agent.

54 f resistance to gemcitabine, a commonly used chemotherapeutic agent.

55 lability limits its further development as a chemotherapeutic agent.

56 onal population to cisplatin, a DNA-damaging chemotherapeutic agent.

57 lammatory cell death induced by SMAC-mimetic chemotherapeutic agents (small-molecule activators of th

58 mary and established cancer cells to current chemotherapeutic agents and an anti-VEGF antibody in mTi

59 s an ABC exporter that extrudes a variety of chemotherapeutic agents and native substrates.

60 ny of the current and newly developed cancer chemotherapeutic agents are nephrotoxic and can promote

61 , which reduces efficacy, and small-molecule chemotherapeutic agents can be absorbed through the urot

62 in patients receiving immunotherapeutic and chemotherapeutic agents creates a pressing clinical need

63 Several chemotherapeutic agents delivered using nanocarriers suc

64 ion, and the potential for developing cancer chemotherapeutic agents discussed in each case.

65 t the difference in mechanisms of actions of chemotherapeutic agents elicit distinct effects on the c

66 esistant neoplasms where it effluxes various chemotherapeutic agents from cells.

67 Anti-cancer chemotherapeutic agents have limited access into the bra

68 eoside analogs DHAs with SIRT6 inhibitors or chemotherapeutic agents in AML due to the role of SIRT6

69 xicity of super-therapeutic acetaminophen or chemotherapeutic agents in children, limited data exists

70 y (MAb) therapy has been combined with other chemotherapeutic agents in human cancer trials.

71 allenges in achieving high concentrations of chemotherapeutic agents in the central nervous system.

72 h cisplatin is one of the most commonly used chemotherapeutic agents in the treatment of non-small ce

73 imilarly, PVOD can develop after exposure to chemotherapeutic agents in the treatment of solid and he

74 tly increase the growth inhibitory effect of chemotherapeutic agents in vitro and in vivo.

75 tudy, we found that treating TNBC cells with chemotherapeutic agents led to a significant accumulatio

76 rgeted anti-cancer compounds and traditional chemotherapeutic agents on the expression of PD-L1 in fo

77 In early-phase clinical trials, chemotherapeutic agents targeting cancer-associated fibr

78 H and cancer have identical characteristics, chemotherapeutic agents targeting the POH-related fibrob

79 pancreatic cancer remains dismal and potent chemotherapeutic agents that selectively target this can

80 he potential to be combined with established chemotherapeutic agents to change the paradigm of NMIBC

81 have been effective for delivery of various chemotherapeutic agents used to combat cancer.

82 necessitated the rapid development of newer chemotherapeutic agents with novel mechanisms of action.

83 rapy dose and exposed cardiac volume, select chemotherapeutic agents, and age at exposure on risk for

84 y injury, whether due to ischemic insults or chemotherapeutic agents, is exacerbated by inflammation,

85 tolerance against unrelated standard-of-care chemotherapeutic agents, such as anthracyclines.

86 rogression, YAP, AXL, and SRC signaling, and chemotherapeutic agents.

87 owth and sensitizes p53-compromised cells to chemotherapeutic agents.

88 nsitize cancer cells to ferroptosis-inducing chemotherapeutic agents.

89 atinum(II) compounds are a critical class of chemotherapeutic agents.

90 ncreasingly prevalent drug class utilized as chemotherapeutic agents.

91 cological synergisms between FPPa-OmoMYC and chemotherapeutic agents.

92 e survival also of cancer cells treated with chemotherapeutic agents.

93 cells were on the average more resistant to chemotherapeutic agents.

94 r exposure to the common inciting trigger of chemotherapeutic agents.

95 gene confer hypersensitivity to DNA-damaging chemotherapeutic agents.

96 ar, kidney disease can arise from the use of chemotherapeutic agents.

97 ir sequential administration after available chemotherapeutic agents.

98 re frequently insensitive to traditional AML chemotherapeutic agents.

99 p mediate resistance of pancreatic tumors to chemotherapeutic agents.

100 DE cultures were exposed to standard-of-care chemotherapeutics agents for 2 weeks, attesting the abil

101 Targeted delivery of chemotherapeutics aims to increase efficacy and lower to

102 daunorubicin-resistant AML cell line to the chemotherapeutic and >100-fold dose reduction of cytarab

103 entify PDLIM2-independent PD-L1 induction by chemotherapeutic and epigenetic drugs as another mechani

104 scape protective immune responses induced by chemotherapeutic and immunotherapeutic drugs, thereby pr

105 r pathological role in neoplastic evasion of chemotherapeutics and antibiotics.

106 were treated with varying concentrations of chemotherapeutics and corresponding miRNAs.

107 on, increase accessibility for DNA targeting chemotherapeutics and reduce cytotoxic drug resistance.N

108 e-negative breast cancer xenograft tumors to chemotherapeutics and reduces metastasis.

109 ancer specificity of prodrugs from classical chemotherapeutics and the potency of mitotic kinase inhi

110 Novel chemoprophylactic and chemotherapeutic antimalarials are needed to support the

111 programs in AML that identify it as a novel chemotherapeutic approach to selectively target human LS

112 iated BBB opening, which may ameliorate DIPG chemotherapeutic approaches in children.

113 m for studying tumor biology and for testing chemotherapeutic approaches tailored to genomic characte

114 esectable disease, locoregional and systemic chemotherapeutics are primary treatment options.

115 DNA-damaging chemotherapeutics are widely used in cancer treatments,

116 network, which enables tumor cells to resist chemotherapeutic as well as metastatic stress.

117 A lesions caused by reactive metabolites and chemotherapeutics, as well as stable nucleoprotein compl

118 A chemotherapeutic assay was conducted to examine dose-dep

119 ion, thereby allowing CDCP1+ CSCs to survive chemotherapeutic attack.

120 ity of AML cells to cytarabine, an essential chemotherapeutic backbone in the therapy of AML.

121 genous alpha7 nAChRs, while a combination of chemotherapeutic Bcl2-inhibitors suppressed neuronal alp

122 y serve as a tailor-made approach to enhance chemotherapeutic benefits in other cancer types.

123 stemic toxicities associated with modern day chemotherapeutics but also address resistance issues tha

124 er cells to PARP inhibitors and DNA-damaging chemotherapeutics by reducing expression of the genes in

125 cells, combining immunotherapy with certain chemotherapeutics can lead to increased efficacy compare

126 Acute treatment with replication-stalling chemotherapeutics causes reversal of replication forks.

127 ated in NSCLC cells after treatment with the chemotherapeutic cisplatin and that overexpression of SO

128 nt to stalled RFs promoted resistance to the chemotherapeutic cisplatin.

129 ead to increased resistance to the frontline chemotherapeutics cisplatin and paclitaxel.

130 ia systemic delivery of an immunostimulatory chemotherapeutic combination in nanoscale coordination p

131 esigning superior synergies while optimizing chemotherapeutic combinations or chemotherapeutics in no

132 anodiscs, revealing a single molecule of the chemotherapeutic compound paclitaxel (Taxol) bound in a

133 tein partners that potentiate the effects of chemotherapeutic compounds and improve cancer treatment

134 itors after application of taxanes (or other chemotherapeutic compounds) strongly potentiates the ant

135 al analyses reveal the binding mode of three chemotherapeutic compounds, demonstrate how these molecu

136 he limited efficacy of existing FDA-approved chemotherapeutic compounds.

137 anism makes these complexes highly promising chemotherapeutic cytotoxicity leads.

138 anin family member, CD82, in response to the chemotherapeutic, daunorubicin.

139 While repeated chemotherapeutic delivery reduced local viable tumor, th

140 The use of nanovesicles (NVs) as chemotherapeutic delivery vehicles has been recently pro

141 To date, there are no effective chemotherapeutics despite a myriad of clinical trials.

142 Interestingly, radiation and antimitotic chemotherapeutics did not increase overall tumor burden

143 coming the Pgp resistance by co-delivering a chemotherapeutic, Doxorubicin (Dox), with a Pgp inhibito

144 ffectively enhances their sensitivity to the chemotherapeutic drug 5-FU.

145 Vincristine is a core chemotherapeutic drug administered to pediatric acute ly

146 In this work, we designed a new chemotherapeutic drug candidate against cancer, namely,

147 l structures available for this enzyme show, chemotherapeutic drug design has centered on stopping th

148 l lines display cross-resistance against the chemotherapeutic drug docetaxel due to MCL1 upregulation

149 fically, PDT in conjugation with widely used chemotherapeutic drug doxorubicin (Dox) proved effective

150 odel, drug eluding beads (DEBs) carrying the chemotherapeutic drug doxorubicin are located at destroy

151 scaffold acts as a container to encapsulate chemotherapeutic drug doxorubicin.

152 Multidrug resistance-1 (MDR1) acts as a chemotherapeutic drug efflux pump in tumor cells, althou

153 ng mice compared to that with the first-line chemotherapeutic drug gemcitabine.

154 peptide that can be conjugated directly to a chemotherapeutic drug or to nanoparticles for targeted d

155 been widely investigated for spatiotemporal chemotherapeutic drug release applications for cancer ch

156 ently increased GB cell death induced by the chemotherapeutic drug temozolomide.

157 Bleomycin is a powerful chemotherapeutic drug used to treat a variety of cancers

158 5-Fluorouracil (5-FU) is a chemotherapeutic drug widely used to treat colorectal ca

159 when the Pt NPs are loaded in vitro with the chemotherapeutic drug, daunorubicin, and the formulation

160 of tumor-bearing mice were injected with the chemotherapeutic drug, vincristine, alone or in combinat

161 Oxaliplatin, a platinum-based chemotherapeutic drug, which is used as first-line treat

162 Our present work thus reveals a chemotherapeutic drug-resistant cancer cell vulnerabilit

163 ptive response in cancer and particularly in chemotherapeutic drug-resistant cells.

164 well as in reactive oxygen species (ROS)- or chemotherapeutic drug-treated cell lines.

165 decrease in flux following treatment with a chemotherapeutic drug.

166 .05-0.001) potentiated the response to three chemotherapeutic drugs (vincristine, etoposide and metho

167 s 31 CAAs that robustly alter response to 56 chemotherapeutic drugs across cell lines representing 17

168 icity after clinically relevant exposures to chemotherapeutic drugs and ionizing radiation, as well a

169 There are currently no effective chemotherapeutic drugs approved for the treatment of dif

170 ticity induced by inflammatory mediators and chemotherapeutic drugs but inhibiting this pathway does

171 enhance the resistance of OvCa cells against chemotherapeutic drugs by activating the Akt pathway.

172 may play roles in modulating the efficacy of chemotherapeutic drugs by modulating DNA repair pathways

173 cer treatment, recent evidence suggests that chemotherapeutic drugs can promote metastasis through po

174 ith high specificity because many classes of chemotherapeutic drugs can themselves cause myocardial d

175 e treated with various concentrations of the chemotherapeutic drugs cyclophosphamide, gemcitabine (GE

176 Since the repeated administration of most chemotherapeutic drugs develops chemoresistance and seve

177 Given that most chemotherapeutic drugs disrupt ER homeostasis as part of

178 sive pediatric cancer for which no effective chemotherapeutic drugs exist.

179 of nanocarriers as drug delivery system for chemotherapeutic drugs has become a research hotspot in

180 mbrane, resulting in inadequate retention of chemotherapeutic drugs in cancer cells.

181 success rate of different nanoparticle based chemotherapeutic drugs is presented.

182 Site-specifically released chemotherapeutic drugs killed cancer cells surviving fro

183 may be ideal as a combination treatment with chemotherapeutic drugs or other immunotherapies.

184 show that activation of DNA-PKcs and ATM by chemotherapeutic drugs promotes NF-kappaB activity, with

185 n pathways that could be targeted by current chemotherapeutic drugs such as cytarabine.

186 ormally reversible, they can be "trapped" by chemotherapeutic drugs such as etoposide and subsequentl

187 Stabilization of this intermediate by chemotherapeutic drugs such as etoposide leads to persis

188 are generally more resistant to conventional chemotherapeutic drugs than are B-cell ALL blasts.

189 vestigate A3B expression upon treatment with chemotherapeutic drugs that activate p53, including 5-fl

190 s for understanding the mutagenic effects of chemotherapeutic drugs that stabilize the Top1cc.

191 tion and are relevant to the clinical use of chemotherapeutic drugs that target Top2.

192 Chemotherapeutic drugs triggered a positive feedback loo

193 f a broad range of bioactive cargos, such as chemotherapeutic drugs, anti-inflammatory agents, antiba

194 and physical DNA insults; oxidative stress, chemotherapeutic drugs, environmental pollutants, and su

195 Using three common chemotherapeutic drugs, gemcitabine (GEM), irinotecan (I

196 hen used in combination with clinically used chemotherapeutic drugs, including temozolomide, reverses

197 as well as xenobiotics including therapeutic/chemotherapeutic drugs, nutrients, carcinogens, and toxi

198 didate for combination therapy with existing chemotherapeutic drugs.

199 PCa tumors and for the targeted delivery of chemotherapeutic drugs.

200 and to evaluate and predict the efficacy of chemotherapeutic drugs.

201 nherent drawbacks, there is a search for new chemotherapeutic drugs.

202 te member involved in the cellular efflux of chemotherapeutic drugs.

203 optosis, as well as enhanced accumulation of chemotherapeutic drugs.

204 s associated with systemic administration of chemotherapeutic drugs.

205 in reduced accessibility to immune cells and chemotherapeutic drugs.

206 llowing real-time monitoring of responses to chemotherapeutic drugs.

207 confers resistance to ionizing radiation and chemotherapeutic drugs.

208 s and improve the pharmacokinetic profile of chemotherapeutic drugs.

209 to structurally- and functionally-divergent chemotherapeutic drugs.

210 rough apoptosis induction in comparison with chemotherapeutic drugs.

211 leading to chemoresistance and a diminished chemotherapeutic effect on liver cancer.

212 in vitro tumor models are more predictive of chemotherapeutic effectiveness than 2D cultures, and thu

213 To enhance the chemotherapeutic efficacy and oxidative phosphorylation

214 sis for access to valuable precursors of the chemotherapeutic etoposide.

215 Many potential chemotherapeutics fail to reach patients.

216 ynamic abilities of porphyrinoids, can carry chemotherapeutics for synergistic modalities, and can be

217 ng strategy to increase the effectiveness of chemotherapeutics for treatment of solid tumors.

218 The enabling concept is the use of a new chemotherapeutic formulation in which chemotherapy drugs

219 reconstructions, radiotherapy treatment and chemotherapeutic guidelines.

220 Conventional chemotherapeutics have been developed into clinically us

221 Genotoxic agents such as radiation and chemotherapeutics have been shown to activate the Wnt/be

222 s and resistances of kinases to DNA-damaging chemotherapeutics have not been possible, partially due

223 To investigate the enhancement of chemotherapeutics in cancer cells, high MGMT expressing

224 optimizing chemotherapeutic combinations or chemotherapeutics in novel delivery systems.

225 he immunostimulatory effects of conventional chemotherapeutics in the context of ICI-based immunother

226 a useful strategy for rescuing DNA-damaging chemotherapeutics in TP53-mutant cancers.

227 tically, we observe that mTOR inhibitors and chemotherapeutics induce translational activation of a s

228 lism which protects breast cancer cells from chemotherapeutic-induced DNA damage.

229 sts and nephrologists to predict and prevent chemotherapeutic-induced nephrotoxicity.

230 findings may have profound implications for chemotherapeutic inefficiency and cancer relapse.

231 activity when combined with non-ICD inducing chemotherapeutics like cisplatin.

232 ong-term vascular access for the delivery of chemotherapeutic medications.

233 for either targeted and sustained release of chemotherapeutic nanodrug for liver cancer treatment, or

234 also used to measure AP sites induced by the chemotherapeutic nitrogen mustard in vitro.

235 atment of glioblastoma and is now becoming a chemotherapeutic option in patients diagnosed with high-

236 hind the blood-brain barrier severely limits chemotherapeutic options.

237 Drug conjugates are chemotherapeutic or cytotoxic agents covalently linked t

238 plementary immunotherapeutic strategies with chemotherapeutics or other oncogenic pathway inhibitors.

239 crobial enzyme inhibitors can improve cancer chemotherapeutic outcomes by protecting the gut epitheli

240 drug allergies to two common platinum-based chemotherapeutics, oxaliplatin and carboplatin.

241 These data indicate that the chemotherapeutic paclitaxel concurrently affects the gut

242 st HER2-positive cells; incorporation of the chemotherapeutic paclitaxel into this targeted carrier e

243 When loaded with a chemotherapeutic payload (i.e., doxorubicin), these cell

244 Resistance development to one chemotherapeutic reagent leads frequently to acquired to

245 Furthermore, patient selection, optimal chemotherapeutic regimen and immunological changes assoc

246 cautioned in cancer patients treated with a chemotherapeutic regimen containing cisplatin.

247 A multidrug chemotherapeutic regimen FOL-F-IRIN-OX (combination of 5

248 ytarabine, melphalan)+antithymocyte globulin chemotherapeutic regimen.

249 Cisplatin-based chemotherapeutic regimens are frequently used for treatm

250 Chemotherapeutic regimens for ovarian cancer often inclu

251 As many the chemotherapeutic regimens have adverse side effects and

252 High-intensity chemotherapeutic regimens have considerably improved ove

253 ess resistance issues that are plaguing many chemotherapeutic regimens.

254 have fewer toxic effects than high-intensity chemotherapeutic regimens.

255 Targeted and on-demand release of chemotherapeutics remains a challenge.

256 s their growth, proliferation, invasiveness, chemotherapeutic resistance and poor therapeutic respons

257 cell cycle delays are sufficient to increase chemotherapeutic resistance in euploid cells.

258 The emerging importance of Mcl-1 protein in chemotherapeutic resistance makes it a high priority the

259 ncing of clonal cell isolates that developed chemotherapeutic resistance to show that chromothripsis

260 c malignancy, frequently relapses because of chemotherapeutic resistance.

261 it has not been evaluated in the context of chemotherapeutic resistance.

262 ous human lung cancer cell lines, as well as chemotherapeutic-resistant patient-derived lung cancer c

263 y shows how a p53-responsive lncRNA mediates chemotherapeutic response by modulating nuclear p53 path

264 ivity to cisplatin and dramatically improved chemotherapeutic response in a highly drug-resistant mou

265 a unique strategy for altering and enhancing chemotherapeutic response.

266 ors and identifying epigenetic modulators of chemotherapeutic responses.

267 Unlike conventional chemotherapeutics, SCNPs cause immunogenic cell death or

268 armacotyping to guide postoperative adjuvant chemotherapeutic selection.

269 typed to derive a population distribution of chemotherapeutic sensitivity at our center.

270 oside levels, and co-treatment with standard chemotherapeutics sensitized cells to mitochondrial memb

271 Several chemotherapeutic strategies have been developed for dise

272 Furthermore, chemotherapeutic stress-induced inflammatory responses w

273 (TNBC) cells subjected to environmental and chemotherapeutic stresses commonly faced by TNBC cells t

274 Background Anthracycline chemotherapeutics, such as doxorubicin, are used widely

275 d 65 (34%) patients, with 36 (19%) requiring chemotherapeutic switch before long-course CRT and subse

276 lete metabolic response, or consideration of chemotherapeutic switch in order to achieve these factor

277 t neoplasms has led to Ras being a desirable chemotherapeutic target.

278 supporting the strategy of using Rh-PPO as a chemotherapeutic targeted to MMR-deficient cancers.

279 At odds with conventional chemotherapeutics, targeted anticancer agents are design

280 Drug resistance to platinum chemotherapeutics targeting DNA often involves abrogatio

281 e-clinical rapid in vivo validation of novel chemotherapeutics targeting early lesions in patients fo

282 or microenvironment mechanics and may reveal chemotherapeutic targets for cancer.

283 itize MB cells to a well-known and tolerated chemotherapeutic, temozolomide (TMZ).

284 rom a drug screen consisting of conventional chemotherapeutics tested on patient-derived cell lines.

285 Doxorubicin is an anthracycline-based chemotherapeutic that causes myotoxicity with symptoms p

286 hat can be exploited for design of potential chemotherapeutics that specifically inhibit CatD and rel

287 trials, and temozolomide is a commonly used chemotherapeutic, this approach is clinically actionable

288 general, the developed approach enables the chemotherapeutic to overcome both BBB and multidrug resi

289 rapy or combination therapy with established chemotherapeutics to improve treatment outcomes in CRC p

290 tumour burden after the targeted delivery of chemotherapeutics to the tumours.

291 individualized disease, predicting the best chemotherapeutic treatment for individual patients can b

292 o try to understand the relationship between chemotherapeutic treatment of cancer and the immune syst

293 repertoire of methods for the detection and chemotherapeutic treatment of prostate cancer (PCa) is c

294 uropathy incidence during the early stage of chemotherapeutic treatment.

295 due to p53 mutations and are insensitive to chemotherapeutic treatments that activate p53.

296 rs remaining after completion of traditional chemotherapeutic treatments.

297 vated ISG15 levels sensitize cells to cancer chemotherapeutic treatments.

298 poisons are one of the most common class of chemotherapeutics used in cancer.

299 nhibitors can (re)sensitize cancer cells for chemotherapeutics via "epigenetic priming".

300 Efficacy of standard-of-care chemotherapeutics was assessed by measuring cell viabili