ライフサイエンスコーパス: cardiotoxicity

1 se-dependent, and sometimes life-threatening cardiotoxicity.

2 es, and response to heart failure therapy of cardiotoxicity.

3 the progression of subclinical and clinical cardiotoxicity.

4 nd 11 required hospitalization for suspected cardiotoxicity.

5 ystematic monitoring of hepatic toxicity and cardiotoxicity.

6 2) increment) were independent correlates of cardiotoxicity.

7 ty of CRC cells and to reduce DOX-associated cardiotoxicity.

8 hout causing significant body weight loss or cardiotoxicity.

9 in the pathogenesis of chemotherapy-induced cardiotoxicity.

10 P18 uptake in a mouse model of anthracycline cardiotoxicity.

11 help to explain and predict Kv11.1-mediated cardiotoxicity.

12 iable strategy to mitigate acute ADR induced cardiotoxicity.

13 e as a mechanistic indicator for Dox-induced cardiotoxicity.

14 d clinical protocols to prevent irreversible cardiotoxicity.

15 ermining the mechanism of sorafenib-mediated cardiotoxicity.

16 to clinical symptoms of acute anthracycline cardiotoxicity.

17 arget molecule to combat doxorubicin-induced cardiotoxicity.

18 lassify patients at risk for therapy-induced cardiotoxicity.

19 tion, and treatment of anthracycline-related cardiotoxicity.

20 t doxorubicin is limited by life-threatening cardiotoxicity.

21 agents to mitigate oxidative stress-induced cardiotoxicity.

22 itical mechanism by which doxorubicin causes cardiotoxicity.

23 ochondria-derived, oxidative stress-mediated cardiotoxicity.

24 nd improves cardiac function in DOXO-induced cardiotoxicity.

25 ines and are therefore at risk of developing cardiotoxicity.

26 oral variability of measurements rather than cardiotoxicity.

27 lays a role in many of the observed signs of cardiotoxicity.

28 serve as predictors for development of late cardiotoxicity.

29 use is limited by cumulative dose-dependent cardiotoxicity.

30 e risk of hERG K(+) channel blockade-induced cardiotoxicity.

31 used as surrogate marker(s) for DOX-induced cardiotoxicity.

32 f tissue necrosis and lethality unrelated to cardiotoxicity.

33 cardiac MRI might allow early recognition of cardiotoxicity.

34 thmogenic substrate in anthracycline-induced cardiotoxicity.

35 potentially contribute to drug efficacy and cardiotoxicity.

36 , pericardial disease, and radiation-induced cardiotoxicity.

37 ted that statins prevent doxorubicin-induced cardiotoxicity.

38 y serve as a surrogate marker of DOX-induced cardiotoxicity.

39 ath, azithromycin is thought to have minimal cardiotoxicity.

40 ay be a valuable preclinical tool to predict cardiotoxicity.

41 herapeutic agent against doxorubicin-induced cardiotoxicity.

42 a cumulative dose that did not induce acute cardiotoxicity.

43 serial (18)F-FDG PET/CT predicts doxorubicin cardiotoxicity.

44 anthracyclines or trastuzumab are at risk of cardiotoxicity.

45 DM1 was well tolerated with no dose-limiting cardiotoxicity.

46 o anthracyclines which at higher doses cause cardiotoxicity.

47 known about the mechanism of this late-onset cardiotoxicity.

48 rious adverse events, autoimmune disease, or cardiotoxicity.

49 cardiac apoptosis and to reduce Dox-mediated cardiotoxicity.

50 ription factor GATA4 antagonizes DOX-induced cardiotoxicity.

51 suggesting that autophagy contributes to DOX cardiotoxicity.

52 xicology revealed a significant dose related cardiotoxicity.

53 increased tissue damage associated with Dox cardiotoxicity.

54 thought to contribute to doxorubicin-induced cardiotoxicity.

55 ithheld from elderly patients because of its cardiotoxicity.

56 s the major contributor to acute doxorubicin cardiotoxicity.

57 a-blockers could prevent trastuzumab-related cardiotoxicity.

58 a drug used to prevent anthracycline-induced cardiotoxicity.

59 nt is associated with both acute and chronic cardiotoxicity.

60 mouse model, revealing a marked reduction of cardiotoxicity.

61 in vitro models of doxorubicin (DOX)-induced cardiotoxicity.

62 hich could implicate Top2beta in doxorubicin cardiotoxicity.

63 g iron-rich chow alone did not result in any cardiotoxicity.

64 ion are not reliably predictive of clinical cardiotoxicity.

65 ed pathway correction prevented drug-induced cardiotoxicity.

66 platform to evaluate potential efficacy and cardiotoxicity.

67 histone antibody treatment abrogated histone cardiotoxicity.

68 2-selective digoxin derivatives for reducing cardiotoxicity.

69 edox cycling has a minor role in doxorubicin cardiotoxicity.

70 he clinical use of doxorubicin is limited by cardiotoxicity.

71 major impact on subsequent treatment-related cardiotoxicity.

72 hagy initiation protects against doxorubicin cardiotoxicity.

73 s, were associated with an increased risk of cardiotoxicity.

74 but its utility is limited by its cumulative cardiotoxicity.

75 pected events, and without evidence of acute cardiotoxicity.

76 lastic agent, is markedly hampered by severe cardiotoxicity.

77 Anthracycline-induced cardiotoxicity (ACT) is a serious adverse drug reaction

78 efulness is limited by anthracycline-induced cardiotoxicity (ACT) manifesting as asymptomatic cardiac

79 but the development of anthracycline-induced cardiotoxicity (ACT) remains a significant concern for m

80 Most cardiotoxicity after anthracycline-containing therapy oc

81 associated with a greater risk of developing cardiotoxicity after anthracyclines and a sequential ant

82 Long-term cardiotoxicity after in utero exposure to ART is unknown

83 to 1989 suggests that initiatives to reduce cardiotoxicity among those treated more recently may be

84 e successful and widely used but suffer from cardiotoxicity and acquired tumor resistance.

85 clinical utility in identifying early-onset cardiotoxicity and areas of reversible myocardial injury

86 d chronic side effects, in particular by its cardiotoxicity and by the rapid development of resistanc

87 ing device also detected doxorubicin-induced cardiotoxicity and can be adapted to detect other molecu

88 ting candidate for prevention of DOX-induced cardiotoxicity and congestive heart failure.

89 nylation serves as a critical determinant of cardiotoxicity and could serve as a mechanistic indicato

90 Exciting new research aimed at predicting cardiotoxicity and developing cardioprotective strategie

91 roach to ameliorate the chemotherapy-induced cardiotoxicity and enhance cancer prognosis.

92 may provide a molecular explanation for the cardiotoxicity and eventual failure of GSK932121 in phas

93 could both recapitulate doxorubicin-induced cardiotoxicity and exhibited insignificant differences o

94 ewer acute toxic effects, and lower risks of cardiotoxicity and leukemia.

95 y are useful in the prediction of subsequent cardiotoxicity and may help guide treatment to avoid car

96 Anthracycline-induced cardiotoxicity and myocardial dysfunction may be associa

97 cyclines and trastuzumab), or definitions of cardiotoxicity and of overweight or obesity.

98 upplemented with screening for biomarkers of cardiotoxicity and perhaps by identification of genetic

99 r a novel in vitro platform for pre-clinical cardiotoxicity and pro-arrhythmia screening of drugs in

100 The mechanisms underlying histone-induced cardiotoxicity and the functional consequences on left v

101 xploit antileukemic synergy while minimizing cardiotoxicity and the severity of differentiation syndr

102 s at the highest risk for the development of cardiotoxicity and to determine strategies for preventio

103 ectrocardiography and laboratory testing for cardiotoxicity and viral culturing of the vaccination si

104 ng new DOXO derivatives endowed with reduced cardiotoxicity, and active against DOXO-resistant tumor

105 of cardioprotective agents for prevention of cardiotoxicity, and advancements in therapies for cardia

106 are generally very sensitive to PAH-induced cardiotoxicity, and adverse changes in heart physiology

107 on risk of developing anthracycline-related cardiotoxicity, and functional analyses suggest that the

108 tratified patient-specific susceptibility to cardiotoxicity, and functional assays in hiPSC-CMs using

109 of cardiac necrosis to predict drug-induced cardiotoxicity, and in the work presented here, an LC/MS

110 atients experienced drug-related symptomatic cardiotoxicity, and no interstitial pneumonitis was repo

111 st that activation of autophagy mediates DOX cardiotoxicity, and preservation of GATA4 attenuates DOX

112 in innately resistant to doxorubicin-induced cardiotoxicity, and therefore tadalafil afforded no addi

113 Early detection and prompt therapy of cardiotoxicity appear crucial for substantial recovery o

114 Three types of anthracycline-induced cardiotoxicities are currently recognized: acute, early-

115 Mechanisms of these cardiotoxicities are not fully understood.

116 Systems that predict cardiotoxicity are of uppermost significance, as approxi

117 allow earlier and more accurate detection of cardiotoxicity are reviewed.

118 enty-six patients (32%, [22%-43%]) developed cardiotoxicity as defined by the Cardiac Review and Eval

119 seem as critical sites of sex differences in cardiotoxicity as evidenced by significant statistical i

120 This article reviews cardiotoxicity associated with 2 major anticancer regime

121 ancer patients survive longer, the impact of cardiotoxicity associated with the use of cancer treatme

122 toxicology study, SI-2 caused minimal acute cardiotoxicity based on a hERG channel blocking assay an

123 s associated with minimal hematotoxicity and cardiotoxicity based on measurements of the left ventric

124 ompound to attempt oncologic therapy without cardiotoxicity, based on targeting KV11.1.

125 rdiac repolarization but is also a source of cardiotoxicity because unintended hERG inhibition by div

126 However, the differential risk for cardiotoxicity between daunorubicin and doxorubicin has

127 whether a difference in doxorubicin-related cardiotoxicity between men and women also exists.

128 S protein assays from our laboratory for two cardiotoxicity biomarkers, Myl3 and NTproBNP.

129 rmacological or genetic approach reduced DOX cardiotoxicity but did not produce additive effects when

130 ter from oiled sites showed modest sublethal cardiotoxicity but no elevated necrosis or mortality.

131 Amrubicin did not induce early cardiotoxicity, but its long-term effects are unknown.

132 ty, and preservation of GATA4 attenuates DOX cardiotoxicity by inhibiting autophagy through modulatio

133 s required for rescue of bupivacaine-induced cardiotoxicity by lipid emulsion in rats.

134 for successful rescue of bupivacaine-induced cardiotoxicity by lipid emulsion.

135 In this article we review the incidence of cardiotoxicity caused by commonly used chemotherapeutic

136 and there may be qualitative differences in cardiotoxicity caused by low and high-potency local anes

137 hypothesized that CMR would identify occult cardiotoxicity characterized by structural and functiona

138 , a drug that attenuates doxorubicin-induced cardiotoxicity, decreased mitochondrial iron levels and

139 most useful parameter for the prediction of cardiotoxicity, defined as a drop in LVEF or heart failu

140 Cardiotoxicity, defined by the Cardiac Review and Evalua

141 elapsed between the end of chemotherapy and cardiotoxicity development was 3.5 (quartile 1 to quarti

142 Here, we found that cardiotoxicity develops through the preferential accumul

143 ents will be affected by doxorubicin-induced cardiotoxicity (DIC).

144 Doxorubicin-induced acute cardiotoxicity did not increase c-kit-derived endothelia

145 However, this larval cardiotoxicity did not manifest in a reduced aerobic sco

146 In a mouse model of cardiotoxicity, doxorubicin treatment is associated with

147 also causes large-scale cell loss, sorafenib cardiotoxicity dramatically increases mortality.

148 s may provide insights into the mechanism of cardiotoxicity due to anticancer PDGFR inhibitors.

149 motherapy, it enhances patient outcomes, but cardiotoxicity due to the trastuzumab treatment poses a

150 s important to be aware of the potential for cardiotoxicity during long-term follow-up and to conside

151 se is limited by tumor resistance and severe cardiotoxicity (e.g., congestive heart failure).

152 However, avoidance of doxorubicin-related cardiotoxicity effects is important to improve long-term

153 lear whether the association between age and cardiotoxicity exists for newer treatments.

154 s study also raises concerns about potential cardiotoxicity for chemotherapeutics that target MCL-1.

155 A damage is the principal pathway of chronic cardiotoxicity for therapeutic doses, leading to a progr

156 overweight and obesity are risk factors for cardiotoxicity from anthracyclines and sequential anthra

157 ions between obesity or being overweight and cardiotoxicity from anthracyclines and sequential anthra

158 ent methods to identify patients at risk for cardiotoxicity from cancer therapy are inadequate.

159 red with doxorubicin to minimize the risk of cardiotoxicity from treatment with trastuzumab and anthr

160 able to discriminate a KI with little or no cardiotoxicity (gefitinib) from one with demonstrated ca

161 and mortality of anticancer therapy-related cardiotoxicity has become more problematic.

162 However, adverse side effects and cardiotoxicity have also been reported.

163 creased probability of anthracycline-related cardiotoxicity have been identified.

164 tion-based studies on cancer therapy-related cardiotoxicity have focused on older women.

165 sequential therapy were at a higher risk of cardiotoxicity (hazard ratio, 1.76 [95% CI, 1.19 to 2.60

166 ent HF, independent of anthracycline-related cardiotoxicity (hazard ratio, 9.0; 95% confidence interv

167 erapeutic use of doxorubicin by reducing its cardiotoxicity; however, it remains unclear whether lipo

168 ired for an ideal in vitro system to predict cardiotoxicity: i) cells with a human genetic background

169 The ability to test for efficacy and cardiotoxicity in a clinically relevant human model syst

170 ntified hypertension-susceptibility loci and cardiotoxicity in a cohort of long-term childhood cancer

171 lance and prevention of chemotherapy-induced cardiotoxicity in adult survivors of breast cancer who h

172 rotein might provide a strategy to limit the cardiotoxicity in cancer patients treated with anthracyc

173 might represent a novel means to circumvent cardiotoxicity in cancer patients whose treatment regime

174 or the prevention of chemotherapy-associated cardiotoxicity in cancer patients.

175 NT-proBNP may hold promise as biomarkers of cardiotoxicity in children with high-risk ALL.

176 The CHAART-2 (HAART-Associated Cardiotoxicity in HIV-Infected Children) study prospecti

177 s a rational means to circumvent doxorubicin cardiotoxicity in human patients with cancer.

178 However, potential cardiotoxicity in humans and contemporary dietary source

179 ependent predictors of susceptibility to DOX cardiotoxicity in man.

180 highly effective anticancer agent but causes cardiotoxicity in many patients.

181 onance to characterize anthracycline-induced cardiotoxicity in mice.

182 tion of myocardial changes and prediction of cardiotoxicity in patients receiving cancer therapy.

183 ere was no clinically significant short-term cardiotoxicity in patients treated with trastuzumab and

184 offer additive information about the risk of cardiotoxicity in patients undergoing doxorubicin and tr

185 strain and blood biomarkers predict incident cardiotoxicity in patients with breast cancer during tre

186 l or multiple biomarkers are associated with cardiotoxicity in patients with breast cancer undergoing

187 hypertrophy, heart failure, and doxorubicin cardiotoxicity in patients.

188 TNF-alpha-mediated cardiotoxicity in SAP-IFN-gamma transgenic mice is indep

189 l and pathological stress induced late-onset cardiotoxicity in the adult doxorubicin-treated mice.

190 trategies for surveillance and prevention of cardiotoxicity in the elderly.

191 thway is an important modulator of sorafenib cardiotoxicity in vitro and in vivo and appears to act t

192 tric model of late-onset doxorubicin-induced cardiotoxicity in which juvenile mice were exposed to do

193 n juvenile salmon, and significantly reduced cardiotoxicity in zebrafish.

194 Mechanisms of air pollution-induced cardiotoxicity include increased generation of reactive

195 The preclinical models for predicting cardiotoxicity, including induced pluripotent stem cells

196 By contrast, cardiotoxicity induced by chronic beta-AR stimulation, a

197 clinical implications for the prevention of cardiotoxicity induced heart failure.

198 Most models of doxorubicin cardiotoxicity involve intraperitoneal injection of high

199 Cardiotoxicity is a leading cause for drug attrition dur

200 Cardiotoxicity is a side effect that plagues modern drug

201 Cardiotoxicity is a well established complication of ant

202 However, anthracycline-related cardiotoxicity is also well recognized and can compromis

203 suggest that, in mice, anthracycline-induced cardiotoxicity is associated with an early increase in c

204 therapeutic agents that prevent TTR-mediated cardiotoxicity is desired.

205 The postulated mechanism of the cardiotoxicity is generation of reactive oxygen and nitr

206 ng individual susceptibility to drug-induced cardiotoxicity is key to improving patient safety and pr

207 failure, suggesting that doxorubicin-induced cardiotoxicity is mediated by topoisomerase-IIbeta in ca

208 Because trastuzumab-related cardiotoxicity is reversible, efforts to improve the ade

209 hracycline exposure are at increased risk of cardiotoxicity, leading to the hypothesis that genetic s

210 monounsaturated fatty acids (LCMUFAs) caused cardiotoxicity, leading, for example, development of Can

211 In an effort to address potential cardiotoxicity liabilities identified with earlier front

212 In case of cardiotoxicity (LVEF decrease >10 absolute points, and <

213 ing improves outcomes but is associated with cardiotoxicity manifested as congestive heart failure (C

214 Ongoing surveillance of DAAs for cardiotoxicities may be beneficial, especially among pat

215 ulating the sox9b gene, we hypothesized that cardiotoxicity might also result from sox9b downregulati

216 species-related mechanisms of air pollution cardiotoxicity might become a valid target in developing

217 In a murine anthracycline-related cardiotoxicity model, increases in cardiovascular magnet

218 But TTT-28 did not induce the toxicity (cardiotoxicity/myelosuppression) of paclitaxel in mice.

219 Survivors previously undiagnosed with cardiotoxicity (n = 108) had a high prevalence of EF (32

220 ment predicted the subsequent development of cardiotoxicity; no significant associations were observe

221 ortantly, these analogues did not induce the cardiotoxicity observed at high nonoptimal doses of the

222 In 98% of cases (n=221), cardiotoxicity occurred within the first year.

223 nued evidence to support the ideas that LAST cardiotoxicity occurs primarily at sodium channels, lipi

224 been hypothesized that doxorubicin-dependent cardiotoxicity occurs through ROS production and possibl

225 ion has been the leading explanation for the cardiotoxicity of 5-fluorouracil and may be the underlyi

226 d myocytes and intact heart protects against cardiotoxicity of beta-adrenergic receptor activation by

227 However, the current means to alleviate the cardiotoxicity of DOX are limited.

228 so provide a new explanation for the reduced cardiotoxicity of EPI compared with other anthracyclines

229 n 2 independent cohorts, suggesting possible cardiotoxicity of LCMUFAs in humans.

230 Herein, we examine the cardiotoxicity of targeted therapeutics, focusing on the

231 en employed to investigate the dose-limiting cardiotoxicity of the common anti-cancer drug doxorubici

232 The underlying mechanisms that drive the cardiotoxicity of the KIs are also examined.

233 this issue appears to be at the core of the cardiotoxicity (often manifest as a dilated cardiomyopat

234 No evidence of acute cardiotoxicity or of acute or delayed systemic toxicity

235 creen drugs that possess cardiac activity or cardiotoxicity, or to assess chemicals that could direct

236 related genes that may underpin the familiar cardiotoxicity phenotype.

237 ixed, but it is likely that local anesthetic cardiotoxicity primarily arises from a blockade of sodiu

238 We have recapitulated drug-induced cardiotoxicity profiles for healthy subjects, long QT sy

239 in basic mechanisms of anthracycline-induced cardiotoxicity provided a unified theory to explain the

240 Potential cardiotoxicity related to anti-human ether-a-go-go potas

241 Cardiotoxicity related to anticancer treatment is import

242 we will discuss the most recent views on the cardiotoxicity related to various classes of chemotherap

243 The mechanisms of doxorubicin-induced cardiotoxicity remain incompletely understood.

244 tment of LAST (particularly local anesthetic cardiotoxicity) remain unclear.

245 s in cancer treatment, anthracycline-related cardiotoxicity remains a major cause of morbidity and mo

246 econdary prevention of anthracycline-induced cardiotoxicity resulting from newly recognized molecular

247 Sorafenib cardiotoxicity results from myocyte necrosis rather than

248 s17249754 were significantly associated with cardiotoxicity risk conferring a protective effect with

249 Cardiotoxicity risk factors at the time of cancer diagno

250 Hazard ratios (HRs) of cardiotoxicity risk were assessed for each biomarker at

251 with DOX-based chemotherapy to identify the cardiotoxicity risk, predict DOX-treatment response and

252 ng Q-T syndrome, and consequently presents a cardiotoxicity risk.

253 e clinical applications, drug discovery, and cardiotoxicity screening by improving the yield, safety,

254 ld be considered prior to pro-arrhythmia and cardiotoxicity screening in drug discovery programs.

255 uld improve on industry-standard preclinical cardiotoxicity screening methods, identify the effects o

256 ildhood cancer treatment protocols to reduce cardiotoxicity should be additionally investigated.

257 Patients at higher risk for cardiotoxicity should receive closer monitoring, cardiop

258 necessary for effective cardiac therapy and cardiotoxicity studies.

259 d dose than the free drug, and moreover, the cardiotoxicity study has evidenced that SQ-Dox nanoassem

260 dict the development of chemotherapy-induced cardiotoxicity, suggesting that prospective clinical tri

261 icity (gefitinib) from one with demonstrated cardiotoxicity (sunitinib).

262 To date hiPSC-CMs used for cardiotoxicity testing display an immature, fetal-like c

263 The improvement of preclinical cardiotoxicity testing, discovery of new ion-channel-tar

264 se modeling, drug discovery, and preclinical cardiotoxicity testing.

265 f malignancies, but it causes a dose-related cardiotoxicity that can lead to heart failure in a subse

266 eat pediatric cancers but is associated with cardiotoxicity that can manifest many years after the in

267 adverse sequelae and long-term effects (eg, cardiotoxicity) that can affect all-cause mortality.

268 selectively enhance anticancer activity over cardiotoxicity, the most significant clinical impediment

269 strategies to prevent anthracycline-induced cardiotoxicity, there is little consensus regarding the

270 recent clinical reports have documented its cardiotoxicity through an unknown mechanism.

271 orubicin is believed to cause dose-dependent cardiotoxicity through redox cycling and the generation

272 d downregulates angiogenesis with negligible cardiotoxicity, thus encouraging its further clinical de

273 identifying patients at risk for DOX-induced cardiotoxicity to prevent permanent cardiac damage.

274 rugs targeting pathways predicted to produce cardiotoxicity, validated inter-patient differential res

275 on cardiac hypertrophy and doxorubicin (Dox)-cardiotoxicity via deacetylation of mitochondrial protei

276 de that Honokiol protects the heart from Dox-cardiotoxicity via improving mitochondrial function by n

277 Pooled odds ratio for cardiotoxicity was 1.38 (95% CI, 1.06 to 1.80; I(2) = 43

278 The risk of cardiotoxicity was 46.5% in patients with the largest ch

279 The overall incidence of cardiotoxicity was 9% (n=226).

280 A greater risk of cardiotoxicity was associated with interval changes in T

281 Recovery from cardiotoxicity was defined as partial (LVEF increase >5

282 Cardiotoxicity was evaluated as the change in indexed le

283 Excess cardiotoxicity was not seen with high doses of D in ADE.

284 Grade 3/4 cardiotoxicity was rare after induction (4 L-DNR vs 5 id

285 No neratinib-related, grades 3 or 4 cardiotoxicity was reported.

286 The role of iron toward doxorubicin (DOX) cardiotoxicity was studied using a rodent model of dieta

287 methyl urea series, as a result of potential cardiotoxicity, was successfully accomplished, resulting

288 sify anthracycline dosage without increasing cardiotoxicity, we compared potentially less cardiotoxic

289 for monitoring both anticancer efficacy and cardiotoxicity, we tested cardiotoxic doxorubicin alone

290 les that identified an unacceptable level of cardiotoxicity were never reached.

291 ew or unexpected adverse events or increased cardiotoxicity were reported during the study.

292 anthracycline doxorubicin is limited by its cardiotoxicity which is associated with mitochondrial dy

293 s are major culprits in chemotherapy-induced cardiotoxicity, which is the chief limiting factor in de

294 servational and clinical trial data, risk of cardiotoxicity with anthracycline-based chemotherapy inc

295 We sought to determine the risk of cardiotoxicity with breast cancer therapy in women with

296 Interestingly, the risk of cardiotoxicity with drugs such as trastuzumab is predict

297 As a result, Honokiol alleviated Dox-cardiotoxicity with improved cardiac function and reduce

298 synthesised to reduce anthracycline-related cardiotoxicity without compromising antitumour efficacy.

299 cardioprotection from doxorubicin-associated cardiotoxicity without compromising the efficacy of anti

300 a model that provokes modest and progressive cardiotoxicity without constitutional symptoms, reminisc