ライフサイエンスコーパス: cardiotoxicity

1 serve as predictors for development of late cardiotoxicity.

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

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

4 in the pathogenesis of chemotherapy-induced cardiotoxicity.

5 arget molecule to combat doxorubicin-induced cardiotoxicity.

6 itical mechanism by which doxorubicin causes cardiotoxicity.

7 thmogenic substrate in anthracycline-induced cardiotoxicity.

8 , pericardial disease, and radiation-induced cardiotoxicity.

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

10 o anthracyclines which at higher doses cause cardiotoxicity.

11 a-blockers could prevent trastuzumab-related cardiotoxicity.

12 ion are not reliably predictive of clinical cardiotoxicity.

13 ed pathway correction prevented drug-induced cardiotoxicity.

14 platform to evaluate potential efficacy and cardiotoxicity.

15 histone antibody treatment abrogated histone cardiotoxicity.

16 2-selective digoxin derivatives for reducing cardiotoxicity.

17 edox cycling has a minor role in doxorubicin cardiotoxicity.

18 he clinical use of doxorubicin is limited by cardiotoxicity.

19 major impact on subsequent treatment-related cardiotoxicity.

20 hagy initiation protects against doxorubicin cardiotoxicity.

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

22 but its utility is limited by its cumulative cardiotoxicity.

23 pected events, and without evidence of acute cardiotoxicity.

24 lastic agent, is markedly hampered by severe cardiotoxicity.

25 fy a gene signature that can predict risk of cardiotoxicity.

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

27 the progression of subclinical and clinical cardiotoxicity.

28 nd 11 required hospitalization for suspected cardiotoxicity.

29 ystematic monitoring of hepatic toxicity and cardiotoxicity.

30 2) increment) were independent correlates of cardiotoxicity.

31 hout causing significant body weight loss or cardiotoxicity.

32 P18 uptake in a mouse model of anthracycline cardiotoxicity.

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

34 iable strategy to mitigate acute ADR induced cardiotoxicity.

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

36 d clinical protocols to prevent irreversible cardiotoxicity.

37 ermining the mechanism of sorafenib-mediated cardiotoxicity.

38 to clinical symptoms of acute anthracycline cardiotoxicity.

39 lassify patients at risk for therapy-induced cardiotoxicity.

40 tion, and treatment of anthracycline-related cardiotoxicity.

41 oteins has been reported, in particular, for cardiotoxicity.

42 t doxorubicin is limited by life-threatening cardiotoxicity.

43 agents to mitigate oxidative stress-induced cardiotoxicity.

44 ochondria-derived, oxidative stress-mediated cardiotoxicity.

45 nd improves cardiac function in DOXO-induced cardiotoxicity.

46 ines and are therefore at risk of developing cardiotoxicity.

47 egulatory roles in minimizing the IR-induced cardiotoxicity.

48 oral variability of measurements rather than cardiotoxicity.

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

50 prior diagnoses contributing to drug related cardiotoxicity.

51 omising drug target for managing DOX-induced cardiotoxicity.

52 eatment to reduce the risk of immune-related cardiotoxicity.

53 channel whose inhibition is associated with cardiotoxicity.

54 sing tracer for imaging chemotherapy-induced cardiotoxicity.

55 t for an imaging approach to detect evolving cardiotoxicity.

56 atic hydrocarbons (PAHs) as key mediators of cardiotoxicity.

57 l promising intervention against Cfz-induced cardiotoxicity.

58 cal use of anthracyclines is associated with cardiotoxicity.

59 rs (MEISi) with no predicted cytotoxicity or cardiotoxicity.

60 9) compared with patients without documented cardiotoxicity.

61 noids can model hypoxia-enhanced doxorubicin cardiotoxicity.

62 P2 poisoning, may play a role in doxorubicin cardiotoxicity.

63 port on DeltaPsi(m) as a readout of evolving cardiotoxicity.

64 nificantly worse in patients with documented cardiotoxicity.

65 dependent mitochondrial fragmentation in Dox cardiotoxicity.

66 in the physiologic range may help reduce Dox cardiotoxicity.

67 tility is severely limited by its associated cardiotoxicity.

68 acers may be suitable for early detection of cardiotoxicity.

69 of cardiovascular disease(1), screening for cardiotoxicity(2) and decisions regarding the clinical m

70 ents, p=0.0002) or stopping early because of cardiotoxicity (61 [3%] of 1939 patients vs 146 [8%] of

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

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

73 Most cardiotoxicity after anthracycline-containing therapy oc

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

75 Late cardiotoxicity after pediatric acute myeloid leukemia th

76 Chronic Dox-cardiotoxicity also exhibited time-dependent accumulatio

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

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

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

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

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

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

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

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

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

86 HER2-positive early breast cancer, with less cardiotoxicity and fewer severe adverse events.

87 immunotherapy responsiveness and its related cardiotoxicity and highlight how patient genetics and ep

88 for the PET imaging of chemotherapy-induced cardiotoxicity and indicates the potential application o

89 Anthracycline-induced cardiotoxicity and myocardial dysfunction may be associa

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

91 in two patients (<1%) in the VRd group (one cardiotoxicity and one secondary cancer) and 11 (2%) in

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

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

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

95 valuated the risk factors for incident early cardiotoxicity and the impacts of cardiotoxicity on even

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

97 lind, multicenter, placebo-controlled trial, cardiotoxicity and treatment interruptions in patients w

98 istant K1 strain, in vitro cytotoxicity, and cardiotoxicity and were addressed through structure-acti

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

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

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

102 associated with cumulative toxicity, such as cardiotoxicity, and can impact quality of life.

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

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

105 Chemotherapy drugs are known to result in cardiotoxicity, and studies have shown that heart failur

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

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

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

109 Mechanisms of these cardiotoxicities are not fully understood.

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

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

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

113 r safety of AIs as upfront treatments, their cardiotoxicity as sequential treatments with tamoxifen r

114 t intended to address the theme of improving cardiotoxicity assessment in drug development.

115 tial and thus an important component of drug cardiotoxicity assessments.

116 today have to be familiar not only with the cardiotoxicity associated with traditional cancer therap

117 By the time cardiotoxicity-associated cardiac dysfunction is detecta

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

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

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

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

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

123 dy was to identify early doxorubicin-induced cardiotoxicity by serial multiparametric cardiac magneti

124 evant cardiotoxicity tools, particularly for cardiotoxicities characterized by contractile dysfunctio

125 The earliest doxorubicin-cardiotoxicity CMR parameter was T(2) relaxation-time pr

126 lar and cellular determinants of doxorubicin cardiotoxicity, contributing to the development of cardi

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

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

129 Cardiotoxicity, defined by the Cardiac Review and Evalua

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

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

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

133 wn molecular pathways related to DOX-induced cardiotoxicity (DIC).

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

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

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

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

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

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

140 Documented cardiotoxicity during on-protocol therapy was significan

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

142 ly expressed transcripts, with enrichment of cardiotoxicity, ECM and inflammatory pathways.

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

144 on EFS were equivalent whether the incident cardiotoxicity event occurred in the absence (HR, 1.6; 9

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

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

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

148 Cardiotoxicity-free survival was longer on both carvedil

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

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

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

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

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

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

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

156 tient groups are consistent with doxorubicin cardiotoxicity having a greater dependence on reduced ce

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

158 al practice guidelines address approaches to cardiotoxicity, however, they focus on specific agents o

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

160 2.5; P = .004) than for infection-associated cardiotoxicity (HR, 1.3; 95% CI, 0.7 to 2.4; P = .387).

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

162 failure therapeutics and reliable testing of cardiotoxicity in a 3-dimensional heart model.

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

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

165 therapeutic agent that causes dose-dependent cardiotoxicity in a subset of treated patients, but the

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

167 further assessing its potential for imaging cardiotoxicity in an acute doxorubicin model.

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

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

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

171 ove risk assessments of antimalarial-related cardiotoxicity in clinical research and practice.

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

173 However, potential cardiotoxicity in humans and contemporary dietary source

174 apsed/refractory myeloma, is associated with cardiotoxicity in humans.

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

176 roach in examining mechanisms of oil-induced cardiotoxicity in marine fish.

177 onance to characterize anthracycline-induced cardiotoxicity in mice.

178 ab, both lisinopril and carvedilol prevented cardiotoxicity in patients receiving anthracyclines.

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

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

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

182 Potential cardiotoxicity in some BKIs led to the continued explora

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

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

185 the earliest marker of anthracycline-induced cardiotoxicity, in the absence of T(1) mapping, ECV, or

186 it has been linked with potentially limiting cardiotoxicity, including emerging reports of profound h

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

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

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

190 Most models of doxorubicin cardiotoxicity involve intraperitoneal injection of high

191 Anthracycline-induced cardiotoxicity is a major cause of morbidity and mortali

192 Anthracycline-induced cardiotoxicity is a major clinical problem, and early ca

193 Although cardiotoxicity is a serious adverse event associated wit

194 Cardiotoxicity is a side effect that plagues modern drug

195 Cardiotoxicity is a well established complication of ant

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

197 Dox cardiotoxicity is closely associated with mitochondrial

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

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

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

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

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

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

204 ckers reduce the rate of trastuzumab-induced cardiotoxicity (left ventricular ejection fraction decre

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

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

207 icity is a major clinical problem, and early cardiotoxicity markers are needed.

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

209 sensitive detection of chemotherapy-induced cardiotoxicity may allow improved treatment strategies a

210 Early treatment-related cardiotoxicity may be associated with decreased EFS and

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

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

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

214 the reduction in OS was more pronounced for cardiotoxicity not associated with infection (HR, 1.7; 9

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

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

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

218 ion (WHO) Evidence Review Group (ERG) on the Cardiotoxicity of Antimalarials.

219 traditional CVD risk factors and also to the cardiotoxicity of cancer treatment.

220 esults obtained highlight the dose-dependent cardiotoxicity of Diclofenac compared to Ketoprofen.

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

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

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

224 great promise for understanding drug-induced cardiotoxicity of oncological drugs that may manifest as

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

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

227 dent early cardiotoxicity and the impacts of cardiotoxicity on event-free survival (EFS) and overall

228 The impact of early-onset cardiotoxicity on treatment outcomes is less well unders

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

230 Approximately 12% of patients experienced cardiotoxicity over a 5-year follow-up, with more than 7

231 Individual cardiotoxicity patient reports for these KIs, obtained f

232 related genes that may underpin the familiar cardiotoxicity phenotype.

233 rties all play a role in doxorubicin-induced cardiotoxicity phenotypes.

234 onstrating feasibility of a new approach for cardiotoxicity prediction.

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

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

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

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

239 Among these, cardiotoxicities remain of prime concern, but vascular t

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

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

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

243 Sorafenib cardiotoxicity results from myocyte necrosis rather than

244 We also identify relationships between cardiotoxicity risk and structural/binding profiles of i

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

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

247 g substructures are predictive of KI-induced cardiotoxicity risk, and that they can be informative fo

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

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

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

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

252 blicly available, this approach may expedite cardiotoxicity screening of compounds as diverse as smal

253 rtantly, Matrix Plus enabled high throughput cardiotoxicity screening using mature human cardiomyocyt

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

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

256 Furthermore, the cardiotoxicity spectrum has broadened to include myocard

257 necessary for effective cardiac therapy and cardiotoxicity studies.

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

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

260 iology, including high-throughput screening, cardiotoxicity testing and personalized medicine assays,

261 re predictive in vitro chronic/repeated dose cardiotoxicity testing assays.

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 ed by the reliance on whole-animal models of cardiotoxicity that may fail to reflect the fundamental

267 limiting adverse effect of anthracyclines is cardiotoxicity that often presents as heart failure due

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

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

272 ative development program for human-relevant cardiotoxicity tools, particularly for cardiotoxicities

273 y cancer) and 11 (2%) in the KRd group (four cardiotoxicity, two acute kidney failure, one liver toxi

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 Cardiotoxicity was also assessed by measuring the heart

281 Cardiotoxicity was ascertained through adverse event mon

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

283 For the entire cohort, cardiotoxicity was comparable in the 3 arms and occurred

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

285 Cardiotoxicity was evaluated as the change in indexed le

286 Together, these results suggested that Dox cardiotoxicity was mediated, at least in part, by the in

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

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

289 data regarding any potential fetal/neonatal cardiotoxicity, we leveraged a unique opportunity in whi

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

291 their response to acute doxorubicin-induced cardiotoxicity were assessed in rats in vivo (10, 15, or

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 doxorubicin is undermined by dose-dependent cardiotoxicity, which may be a function of futile redox

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

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

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

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

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