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1  produce high response rates but may also be cardiotoxic.
2 rom both plasma and kidneys of CKD mice were cardiotoxic.
3 k or whether certain manifestations are more cardiotoxic.
4 and during normal (1 microM, n = 6) and high cardiotoxic (50 microM, n = 11) dose infusions of the di
5 ot be 1 facet of depression that is the most cardiotoxic across all contexts.
6 ype TRalpha(wt), that is associated with the cardiotoxic actions of T3.
7 sets has revealed that ponatinib is the most cardiotoxic agent among all Food and Drug Administration
8 analyzed the effects of doxorubicin, a known cardiotoxic agent, on human cardiomyocytes (CMs) as meas
9 erns similar to that seen with several known cardiotoxic agents such as doxorubicin.
10 lines) and radiation had been well-described cardiotoxic agents, with anthracycline-associated heart
11 BRs) catalyze reduction of anthracyclines to cardiotoxic alcohol metabolites.
12                              The use of less cardiotoxic alternatives, such as liposomal doxorubicin,
13 ared with doxorubicin, daunorubicin was less cardiotoxic among survivors of childhood cancer than mos
14 cumulation within the myocardium is directly cardiotoxic and causes left ventricular remodeling and d
15 ally elevated cytokines are also known to be cardiotoxic and have the potential to result in profound
16 mor growth and demonstrated markedly reduced cardiotoxic and nephrotoxic effects, as well as better t
17 ture, particularly ways that could avoid the cardiotoxic and neurotoxic effects of current agents suc
18 e dissolved phase of runoff (e.g., PAHs) are cardiotoxic and that soil bioretention protects against
19 osed in heart muscle cell death triggered by cardiotoxic anti-cancer drugs, given its reported activa
20                 Here we demonstrate that the cardiotoxic anticancer agent doxorubicin (adriamycin) in
21 e of low LV mass was independent of previous cardiotoxic anticancer therapy.
22                         Doxorubicin (Dox), a cardiotoxic antineoplastic drug, disrupts the cardiac-sp
23                               Doxorubicin, a cardiotoxic antineoplastic, disrupts the cardiac-specifi
24   Ibrutinib has been associated with serious cardiotoxic arrhythmias.
25         ACSL1 prevented de novo synthesis of cardiotoxic C16- and C24-, and C24:1 ceramides and incre
26  era, diagnosis of diabetes, and exposure to cardiotoxic cancer therapies.
27 se results indicate that previously regarded cardiotoxic cancer therapy adversely increases thoracic
28 ostication of patients receiving potentially cardiotoxic cancer therapy has involved relatively small
29  among patients with breast cancer receiving cardiotoxic cancer therapy, and its use warrants further
30 red risk factors and exposure to potentially cardiotoxic cancer therapy.
31 d adult cancer survivors who had exposure to cardiotoxic cancer treatment and/or previous cardiovascu
32 re related to prior receipt of a potentially cardiotoxic cancer treatment regimen.
33 lian cytotoxicity > 15% and those containing cardiotoxic cardiac glycosides were eliminated.
34 ticularly in patients with prior exposure to cardiotoxic chemotherapies e.g., anthracyclines.
35 may lead to changes in the administration of cardiotoxic chemotherapies.
36 related to the administration of potentially cardiotoxic chemotherapy in human subjects.
37 ac safety in patients with cancer undergoing cardiotoxic chemotherapy not only for the early detectio
38 re and 3 months after initiating potentially cardiotoxic chemotherapy using blinded, unpaired analysi
39 ar biomarkers for risk stratification during cardiotoxic chemotherapy.
40 es 3 months after the receipt of potentially cardiotoxic chemotherapy.
41 tion in human subjects receiving potentially cardiotoxic chemotherapy.
42                     Epirubicin (EPI) is less cardiotoxic compared with other canonical anthracyclines
43 ce, detection, and differential diagnosis of cardiotoxic complications.
44 tress and thereby cardiac injury, as a model cardiotoxic compound and observed changes in the Mrp1 ex
45  increase in carbonylation under Dox-induced cardiotoxic conditions in a spontaneously hypertensive r
46 ified specific serum proteins oxidized under cardiotoxic conditions.
47 ellular calcium overload, and the release of cardiotoxic cytokines.
48 t was less efficacious with the higher, more cardiotoxic dose of DOX.
49 ancer efficacy and cardiotoxicity, we tested cardiotoxic doxorubicin alone and in combination with an
50  that reproduces susceptibility to develop a cardiotoxic drug response.
51 afish model of cardiomyopathy induced with a cardiotoxic drug.
52 iduals exhibit different susceptibilities to cardiotoxic drugs and that use of disease-specific hiPSC
53 monstrated increased susceptibility to known cardiotoxic drugs as measured by action potential durati
54 markers that were increased upon addition of cardiotoxic drugs, prior to the onset of tissue demise.
55                 However, excess iron is also cardiotoxic due to its ability to catalyze the formation
56                    Women developing HF after cardiotoxic EBC chemotherapy have fewer comorbidities th
57 itochondrial function, could detect an acute cardiotoxic effect of doxorubicin (DOX) in a large anima
58 ve courses of chemotherapy agents with known cardiotoxic effects (including anthracyclines, taxanes,
59  for the first time, that 3NPA has important cardiotoxic effects as well as neurotoxic effects, and t
60                                        These cardiotoxic effects can be acute, such as changes in ele
61                                              Cardiotoxic effects can occur immediately during adminis
62 aromatic hydrocarbons that cause a number of cardiotoxic effects in marine fishes across all levels o
63 ervations: The old paradigm of anthracycline cardiotoxic effects is replaced by new insights that ant
64 at Edg-mediated Sph1P negative inotropic and cardiotoxic effects may play important roles in acute my
65 lated cardiomyopathy in mice, resembling the cardiotoxic effects observed in a subset of breast cance
66 n appearing more susceptible than men to the cardiotoxic effects of alcohol.
67 that oxidized myocardial CaMKII mediates the cardiotoxic effects of aldosterone on the cardiac matrix
68 n or hypertension, suggesting that potential cardiotoxic effects of arsenic might be more pronounced
69                                 Although the cardiotoxic effects of cocaine are universally recognize
70 ignaling axis that functionally connects the cardiotoxic effects of DOX to proteasomal degradation of
71 a new therapeutic target in ameliorating the cardiotoxic effects of DOX treatment in cancer patients.
72 supporting the idea that Bnip3 underlies the cardiotoxic effects of DOX.
73                            Despite the known cardiotoxic effects of doxorubicin and other anthracycli
74                                          The cardiotoxic effects of doxorubicin are cumulative, which
75               These results suggest that the cardiotoxic effects of doxorubicin develop from mitochon
76 may be further explored in view of potential cardiotoxic effects of FLT3-targeting anticancer therapy
77 ikely to be the primary target for the known cardiotoxic effects of other, related antihistamines.
78 s of obesity, which, in combination with the cardiotoxic effects of specific cancer therapies, places
79 ing that oxidative stress may exacerbate the cardiotoxic effects of the PLN(R9C) mutant.
80             More research is needed into the cardiotoxic effects of these therapies.
81                                The on-target cardiotoxic effects of trastuzumab were owing to a prosu
82 logical mechanisms underlying such potential cardiotoxic effects remain unclear.
83                  Prevention of anthracycline cardiotoxic effects should be based on inhibiting or deg
84                   However, imatinib also has cardiotoxic effects traceable to its impact on the C-Abl
85                                     No acute cardiotoxic effects were observed with either treatment,
86                                              Cardiotoxic effects were reported in 15 (5%) of 291 chil
87 C, HEK-293, and MCF-7 cells, did not present cardiotoxic effects, and did not affect P-gp transport a
88  with increased risk of febrile neutropenia, cardiotoxic effects, and secondary malignant neoplasms.
89 icity of anthracyclines while reducing their cardiotoxic effects, we have developed a novel class of
90 ak may contribute to AMT's proarrhythmic and cardiotoxic effects, which may be counteracted by interv
91                      The primary outcome was cardiotoxic effects, which were defined as the incidence
92 ores, myofibrillar degeneration, and related cardiotoxic effects.
93 drawn even later from the marketplace due to cardiotoxic effects.
94 ficial in preventing the development of late cardiotoxic effects.
95 ER2/neu) correlates with trastuzumab-related cardiotoxic effects.
96 are at increased risk of trastuzumab-related cardiotoxic effects.
97 omarkers have allowed for early detection of cardiotoxic effects.
98 on for the prevention of trastuzumab-related cardiotoxic effects.
99 oprotective agents may prevent some of these cardiotoxic effects.
100 al sites, or for i.v. therapeutics or during cardiotoxic episodes.
101 uary, 2004, following clinically significant cardiotoxic events (nine events in eight of 77 patients)
102     The frequency and clinical phenotypes of cardiotoxic events in chimeric antigen receptor (CAR) T-
103 studies have uncovered excess risks of these cardiotoxic events, especially in traditionally underrep
104 elopment carries a higher risk of subsequent cardiotoxic events.
105 rt radiotherapy; n = 246) were compared with cardiotoxic-exposed survivors of European ancestry (n =
106 2017 (the EBC-HF cohort) were categorized by cardiotoxic exposure (anthracycline alone, trastuzumab a
107                   PCP documentation of prior cardiotoxic exposures was low compared with known exposu
108  breast cancer, and proved to be excessively cardiotoxic for use in the adjuvant setting.
109                                              Cardiotoxic free radicals are generated by ischemia-repe
110  peptide angiotensin II (Ang II) is a potent cardiotoxic hormone whose actions have been well studied
111 ibitor asymmetric dimethylarginine (ADMA), a cardiotoxic hormone whose effects can be prevented by l-
112                           Anthracyclines are cardiotoxic; however, there are limited data characteriz
113 iac inflammatory reactions, showing that the cardiotoxic IFN-gamma effect operative in SAP-IFN-gamma
114                                     Although cardiotoxic impacts have been widely reported, the mecha
115                     CKD-EV-miRNA mimics were cardiotoxic, impairing contractility and downregulating
116                          They also were less cardiotoxic in cell culture.
117 dy, we tested the hypothesis that ONOO(-) is cardiotoxic in crystalloid cardioplegia but cardioprotec
118 linical study suggested that imatinib may be cardiotoxic in some patients.
119 neered the amino acid sequence of the highly cardiotoxic LC H6 by introducing three residue mutations
120 ompounds and identified those with potential cardiotoxic liabilities in iPSC-CMs using a single-param
121 and utilization leads to the accumulation of cardiotoxic lipid species, and to establish a mouse mode
122 cardiotoxicity, we compared potentially less cardiotoxic liposomal daunorubicin (L-DNR) to idarubicin
123 IV-induced elevation of pro-inflammatory and cardiotoxic long-chain acylcholines to preinfection leve
124                                              Cardiotoxic manifestation associated with breast cancer
125                   Our findings demonstrate a cardiotoxic mechanism by which crude oil affects the reg
126          We next address the pollution-based cardiotoxic mechanisms first identified in fish followin
127 e showed decreased circulating levels of the cardiotoxic metabolite, doxorubicinol, after administrat
128 sequent decrease in the concentration of its cardiotoxic metabolite.
129 d did not (no risk [NR]) receive potentially cardiotoxic modalities, and with values expected for com
130               However, it is one of the most cardiotoxic of the FDA-approved TKIs.
131 f the BCR-ABL oncogene and is among the most cardiotoxic of TKIs.
132  in association with other drugs that may be cardiotoxic or for patients with conduction disorders.
133                                          The cardiotoxic, oxidative, and abnormal electric performanc
134             However, the precise identity of cardiotoxic PAHs, and the mechanisms underlying contract
135 w a broad framework of the global problem of cardiotoxic pollution to be established.
136                       Mortality is caused by cardiotoxic polycyclic aromatic hydrocarbons (PAHs), ubi
137 strate that R406W-desmin provokes its severe cardiotoxic potential by a novel pathomechanism, where t
138  not support a clinically relevant ischaemic cardiotoxic potential of AIT in patients with early brea
139 ), alongside cancer treatments received with cardiotoxic potential.
140 t a direct SERCA2a activator does not induce cardiotoxic pro-arrhythmogenic events in human cardiac c
141 eted therapy, warranting evaluation of their cardiotoxic profiles.
142 -to-treat cancers but have also revealed new cardiotoxic profiles.
143                            Its antitumor and cardiotoxic properties have been ascribed to anthracycli
144  of diffuse interstitial fibrosis indicate a cardiotoxic response on a similar scale as previously se
145  small molecule and correctly determined the cardiotoxic response to its metabolite in the heart:live
146 ists on other immune subsets involved in the cardiotoxic response.
147 rexpressing Beclin 1 manifested an amplified cardiotoxic response.
148 y fail to reflect the fundamental biology or cardiotoxic responses of the human myocardium.
149 ence for the role of catalase in doxorubicin cardiotoxic responses.
150 hat particular levels of hyperkalemia confer cardiotoxic risk have been challenged by several reports
151 n in patients or has implications for future cardiotoxic risk is unknown.
152  and its presence was associated with higher cardiotoxic risk.
153 ess the rapidly growing problem of disparate cardiotoxic risks among women and underrepresented patie
154 otheraputic use of antineoplastic drugs with cardiotoxic side effects (i.e., doxorubicin).
155                However, due to its extensive cardiotoxic side effects a lifetime cumulative dose limi
156                                 For example, cardiotoxic side effects of the cancer drug imatinib mig
157 ugs is restricted owing to potentially fatal cardiotoxic side effects.
158 n is an effective anticancer drug with known cardiotoxic side effects.
159 ts clinical use is limited because of severe cardiotoxic side effects.
160 ut its application is limited because of its cardiotoxic side effects.
161 and identified chemical frameworks that show cardiotoxic signal in iPSC-CMs.
162 bb, Princeton, NJ) and r-verapamil, the less cardiotoxic stereoisomer, in heavily pretreated patients
163 of cardiovascular complications secondary to cardiotoxic systemic and radiation therapies.
164                          Ropivacaine is less cardiotoxic than bupivacaine and, at low concentrations,
165  Lidocaine is generally considered much less cardiotoxic than other local anesthetics and is used com
166 as the advantage of being significantly less cardiotoxic than racemic bupivacaine, which suggests tha
167 cer survivors of African ancestry exposed to cardiotoxic therapies (anthracyclines and/or heart radio
168 rd ratio [HR], 2.15 [95% CI], 1.37 to 3.38), cardiotoxic therapies (anthracyclines: HR, 2.35 [95% CI,
169      Childhood cancer survivors treated with cardiotoxic therapies are recommended to have routine ca
170 ected radiotherapy are the most well-studied cardiotoxic therapies, and dose reduction, use of cardio
171 al dysfunction in patients who are receiving cardiotoxic therapies.
172 long-term risks of cardiac dysfunction after cardiotoxic therapy (anthracyclines, trastuzumab/pertuzu
173 graphic surveillance for several years after cardiotoxic therapy and also suggest a need to examine t
174 ty between survivors exposed or unexposed to cardiotoxic therapy and control subjects, and to evaluat
175 Childhood Cancer Survivor Study who received cardiotoxic therapy and reported no history of cardiomyo
176 tricular ejection fraction (LVEF) <50% after cardiotoxic therapy initiation and included early- and l
177 om 1.8% at 2 years to 15.3% at 15 years from cardiotoxic therapy initiation.
178    Patients with breast cancer who completed cardiotoxic therapy underwent echocardiographic screenin
179 ociated with cardiovascular risk factors and cardiotoxic therapy were assessed in multivariable Poiss
180 e intolerance in survivors exposed or not to cardiotoxic therapy, and associations among organ system
181 in any survivor who has received potentially cardiotoxic therapy.
182 rove the care of oncology patients receiving cardiotoxic therapy.
183 ith CKD, but not from healthy controls, were cardiotoxic; they significantly induced apoptosis both i
184                Cellular pathways affected by cardiotoxic TKIs include energy metabolism, contractile,
185 act ERK axis, which blunted the induction of cardiotoxic transcripts, in part by enhanced serine 273
186 cumentation of participants' cancer history, cardiotoxic treatment exposures, and survivorship care p
187 hildhood cancer with and without exposure to cardiotoxic treatments at a median of 11 years after dia
188  increased in other cancer populations where cardiotoxic treatments have been used.
189     Childhood cancer survivors not receiving cardiotoxic treatments nevertheless have cardiovascular
190                       The use of potentially cardiotoxic treatments should be reconsidered for high-r
191 gavon, United Kingdom) is effective and less cardiotoxic, which is important in this setting.

 
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