Disease relevance of Epirubicin

• Two patients treated with TEF developed transient cardiac toxicity (dilatative cardiomyopathy and coronary subtotal stenosis requiring stenting) after cumulative E doses of 400 mg and 1,100 mg/m(2), respectively [1].
• Data from four randomized trials evaluating the role of ANT combinations in patients with relapsed ovarian cancer suggest that the addition of EPI or DOX to paclitaxel does not lead to better outcomes in patients with platinum- refractory or resistant disease [2].

High impact information on Epirubicin

• Changes in tumor area paralleled changes in PDI in the EPI group [3].
• Increased IFN-gamma release was also observed after stimulation of T lymphocytes with DC loaded with doxo- and epi-treated (p< 0.02 and p< 0.005, respectively) but not with cis-treated DC [4].
• Doxo and epi increased tumor expression of heat shock protein (hsp) 70 and uptake of tumor cell components by DC, whereas cis treatment had no effect on hsp70 and was associated with poor tumor uptake by DC [4].
• After treatment with Cis-platin (cis), all dying cells were in early apoptosis, whereas secondary necrosis was the prevalent death pattern observed after epirubicin (epi) and doxorubicin (doxo) [4].
• DOX caused greater inactivation of aconitase than EPI, a finding consistent with the higher formation of DOXol vs EPIol [5].

Biological context of Epirubicin

• RESULTS: The IC50 values of EPI in MCF-7 cells were 1.0, 0.7 and 0.5 ng/ml respectively for 24, 48 and 72 h applications [6].

Anatomical context of Epirubicin

• To evaluate this possibility, we compared the activity of doxorubicin (DOXO), epirubicin (EPI), idarubicin (IDA) and mitoxantrone (MITO) on a murine, multidrug resistant, leukaemic cell line (P-388/Dx) cultured in vitro [7].

Associations of Epirubicin with other chemical compounds

• Compared with epirubicin (EPI), IDA and MX2 were 17- and eightfold more effective in the CEM/A7R line respectively [8].
• Verapamil (5 microM) and PSC 833 (1 microM), which dramatically reversed resistance to EPI in the CEM/A7R line, had no sensitizing effect on the resistance of this line to MX2, but slightly decreased resistance to IDA [8].
• Simultaneously enzymatic activity of glutathione S-transferase, glutathione peroxidase, GSH and expression of GST-pi, NADPH-CYP-450 reductase were increased in EPI (1 ng/ml) - treated cells at the end of the 24 h incubation [6].

Gene context of Epirubicin

• Addition of superoxide dismutase, catalase and GSH decreased cytotoxicity of EPI [6].
• In particular, a significant increase in lifespan (T/C> 150%) and tumour growth inhibition (> 90%) was observed in animals with Sp2/0 tumours with EPI/P85 and DOX/L61 compositions [9].
• AIM: To evaluate protective effect of antioxidant enzymes against epirubicin-HCI (EPI) cytotoxicity in vitro [6].
• It is concluded that both EPI and PLD can be recommended as a reasonable single-agent treatment option for relapsed patients, with a preference for PLD taking into account its more favorable toxicity profile [2].
• Patients in group A (n=18) received low-dose (2-4 mg) mitomycin C (MMC) as the anticancer drug when the tumor was less than 5 cm in diameter; when the tumor ranged from 5 and 8 cm in diameter, 4-6 mg MMC along with 10 mg epirubicin (EPI) was given, and in cases of even larger tumors, 6-8 mg MMC, 10 mg EPI and 100 mg CBP were prescribed [10].

Analytical, diagnostic and therapeutic context of Epirubicin

• RESULTS: Compared with the control group, EPI induced an arrest in tumor growth [3].
• Under chemotherapy (MMC or EPI) all 4 treated patients suffered recurrences (100%) [11].

References