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1  anthracyclines, taxanes, camptothecins, and epipodophyllotoxins.
2 thracyclines (20% v 8%; HR, 2.86; P < .001), epipodophyllotoxins (23% v 1%; HR, 12.20; P < .001), or
3 ng plan support the relative safety of using epipodophyllotoxins according to the therapeutic plans o
4 s are caused by platinum compounds, taxanes, epipodophyllotoxins and asparaginase.
5         Cytochrome P450 (CYP) 3A metabolizes epipodophyllotoxins and other chemotherapeutic agents.
6                                              Epipodophyllotoxins are associated with leukemias charac
7 ive doses of alkylators, anthracyclines, and epipodophyllotoxins are below thresholds usually associa
8                                     Although epipodophyllotoxins are commonly used in contemporary tr
9 oup clinical trials were identified that use epipodophyllotoxins at low (<1.5 g/m2 etoposide), modera
10  Tumor cell resistance to anthracyclines and epipodophyllotoxins can be due to reduced drug accumulat
11 cer mortality (radiation, alkylating agents, epipodophyllotoxins), cardiac mortality (chest irradiati
12                   CYP3A metabolism generates epipodophyllotoxin catechol and quinone metabolites, whi
13   The variant may decrease production of the epipodophyllotoxin catechol metabolite, which is the pre
14 pipodophyllotoxin is identical to etoposide, epipodophyllotoxin contains a 4'-methoxyl group on the E
15 toxin treatment and the relationship between epipodophyllotoxin cumulative dose and risk are not well
16                    Within the context of the epipodophyllotoxin cumulative dose range and schedules o
17 ubicin, and other agents, factors other than epipodophyllotoxin cumulative dose seem to be of primary
18 4beta-[(4' '-benzamido)-amino]-4'-O-demethyl-epipodophyllotoxin derivatives (11-23) were designed to
19 s shall aid in future design of novel potent epipodophyllotoxin derivatives.
20            Topoisomerase poisons such as the epipodophyllotoxin etoposide are widely used effective c
21 as anthracyclines (e.g., doxorubicin) or the epipodophyllotoxin etoposide.
22 on attributable to the PRS were greatest for epipodophyllotoxin-exposed (AUC, 0.71 v 0.63) and platin
23 s with MLL gene translocations that followed epipodophyllotoxin exposure were compared with the same
24 s and could be categorized into five groups: epipodophyllotoxins (group 1), inducers of DNA damage (g
25            Except for the sugar, 4'-demethyl epipodophyllotoxin is identical to etoposide, epipodophy
26 f DNA topoisomerase II covalent complexes by epipodophyllotoxins may play a role in the genesis of le
27 risk for treatment-related leukemia and that epipodophyllotoxin metabolism by CYP3A4 may contribute t
28         This PRS also significantly modified epipodophyllotoxin-related SMN risk among nonirradiated
29 ng agents (RR, 2.2; 95% CI, 1.6 to 3.0), and epipodophyllotoxins (RR, 2.3; 95% CI, 1.2 to 4.5) increa
30 od to develop predictive QSAR models for 157 epipodophyllotoxins synthesized previously in our ongoin
31                    We found that the group 1 epipodophyllotoxins (teniposide and etoposide) consisten
32 approximately 140-fold more resistant to the epipodophyllotoxin, teniposide (VM-26), than the parenta
33    The incidence of secondary leukemia after epipodophyllotoxin treatment and the relationship betwee
34 ates of the risk of secondary leukemia after epipodophyllotoxin treatment.
35 ion results in resistance to anthracyclines, epipodophyllotoxins, vinca alkaloids, and some alkylatin
36 amptothecin-(para)-4beta-amino-4'-O-demethyl Epipodophyllotoxin (W1), and camptothecin-(ortho)-4beta-
37 mptothecin-(ortho)-4beta-amino-4'-O-demethyl Epipodophyllotoxin (W2)] on cleavable complex formation