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The second trial (n=55) was performed in the Hôpital Cochin (Paris) to study the relationship between docetaxel toxicity and genetic polymorphisms (Tran et al, 2006).
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However, mechanistic insights are not yet elucidated for different sensitivity to docetaxel toxicity between Japanese and Western populations.
We conclude that ATRA synergistically enhances docetaxel toxicity by down-regulating Bcl-2 expression and partially reverses the docetaxel-induced G2/M arrest by inhibiting docetaxel-induced cdc2 phosphorylation in a pathway that is dependent on MAPK.
Patients were randomized in a 1 1 fashion between docetaxel and docetaxel and ganetespib therapy.
In a tumour-bearing mouse model, therapeutic synergy was observed between docetaxel and 5-FU, and 70% of the highest nontoxic dose of each agent could be administered in combination without any additional toxicity (Bissery et al, 1995).
As there is potential synergy between docetaxel and capecitabine (Nadella et al, 2002), thought to be mediated through activation of thymidine phosphorylase by docetaxel, we also aimed to explore the activity of a doublet regimen, thereby avoiding the potential toxicity of cisplatin.
Nevertheless, the addition of docetaxel increases hematological toxicity and infectious complications.
Docetaxel has relatively greater hematologic toxicity and is more commonly associated with edema than paclitaxel [ 53].
Our goals were to [1] evaluate the toxicity and maximum-tolerated dose of docetaxel with imatinib, and [2] evaluate the decline of prostate-specific antigen (PSA) induced by imatinib alone, and imatinib and docetaxel.
Herein, we characterized the efficacy, toxicity and pharmacokinetic properties of NP docetaxel formulations that have differential drug loading but are otherwise identical.
The other docetaxel-related chronic toxicities (i.e. skin toxicity and nail disorders) were infrequent and never severe.
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