The neoplasm subsequently metastasized and required additional VP-16 and carboplatin for control.
2
Cisplatin and VP-16 combination can be considered as a salvage treatment in heavily pretreated patients with advanced breast cancer.
3
Fas-FasL system participated in the apoptosis induced by DEX and VP-16; different drugs induce apoptosis by different pathway of signal transduction.
4
Chromatin condensation was morphologically evident only when cells detached from the monolayer; untreated or VP-16-treated attached cells retained a normal morphology.
5
This effect was even more pronounced when cells were exposed to VP-16 4 hours before gemcitabine.
6
The combination of VP-16 and gemcitabine, however, resulted in the formation of more DSBs in this cell line than each drug alone.
7
These data indicate mechanisms other than those attributable to decreased drug uptake or altered topoisomerase II exist for clinical resistance to VP-16.
8
In a multiple linear regression model, HDC plus VP-16 resulted in a higher PBPC yield than HDC but all other regimens did not.
9
It has been recently shown that VP-16-213, a semi-synthetic derivative of podophyllotoxin, inhibits the function of mammalian DNA topoisomerase II.
10
The mean number of days to mobilization with HDC was 10.2 days, 17.1 days for HDC plus VP-16, and 14.2 days for all other regimens.