TY - JOUR
AU - Middleton, Mark
AB - A10 Melanoma Research 2007, Vol 17 No 1 DTIC plus antisense against bcl-2 (genasense) showed mechanistic basis for treatment and determinants of an increased response rate (11.7 vs. 6.8, P¼0.019) and survival in metastatic melanoma. For successful treatments time to progression (78 vs. 49 days, P¼0.01) for the to emerge from this field we require, besides drugs that combination arm but only a trend for overall survival target resistance mechanisms, better identification of (9.1 vs. 7.9 months, P¼0.18). However, durable remis- pathways critical to tumour cell survival, better and more sions exceeding 2 years were significantly more common realistic trial designs and the means to evaluate multiple in the antisense arm (seven of 11 vs. one of two patients). agents simultaneously. The next step will be to incorporate genasense with other agents and particularly with biochemotherapy. Although INV 22 sorafenib, a multi-tyrosine kinase inhibitor, is not active as a single agent, the combination of sorafenib with carboplatin and paclitaxel in a phase I/II study showed an Drug resistance mechanisms overall response rate of 31%. This strategy is currently being evaluated by various investigators. Suzanne Egyhazi Karolinska Institute, Stockholm, Sweden Conclusion Only a better understanding of the mechan- isms of 
TI - INV 21 Clinical strategies to overcome resistance to DNA-damaging drugs
JO - Melanoma Research
DA - 2007-02-01
UR - https://www.deepdyve.com/lp/wolters-kluwer-health/inv-21-clinical-strategies-to-overcome-resistance-to-dna-damaging-zynlu1GuTi
SP - A10
EP - A10
VL - 17
IS - 1
DP - DeepDyve
ER -