Abstract
Therapeutic targeting of tumours on the basis of molecular analysis is a new paradigm for cancer treatment but has yet to fulfil expectations. For many solid tumours, targeted therapeutics, such as inhibitors of oncogenic kinase pathways, elicit predominantly disease-stabilizing, cytostatic responses, rather than tumour regression. Combining oncogenic kinase inhibitors with direct activators of the apoptosis machinery, such as the BH3 mimetic ABT-737, may unlock potent anti-tumour potential to produce durable clinical responses with less collateral damage.
MeSH terms
-
Animals
-
Antineoplastic Agents / pharmacology*
-
Antineoplastic Combined Chemotherapy Protocols / therapeutic use
-
Apoptosis / drug effects
-
Biphenyl Compounds / pharmacology*
-
Fusion Proteins, bcr-abl / antagonists & inhibitors
-
Humans
-
Nitrophenols / pharmacology*
-
Piperazines / pharmacology
-
Protein Kinase Inhibitors / pharmacology*
-
Proto-Oncogene Proteins c-bcl-2 / analysis
-
Proto-Oncogene Proteins c-bcl-2 / physiology
-
Sulfonamides / pharmacology*
Substances
-
ABT-737
-
Antineoplastic Agents
-
Biphenyl Compounds
-
Nitrophenols
-
Piperazines
-
Protein Kinase Inhibitors
-
Proto-Oncogene Proteins c-bcl-2
-
Sulfonamides
-
Fusion Proteins, bcr-abl