Classical chemotherapeutic agents such as mitotic inhibitors (spindle poisons), alkylating agents, antimetabolites, topoisomerase
inhibitors, and anthracenediones (anthracyclines) inhibit DNA synthesis and mitosis, thereby killing or impeding the proliferation of
rapidly dividing cells. During the last decade, targeted therapy has gained advantage over conventional treatment regimens, as it is more
effective against cancer and also much less harmful to normal cells, thus minimizing the side-effects of chemotherapy. This type of
treatment blocks the proliferation of cancer cells by inhibiting the function of specific targeted molecules needed for tumor growth and
metastasis. Targeted therapy agents include monoclonal antibodies and small-molecule inhibitors, which most commonly target receptor
and/or non-receptor tyrosine kinases. Most members of the BCL2 apoptosis-related family regulate cellular fate as a response to
antineoplastic agents. Modulations at the mRNA and protein levels of these genes are usually associated with sensitivity or resistance of
various types of cancer cells to chemotherapeutic drugs. Moreover, alterations in expression of BCL2-family members, induced by
anticancer drug treatment, can trigger or simply facilitate apoptosis. In this review, we summarize information about changes in
apoptosis-related gene expression caused directly or indirectly by antineoplastic agents, as well as about the impact of BCL2-family
members on the chemosensitivity or chemoresistance of cancer cells.
Anticancer agents, antineoplastic agents, chemotherapeutic drugs, molecular tumor markers, monoclonal antibody therapy,
Department of Biochemistry and Molecular Biology, University of Athens, Panepistimiopolis, Athens 15701, Greece.