ABSTRACT
Amongst all currently used drugs in the field of cancer therapy, the most prominent group of agents which induce DNA, damage both directly or indirectly. Intuitively DNA should not be a perfect target for relatively unspecific small molecular weight drugs. However, the current understanding is that not damage per se but cellular response to DNA damage induced by antitumor agents is responsible for their specific targeted effect towards cancer cells in comparison to the normal cells. DNA damaging chemotherapeutics include compounds with diferent activities namely: directly or indirectly induce DNA strand breaks, covalently modify DNA bases, change the chromatin structure and topology by inhibiting chromatin-modifying enzymes. In this special issue of Current Medicinal Chemistry entitled....
Subject(s)
Antineoplastic Agents/toxicity , DNA Damage/drug effects , Antineoplastic Agents/chemistry , Antineoplastic Agents/therapeutic use , Chromatin/chemistry , Chromatin/metabolism , Humans , Neoplasms/drug therapy , Neoplasms/pathologyABSTRACT
Chronic lymphocytic leukemia (CLL), a clonal expansion of B CD5+ cells, is the most common type of adult leukemia in western countries. The accumulation of neoplastic B-cells is primarily caused by prolonged life-span of these cells due to deregulation of apoptosis, and only marginally due to a higher proliferation rate. In spite of numerous reports characterizing particular mechanisms of B-CLL cell apoptosis, still relatively little is known about the complex regulation of this process. Therefore, more detailed research is required to understand the complicated mechanisms and regulatory processes of apoptosis in neoplastic B lymphocytes.
