Apoptosis: its role in the development of malignancies and its potential as a novel therapeutic target.
OBJECTIVE
To review the current literature regarding the role of apoptosis in the development of malignant cells and how the induction of this pathway could be used in cancer therapy.


METHODS
A MEDLINE search of basic science articles pertinent to the understanding of the normal physiologic process of apoptosis was conducted.


METHODS
Because of the rapidly growing literature regarding apoptosis, only articles describing key processes in the biology of the cell and the genetic control of apoptosis were included.


RESULTS
Apoptosis is imperative for host survival since it discards unwanted, damaged, and atypical cells. The process is therefore implicated in the continuous regulation of development, differentiation, and homeostasis. Furthermore, apoptosis is a response to physiologic and pathologic stresses that disrupt the balanced rates of cell generation and elimination. In a disease such as cancer, there is a lack of equilibrium between the rates of cell division and cell death; agents that promote or suppress apoptosis can manipulate these rates, influencing the anomalous accumulation of neoplastic cells. Pharmacologic manipulation of apoptosis can manipulate these rates, influencing the anomalous accumulation represents a novel approach in targeting malignant cells and has far-reaching implications for new directions in cancer therapy.


CONCLUSIONS
Apoptosis is a highly organized physiologic mechanism of destroying injured and abnormal cells as well as maintaining homeostasis in multicellular organisms. Both the activation and inhibition of apoptosis are tightly controlled. Pharmacologic manipulation of this pathway is a novel therapeutic target in cancer therapy.
Dixon
S C
SC
Clinical Pharmacokinetics Section, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Soriano
B J
BJ
Lush
R M
RM
Borner
M M
MM
Figg
W D
WD
D000818:Animals; D017209:Apoptosis / Q000235:genetics* / Q000502:physiology*; D016923:Cell Death / Q000235:genetics / Q000502:physiology; D006801:Humans; D009369:Neoplasms / Q000628:therapy*