A cell is a potentially dangerous thing. In unicellular organisms, cells di
vide and multiply in a manner that is chiefly determined by the availabilit
y of nutritional substrates. In a multicellular organism, each cell has a d
istinct growth potential that is designed to subsume a role in the function
of the whole body. Departure from this path to one of uncontrolled cellula
r proliferation leads to cancer. For this reason, evolution has endowed cel
ls with an elaborate set of systems that cause errant cells to self-destruc
t. This process of cell suicide is known as apoptosis or programmed cell de
ath and it plays a crucial role in the growth of both normal and malignant
cells. In this review, we describe the mechanisms whereby programmed cell d
eath is induced and executed. In particular, we concentrate on how anti-apo
ptotic signals generated by cytokines promote cell survival and how these s
ignal transduction pathways may be involved in the pathogenesis of neoplasi
a. Understanding how these processes contribute to tumorigenesis may sugges
t new therapeutic options.