THE ROLE OF APOPTOSIS IN GYNECOLOGICAL MALIGNANCIES

Apoptosis is a process of single-cell deletion requiring active partic ipation of the cell in its own demise, First described in 1972, it is now known to pray a major role in embryogenesis, tissue homeostasis an d neoplasia. Apoptosis can be initiated when DNA damage occurs causing the cell to pause in its reproductive cycle, If the DNA damage is bey ond repair, the eel proceeds to apoptotic cell death, When the genetic mechanism(s) involved in the pathway of apoptosis is altered, the cel l does not die. Further mutations occur by proliferation and such mult iple mutational events can leed to a malignant phenotype and cancer gr owth. The tumour suppressor gene p53 causes a DNA-damaged cell to rest and attempt repair, if damage is irreparable, p53 levels will continu e to increase, initiating apoptosis, Mutation of p53, found in approxi mately 50% of cancers, can stop the apoptotic process, Increased bcl-2 expression, an apoptosis inhibitor, also plays a role in cellular tra nsformation and cancer growth. Its altered expression occurs in the pr esence of oncogene expression. This paper reviews the role of apoptosi s in malignant transformation, cancer growth, and response to therapy for gynaecological cancers. For cervical cancer and its precursors, da ta on apoptotic index, bcl-2 and Bar expression are presented and disc ussed in relationship to human papillomavirus expression. In ovarian e pithelial malignancies, the role that apoptosis plays in chemotherapeu tic responses is reviewed, The data for endometrial cancer are current ly limited to apoptotic index.