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Background. Radiotherapy plays a vital role in the management of cervical cancer. However, because of high patient load and limited resources, waiting lists are unacceptably long. This is a highly curable malignancy that often occurs in economically active, relatively young women. The impact of treatment delays on society is therefore disproportionately large when compared with many other malignancies. Delays also impact negatively on the healthcare system and place further stress on an already burdened department. Objective. To evaluate the potential impact of radiotherapy delays. Methods. Eighty-one patients requiring radical radiotherapy for cervical cancer were selected. Patients were re-evaluated every 4 weeks while waiting, and again at simulation. Results. Median delay from first consultation to simulation was 55 days. Longer delays were not statistically correlated to tumour progression. Most of the upstaging occurred around 40 -65 days. One in four patients received blood transfusions and required hospital admission. Four patients needed haemostatic brachytherapy for bleeding. Conclusion. A relationship between time waited and disease progression could not be proven. However, numbers were small and statistical tests were probably underpowered. The study does, however, highlight unacceptably long delays for radiotherapy, and a wait of less than 40 days is recommended. Despite significant advances in screening and management over the past few decades, cervical cancer remains a significant burden, particularly in developing countries, where more than 80% of cases are diagnosed.[1] Cervical cancer comprises 22.2% of all cancers in women of sub-Saharan Africa and carries the highest rate of cancer-related mortality.[2]

Following exposure of cells to gamma-radiation, a cascade of intracellular consequences may be observed in a semitemporal manner. This includes deoxyribonucleic acid (DNA) damage and reactive oxygen species (ROS) accumulation initially, with consequent signaling for DNA repair and facilitative regulation of the cell cycle. Failure to rectify the damage or ROS levels leads to induction of senescence or apoptosis. 2-Ethyl-3-O-sulfamoyl-estra-1,3,5(10),15-tetraen-17-ol (ESE-15-ol), a 2-methoxyestradiole analog designed in silico for superior pharmacokinetics, was investigated for its potential to enhance apoptotic signaling and decrease the long-term survival of cells exposed to radiation. Sequential early intracellular effects within radiation-treated MCF-7 breast- and A549 lung cancer cells pre-exposed to low-dose ESE-15-ol were investigated using various flow cytometric protocols, spectrophotometry, and microscopy. Long-term cellular survival and proliferation was examined using clonogenic studies, which demonstrated a significant decrease in the presensitized cells. Combination-treated cells exhibited increased superoxide formation, and decreased Bcl-2 expression and -phosphorylation. Induction of apoptosis and elevation of the sub-G1 phase was evident in the pre-exposed MCF-7 cells, although only minimally in the A549 cells at 48-h. These results indicate that low-dose ESE-15-ol may increase tumor response to radiation. Future studies will investigate the effect of ESE-15-ol pre-exposure on radiation-induced DNA damage and repair mechanisms.

Endemic African Kaposi’s sarcoma is a common neoplastic disorder in the sub-Saharan region of Africa. We present a retrospective analysis of 47 black patients with the endemic African (HIV-negative) variant of Kaposi’s sarcoma treated and followed up in the Johannesburg General Hospital between 1980 and 1990. Four patients (8%) presented with simultaneous Kaposi’s sarcoma plus malignant lymphoma, indicating a low but significant association with lymphoproliferative disorders. Of 47 patients seen, 29 presented with localized disease and were treated by means of local radiation therapy. Seventeen patients received chemotherapy. The objective response rate was > 80% irrespective of the treatment modality. We conclude that endemic African Kaposi’s sarcoma is a chemo- and radiosensitive tumour.

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