Little quantitative data exist on the extent of apoptosis (genetically-mediated cell deletion) in different human tumor types. Hematoxylin and eosin-stained paraffin sections of 102 malignant tumors (58 types) were evaluated for apoptotic cells and apoptotic bodies, using the 40x objective with a calibrated eye-piece and avoiding necrotic zones. The percentage of apoptotic cells and apoptotic bodies in the total number of tumor cells examined was designated as the apoptotic index (AI) for each case. There was a wide range in the AI for different tumor types: 45 tumors had AI < 1% and 93 had an AI of < 7%. In 107 additional tumors (11 types), the AI was determined to be within the same low, intermediate, or high range as the index cases. Apoptotic nuclear material was usually more prominent than mitoses. These results suggest that each tumor type has a characteristic AI that reflects innate tumor cell susceptibility to undergo apoptosis. Additional data are needed to determine whether significant variations in AI correlate with altered proliferative indices, aberrant oncogene/tumor suppressor gene expression, and standard clinicopathologic variables.
Certain oncogenes and tumour suppressor genes are known to modulate apoptosis. To investigate whether overexpressed bcl-2 and abnormally stabilized p53 are associated with reduced apoptosis in paraffin sections of non-small cell lung carcinoma, apoptotic, mitotic, and Ki-67 labelling indices were determined and correlated with bcl-2 and p53 immunoreactivity in 54 squamous cell carcinomas and 22 adenocarcinomas. Nineteen squamous cell carcinomas (35.2%) showed over-expression of bcl-2, but all 22 adenocarcinomas were bcl-2 negative. Thirty-seven squamous cell carcinomas (68.5%) and 13 adenocarcinomas (59.1%) showed p53 over-expression. Apoptotic tumour cells were identified among p53 positive and bcl-2 positive tumour cells. There was a significant linear correlation between apoptotic indices and mitotic indices. bcl-2 over-expression and p53 over-expression were not associated with attenuated apoptosis, or altered mitotic or Ki-67 labelling indices in either tumour type. Neither bcl-2 nor p53 was of prognostic significance. These results suggest that apoptosis in non-small cell lung carcinoma occurs independently, and is not modulated primarily by, bcl-2 or p53. It is likely that the effects on apoptosis of bcl-2 and p53 are countered by those of other oncogene products and/or additional factors that regulate apoptosis in vivo.
We have examined 26 human AIDS brains obtained at post mortem for infection by human immunodeficiency virus (HIV) and human cytomegalovirus (HCMV), and for dual infection of cells by both viruses. The techniques used were enzyme-linked immunocytochemistry for HCMV and in situ hybridisation using a cDNA probe for HIV. Using these techniques, HCMV infection was detected in 14 brains, HIV infection in 14 brains, and coinfection with HIV and HCMV in 7 brains. Four case of dual HIV/HCMV infection were found where no colocalisation could be detected. In randomly chosen dually infected areas 19.2% of infected cells were coinfected with both viruses. Although cells identified morphologically as macrophages were the most common infected cell type, astrocytes and neurons were both singly and doubly infected with HIV and HCMV. Complete clinical data were available for 4 of the 7 cases with coinfection and each had AIDS dementia complex.
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