It has long been hypothesized that body tissue uptake of
aluminum may have
biological implications in
breast cancer. In vitro and in vivo studies have shown that
aluminum may trigger
genomic instability by interfering with
DNA strands. The objective of this study was to examine the relationship between
aluminum concentrations in the peripheral and central areas of
breast tumors with the instability of three key genes in
breast cancer, ERBB2, C-MYC, and CCND1 and
aneuploidy of the chromosomes harboring these genes. Tissue samples of 118 women treated for
breast cancer were obtained. Evaluation of
aluminum content was carried out using
graphite furnace atomic absorption spectrometry. A tissue microarray slide containing the
tumor samples was used in FISH assays to assess ERBB2, C-MYC, and CCND1 expressions as well as the statuses of their respective chromosomes 17, 8, and 11. Clinicopathological data were obtained from patient's records.
Aluminum levels of >2.0 mg/kg were found in 20.3 and 22.1% of the central and peripheral
breast tumor areas, respectively. Amplification and/or
aneuploid-positive statuses for ERBB2/CEP17, C-MYC/CEP8, and CCND1/CEP11 were detected in 24, 36.7, and 29.3% of the
tumors, respectively. We found that
aluminum concentration was not related to these altered gene statuses. Our findings suggest that
aluminum concentration does not affect
genomic stability in breast tissues. Tissue microenvironment modifications, due to the presence of
aluminum compounds, seem more appealing as a possible target for future studies to determine the implications of
aluminum in breast
carcinogenesis.