Tissue Aluminum Concentration Does Not Affect the Genomic Stability of ERBB2, C-MYC, and CCND1 Genes in Breast Cancer

Abstract

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.

Aluminium in cosmetics and personal care products

“…The metals that change the oestrogen hormone level are called metalloestrogen. The unwanted oestrogenic effects of aluminium, such as altered protein expression, change in puberty signs and tumour development, may be seen (House et al, 2013; Mandriota et al, 2016; Mannello et al, 2013; Pineau et al, 2014; Rodrigues‐Peres et al, 2013a, 2013b; Wallace, 2015). Overall metalloestrogenic effects of aluminium may potentiate the breast's changes (Darbre, 2009; Darbre, Mannello, & Exley, 2013; Wallace, 2015).…”

“…Rodrigues‐Peres et al (2013b) measured aluminium concentration in central and peripheral parts of breast tumours. They found no significant difference between aluminium concentration in the tumour and the healthy tissue around the tumour.…”

“…The human body is exposed to cosmetics and personal care products that contain aluminium salts daily. It has been hypothesized that aluminium in these products may harm human health; therefore, it should be removed from cosmetics and personal care products (Darbre, 2016; Fakri et al, 2006; Flarend et al, 2001; Rodrigues‐Peres et al, 2013a, 2013b). However, antiperspirants are still prescribed in hyperhidrosis (HH) treatment (Brown et al, 2014; Hosp & Hamm, 2017).…”

Genotoxic Effects of Aluminum Chloride and Their Relationship with N-Nitroso-N-Methylurea (NMU)-Induced Breast Cancer in Sprague Dawley Rats

“…For example, cadmium reportedly induces DNA fragmentation and tumorigenesis, but not the expression of genes such as bcl-x or MT-1 in Wistar rat testis and prostate [90]. Rodrigues-Peres et al [91] found no ERBB2, C-MYC, and CCND1 gene instability when assessing the correlation between aluminum and genomic instability in cancerous human breast tissues and healthy tissues. Additionally, as previously reported, the changes were observed at extremely low or nanomolar concentrations of aluminum, with the ability to induce the expression of pro-inflammatory and pro-apoptotic genes.…”

Molecular Subtypes of Breast Cancer Are Not Associated with the Clinical Under- or Overstaging of Breast Cancer

“…We performed a secondary analysis of data collected from other studies linked to our study group. [8][9][10][11][12] The principal investigator (Juliana Pinho Espinola -JPE) conducted a further review of 226 medical records, specifically for the present report, in order to obtain data regarding clinical staging, exams, and pathological staging. Clinical and epidemiological data are from January 2008 to September 2010.…”