Cadmium (Cd), a heavy metal with strong carcinogenic properties has been linked with breast cancer risk. Epidemiological data on the association between Cd exposure and breast cancer are not consistent and suggest that this relationship may be modulated by a number of different factors. The mechanisms of action underlying the molecular effects of Cd, especially in terms of its carcinogenicity, are generally not well understood. Specifically, in the mammary gland, the effects of Cd are considered to be related mainly to its oestrogenic potential, however, several other mechanisms have also been suggested, such as epigenetic alterations, inhibition of DNA repair pathways, induction of oxidative stress, interference with metallothioneins, cadherins and integrins, as well as interactions with xenobiotics. This review summarizes the current state of knowledge in this field, including potential mechanisms of action of Cd in breast cancer initiation and progression, as well as possible ways of protection against its toxicity. Importantly, there are many research gaps in this area since limited evidence is available from experimental studies. Important issues to be further investigated concern exact molecular mechanisms of Cd accumulation in the tissues and Cd-induced activation of eostrogen receptors. Impact on DNA damage and epigenome upon Cd exposure in breast cancer development remains still highly unexplored area and should gain more interest.

Cervical cancer is a common female cancer. It is strongly associated with human papillomavirus (HPV) infection. However, HPV infection alone is not sufficient to induce cervical cancer because its development is dependent on the coexistence of several factors that enable the virus to overcome the host immune system. These include individual genetic background, environmental factors, or diet, including dietary selenium intake. Selenium is an essential trace element with antiviral properties and has been shown to exert antitumor effects. Surprisingly, the role of selenium in cervical cancer has not been studied as intensively as in other cancers. Here, we have summarized the existing experimental data on selenium and cervical cancer. It may be helpful in evaluating the role of this nutrient in treatment of the mentioned malignancy as well as in planning further studies in this area.

Alterations in brain-derived neurotrophic factor (BDNF) expression have been suggested to mediate the influence of environmental factors on the emergence of depression through epigenetic modifications. However, research on this subject in the developmental population is lacking and the pathophysiology of adolescent depression remains unclear. We aimed to investigate the alterations in BDNF expression and global DNA methylation in depression among adolescent girls. Thirty female inpatients with the initial diagnosis of depression were assessed before and after the period of antidepressant treatment and compared with thirty age-matched healthy controls. The assessment involved BDNF and proBDNF serum levels, the BDNF gene exon IV promoter methylation, and global DNA methylation. The methylation level in the BDNF gene exon IV promoter was significantly lower in the studied group compared with the control and correlated negatively with the severity of depression. The test distinguished the studied group from the controls with a sensitivity of 37% and specificity of 90%. The differences were no longer present after the period of antidepressant treatment. No differences in the global DNA methylation, BDNF, and proBDNF levels were found. We concluded that decreased methylation in the BDNF exon IV promoter could be considered as a biomarker of a depression state among adolescent girls.

Background: There is substantial evidence supporting the role of genetic alterations in chemically induced carcinogenesis. We analyzed the existing literature to gather data on genetic alterations linked to human carcinogens and their possible connection to genotoxic outcomes. The review emphasizes carcinogenic substances and occupational exposures identified as “carcinogenic to humans”. In particular, we searched for studies describing genotoxic alterations linked to agents and occupational exposures for which the International Agency for Research on Cancer has found sufficient evidence of an association with bladder cancer. Methods: The review was carried out in compliance with the PRISMA standards. A comprehensive search of the PubMed database was conducted to identify studies published through March 2024. Results: We identified 60 studies that evaluated genetic alterations for 16 carcinogenic agents and occupations (such as aluminum production, 4-aminobiphenyl, auramine production, benzidine, chlornaphazine, cyclophosphamide, firefighters, magenta production, 2-naphthylamine, opium consumption, ortho-toluidine, painters, the rubber manufacturing industry, Schistosoma haematobium infection, X-radiation, gamma-radiation) in healthy humans. Conclusions: The genotoxic effects of chemical agents in healthy individuals have been well studied and characterized. Additionally, this review presents numerous studies concerning occupational exposure but not exclusively. Genotoxicity assessments have mainly been conducted on biological materials such as blood, peripheral blood lymphocytes, urine, and buccal epithelial cells. The most frequently examined genotoxic effects were DNA damage, chromosomal abnormalities, and micronuclei. Standardized data to clearly define a dose–response relationship for predicting delayed health effects are still lacking.

Background: Selenium (Se) and selenoproteins have been shown to be involved in lipid metabolism mainly due to their ability to modulate redox homeostasis in adipose tissue. The underlying mechanisms are yet to be evaluated. In the light of few data related to the association between polymorphic variants of selenoprotein encoding genes and metabolic syndrome or obesity in humans, the role of selenoprotein polymorphisms in lipid metabolism remains unclear. The aim of this study was to investigate the impact of allelic combination within selenoprotein and redox related genes on the markers of lipid metabolism and oxidative stress. Methods: The study comprised 441 healthy individuals from Poland, in the 18-74 year age group. Allelic combinations were investigated within the polymorphic variants of four selenoprotein encoding genes (GPX1 rs1050450, GPX4 rs713041, SELENOP rs3877899 and SELENOF rs5859) and the redox related gene (SOD2 rs4880). The impact of the most common allelic GPX1-GPX4-SELENOP-SELENOF-SOD2 combinations was assessed on the following markers: triglycerides (TG), total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C), glutathione peroxidase activities (GPX1, GPX3), lipid peroxidation (as TBARS), ceruloplasmin (Cp) and superoxide dismutase 1 (SOD1). Results: Multivariable analysis revealed significant associations between three allelic combinations and markers of lipid metabolism, including HDL-C and TC/HDL-C ratio (AAAAa), LDL-C (aaAaa), and triglycerides (aaaaA), whereas two allelic combinations (aAaAA, aaaAA) were associated with GPX3 activity. Conclusion: This study confirms the possible implication of selenoproteins in lipid metabolism and warrants further research on specific allele combinations within selenoprotein and redox related genes in order to identify functional genetic combinations linked to metabolic phenotype.

Objectives: Triple-negative breast cancer (TNBC) is an aggressive cancer subtype with limited treatment options due to the absence of estrogen, progesterone receptors, and HER2 expression. This study examined the impact of DNA methylation and demethylation markers in tumor tissues on TNBC patients’ response to neoadjuvant chemotherapy (NACT) and analyzed the correlation between 5-methylcytosine (5-mC) and 5-hydroxymethylcytosine (5-hmC) and clinicopathological characteristics, offering new insights into the predictive value of these epigenetic markers. Methods: The study included 53 TNBC female patients, 19 of whom received neoadjuvant chemotherapy (NACT) before surgery. Global DNA methylation and demethylation levels were quantified using an ELISA-based method to measure 5-mC and 5-hmC content in DNA isolated from pre-treatment biopsy samples (in patients undergoing NACT) and postoperative tissues (in patients without NACT). Results: In patients who received NACT, those with disease progression had significantly higher pretreatment levels of 5-hmC (p = 0.028) and a trend toward higher 5-mC levels (p = 0.054) compared to those with pathological complete response, partial response, or stable disease. Higher 5-mC and 5-hmC levels were significantly associated with higher tumor grade (p = 0.039 and p = 0.017, respectively). Additionally, a positive correlation was observed between the Ki-67 proliferation marker and both 5-mC (rS = 0.340, p = 0.049) and 5-hmC (rS = 0.341, p = 0.048) levels in postoperative tissues. Conclusions: Our study highlights the potential of global DNA methylation and demethylation markers as predictors of tumor aggressiveness and chemotherapy response in TNBC. Further research in larger cohorts is necessary to validate these markers’ prognostic and predictive value.