The dietary recommendation encourages reducing saturated fatty acids (SFA) in diet and replacing them with polyunsaturated fatty acids (PUFAs) n–3 (omega–3) and n–6 (omega–6) to decrease the risk of metabolic disturbances. Consequently, excessive n–6 PUFAs content and high n–6/n–3 ratio are found in Western-type diet. The importance of a dietary n–6/n–3 ratio to prevent chronic diseases is linked with anti-inflammatory functions of linolenic acid (ALA, 18:3n–3) and longer-chain n–3 PUFAs. Thus, this review provides an overview of the role of oxylipins derived from n–3 PUFAs and oxylipins formed from n–6 PUFAs on inflammation. Evidence of PUFAs’ role in carcinogenesis was also discussed. In vitro studies, animal cancer models and epidemiological studies demonstrate that these two PUFA groups have different effects on the cell growth, proliferation and progression of neoplastic lesions.

The degree of differentiation of mast cell tumours (MCTs) is the most important feature and reflects the morphological characteristics and metastatic potential of the tumour and its likely response to treatment and the prognosis. The aim of this study was to epidemiologically analyse the risk of MCT development in dogs according to breed, age, sex, size and anatomical location of the tumour using the Kiupel grading system. The analysis involved 492 dogs selected based on a histopathological assessment of 2763 canine skin tumours. A logistic regression analysis was performed to determine the odds ratios (ORs) with 95% confidence intervals. Mast cell tumours accounted for 17.8% of all diagnosed canine skin tumours. The highest risk of high-grade MCTs was noted in the Shar-Pei (OR 28.18, P < 0.001) and Weimaraner (OR 6.45, P = 0.023). The highest risk of low-grade MCTs was determined in the Boxer (OR 6.72, P < 0.001), and Pug (OR 6.13, P = 0.027). The scrotum (OR 31.72, P < 0.001), inguinal area (OR 17.69, P < 0.001) and axilla (OR 6.30, P < 0.001) had the highest risk of high-grade MCTs. The risk of high-grade MCTs increased with age and peaked in the oldest dogs, aged 11–16 years (OR 9.55, P < 0.001). A higher risk of low-grade tumours was noted in younger dogs (aged 4–6 years) (OR 8.54, P < 0.001) and females (OR 1.43, P = 0.001). Statistical analysis further revealed a higher risk of both low (OR 3.47, P < 0.001) and high-grade MCTs (OR 1.71, P = 0.006) in medium-sized dogs. This study demonstrated relationships between Kiupel grading system and phenotypic traits, age and location of canine MCTs confirming the complex biological nature of this tumour.

The role of the mitochondria in the process of carcinogenesis, mainly oxidative phosphorylation, mostly concerns their participation in the production of free radicals and ATP and in the process of apoptosis. The purpose of this study was to detect potential changes in the genes encoding the subunits 6 and 8 of the ATP synthase and their impact on the enzyme's biochemical properties, structure and function in patients with breast tumors. The tested material was mitochondrial DNA (mtDNA) isolated from specimens of ductal carcinoma (carcinoma ductale) Tp1-2Np0-1Mp0, blood and non-cancerous tissue of mammary gland (control), sampled from 50 patients who had been operated for breast cancer. In the case of missense-type changes in the mtDNA, protein prediction software was used to assess their effect on the biochemical properties of the protein, its structure and function. We identified 8 changes in the ATP6 gene in 36/50 examined breast cancer cell samples and 5 changes in the ATP8 gene (10/50). Most of them were homoplasmic changes of missense type. Four of the changes (A8439C, G8858C, C9130G and T9119G) had not been described in the literature before. The identified mutations and polymorphisms, especially those of missense type, can affect mitochondrial functions, especially if the conservative domain of the protein is concerned. Replacement of ‘wild-type’ mtDNA by mutated mtDNA can be an important event in carcinogenesis.

Complex I NADH-oxidoreductase-ubiquinone transports reducing equivalents from the reduced form of NADH to ubiquinone (coenzyme Q-CoQ). The purpose of this study was to analyze mutations in MT-ND1, MT-ND2, MT-ND3 and MT-ND6 genes and their effect on the biochemical properties, structure and functioning of proteins in patients with breast tumours. In research materials, in 50 patients, 28 total polymorphisms and five mutations were detected. Most detected polymorphisms (50 %, 14/28) were observed in MT-ND2 gene. Most of them were silent mutations. Five polymorphisms (m.G3916A, m.C4888T, m.A4918G, m.C5363T, m.C10283T) do not exist in the database. A total of five mutations in 13 patients (13/50) were detected, including two not described in the literature: m.C4987G and m.T10173C. It cannot be excluded that, through the mutations and polymorphism impact on the protein structure, they may cause mitochondrial dysfunction and contribute to the appearance of other changes in mtDNA. The results of our study indicate the presence of homological changes in the sequence of mtDNA in both breast cancer and in some mitochondrial diseases. Mutations in the examined genes in breast cancer may affect the cell and cause its dysfunction, as is the case in mitochondrial diseases.

The role of the mitochondria in the process of carcinogenesis has drawn researchers' attention since the discovery of respiratory deficit in cells, particularly those characterized by rapid proliferation. The deficit was assumed to stimulate further differentiation of the cells and initiate the process of neoplastic transformation. As many as 25-80% of somatic mutations in mitochondrial DNA (mtDNA) are found in various neoplasms. These mutations are considered to trigger the neoplastic transformation through shifts of cell energy resources, an increase in the mitochondrial oxidative stress and modulation of apoptosis. The question arises as to whether the mtDNA mutations precede a neoplasm or whether they are a result of changes and processes that take place during neoplastic proliferation.