Canine mammary gland tumors (CMTs) are one of the most prevalent cancers in dogs and a good model for human breast cancer (BC), however gene expression analysis of CMTs is scarce. Although divergence of genes expression has been found in BC of different human races, no such research of different dog’s breeds has been done. The purpose of this study was to investigate expression of the VEGF-B, VEGF-A, FLT-1, KDR, ERBB2, EGFR, GRB2, RAC1, CDH1 and HYAL-1 genes of canine mammary carcinomas, compare the expression levels with clinicopathological parameters and analyze expression disparities between different breeds. Carcinomas and adjacent tissues were collected from female dogs to perform routine histopathology, immunohistochemistry (IHC) and quantitative real-time polymerase chain reaction (qRT-PCR). We found that VEGF-B and EGFR genes were overexpressed in the mammary gland carcinomas compared to adjacent tissue. VEGF-B gene expression had associations with different parameters (tumor size, grade, and absence of metastasis). Furthermore, differences in VEGF-B, FLT1, ERBB2, GRB2, RAC1, CDH1 and HYAL-1 genes expression have been found in different breed dogs (German Shepherd, Yorkshire Terrier) and mixed-breed dogs indicating that a dog’s breed could determine a molecular difference, outcome of cancer and should be accounted as a confounding factor in the future gene expression research.

BackgroundRecent achievements have established that the very first years since the development of the RA are decisive in terms of the progression of the pathological process and the prediction of its remote consequences. This substantiated the need to reflect the heterogeneity and stage of the RA. First of all it concerns the early RA – a time point when the pathological process is in the primary exudative phase and its reversibility is significantly higher, because of not completely formed autoimmune mechanisms and the absence of pannus.ObjectivesOur aim was to establish the relationship between the levels of Anti-Citrullinated Peptide Antibody (ACPA), cartilaginous oligomeric matrix protein (COMP) and radiographic progression in patients with early RAMethods75 patients with a diagnosis of early RA were examined, the duration of symptoms was less than 1 year (on average – 4.91±2.90 month) that were observed repeatedly on average after 12 months (11.8±1.2 months). The average age of patients was 46.4 years (from 34 to 62 years), 69.33% of the examined ones were women, the average duration of the disease at the time of the initial study was 107 days (57–194 days). Immune dysregulation in early RA was confirmed with the evaluation of the key proinflammatory cytokines – ACPA and COMP by the enzyme-linked immunosorbent assay (ELISA) according to the instructions for diagnostic kits. For the testing of articular cartilage lesions and injury of flexor’s and extensor’s tendons, MRI (1.5 T) and ultrasound diagnostics (US) were performedResultsImmunological analysis of serum samples of ACPA, COMP was shown the role of these cytokines as prognostic factors of development and prognosis of early RA. The serological features of the obtained data revealed a correlation between the increased concentration of COMP and the progression of joint lesions without ACPA level increase. According to the baseline US data, the tendons of general flexor muscles and extensor brushes were most commonly observed in the examined patients: in general, 52 patients (69.3%) and 23 (30.7%), respectively. The injury of the tendons of individual fingers (I-V) in the mode of longitudinal and transverse scanning had its own patterns (table 1).ConclusionsIn patients with seronegative (normal ACPA ranges) early RA and high levels of COMP – the highest frequency of erosive and destructive changes can be observed.Injury of the tendons of flexors and extensors determined in major part of the patients with early RA.Abstract AB0218 – Table 1Injury of the flexor’s and extensor’s tendonsFingersInjury of flexor tendonsInjury of extensor tendons Totally, n (%)Exudative tenosinovite,n (%)Exudative – proliferative tenosinovitis,n (%)Totally, n (%)Exudative tenosinovite,n (%)Exudative – proliferative tenosinovitis,n (%) I1 (1,3)1 (1,3)0 (0,0)4 (5,2)3 (3,9)1 (1,3)II58 (77,3)52 (69,3)6 (8,0)26 (34,7)24 (32,0)2 (2,6)III36 (48,0)35 (46,7)1 (1,3)18 (24,0)18 (24,0)0 (0,0)IV22 (29,3)20 (26,7)2 (2,7)12 (16,0)9 (12,0)3 (3,9)V13 (17,3)13 (17,3)0 (0,0)6 (8,0)6 (8,0)0 (0,0)Abstr...

No abstract