The extracellular matrix is a structure composed of many molecules, including fibrillar (types I, II, III, V, XI, XXIV, XXVII) and non-fibrillar collagens (mainly basement membrane collagens: types IV, VIII, X), non-collagenous glycoproteins (elastin, laminin, fibronectin, thrombospondin, tenascin, osteopontin, osteonectin, entactin, periostin) embedded in a gel of negatively charged water-retaining glycosaminoglycans (GAGs) such as non-sulfated hyaluronic acid (HA) and sulfated GAGs which are linked to a core protein to form proteoglycans (PGs). This highly dynamic molecular network provides critical biochemical and biomechanical cues that mediate the cell–cell and cell–matrix interactions, influence cell growth, migration and differentiation and serve as a reservoir of cytokines and growth factors’ action. The breakdown of normal ECM and its replacement with tumor ECM modulate the tumor microenvironment (TME) composition and is an essential part of tumorigenesis and metastasis, acting as key driver for malignant progression. Abnormal ECM also deregulate behavior of stromal cells as well as facilitating tumor-associated angiogenesis and inflammation. Thus, the tumor matrix modulates each of the classically defined hallmarks of cancer promoting the growth, survival and invasion of the cancer. Moreover, various ECM-derived components modulate the immune response affecting T cells, tumor-associated macrophages (TAM), dendritic cells and cancer-associated fibroblasts (CAF). This review article considers the role that extracellular matrix play in breast cancer. Determining the detailed connections between the ECM and cellular processes has helped to identify novel disease markers and therapeutic targets.

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Objectives: The tests conducted were intended to analyze the concentration of p53 protein and anti-p53 autoantibodies in serum of women with ovarian tumours. Material and methods: The study included patients with diagnosed ovarian cancer: Cystadenoma serosum or Cystadenocarcinoma papillare serosum at IIIc stage (including 10 women who had G1, 14 women who had G2 and 30 women who had G3 staging). Concentrations of parameters were measured by ELISA. Results: The analysis of the obtained results showed statistical significance between the concentration of p53 protein depending on the degree of differentiation of G1 and G3 (p < 0.001) and anti-p53 autoantibodies depending on the degree of differentiation of G1 and G2 (p < 0.05) as well as G2 and G3 (p < 0.01). In addition, the determined p53/anti-p53 autoantibodies ratio was only significant between G1 and G2 (p < 0.05), as was the assessment of the percentage of the tested parameters in the immune complex. Conclusions: Immune system disorders involving the p53 protein and anti-p53 autoantibodies may be one of the immune mechanisms involved in the pathogenesis of ovarian serous cancer.