# Tumor Microenvironment and Dermatological Conditions in Prostate Cancer
### Mechanisms of PCa Progression  
Inflammation is an innate defense mechanism of the body against various infectious and allergic or toxic stimuli. The inflammatory process involves the accumulation of cells such as macrophages, polymorphonuclear cells, and lymphocytes in the vessels and then their extravasation into the tissue. Over 150 years ago, [PERSON] stated that the main process involved in the appearance of cancer is inflammation. This is also confirmed by epidemiological studies that have shown that patients with inflammatory diseases have a higher risk of developing malignancies than the rest of the population [15]. Studies have shown that in almost 90% of PCa cases, histopathological examination highlights the presence of inflammatory infiltrate. In addition, a direct correlation was observed between the extent of inflammation and the grade of the tumor. The mechanisms by which chronic inflammation appears in the prostate are not fully known, but it seems that the microbial flora in the urinary tract could play a key role. The inflammatory infiltrate contains numerous types of cells that form a network, being interconnected, a network that will release a series of mediators with essential effects in tumor progression. The most important cells identified in the tumor infiltrate are CD3+ T cells (70-80%, largely CD4+ T cells), CD20+ B cells (10-15%), and macrophages (10-15%) [16]. Initially, neoplasia was considered a pathologic process that involves cell and gene expression; however, today we know that it is a disease of the tumor microenvironment (TME) [17; 18; 19]. In PCa, the mechanisms of cancer progression may be due to TME het erogeneity and aberrant activation of epithelial-mesenchymal transition (EMT). The TME supports tumor cell mobility, metastasis, and cell survival in distant organs, and EMT promotes tumor invasion and metastasis [13; 20; 21]. The TME is a dynamic system in which the tumor interacts with multiple host cells [17]. Host components include various cells, including stromal, endothelial, or immune cells, which interact with the extracellular matrix and soluble factors (e.g., cytokines, chemokines, etc.). Tumor cells in the TME stimulate angiogenesis and the release of growth factors, support the aggressiveness of the tumor, and increase the Gleason score [10]. PCa cells can use hexoses as an energy source. PCa overexpresses fructose transporters, but not glucose transporters, compared to benign cells. Therefore, fructose can modulate the biology of PCa. As tumors progress, a series of complex transformations take place in the microenvironment due to the interplay between cancer cells and the surrounding cells [22]. The occurrence of cancer is largely driven by the bidirectional relationship between cancer cells and the tumor microenvironment. These interactions can have significant impacts, influencing tumor cell survival, growth, the formation of new blood vessels, resistance to treatments, evasion of immune detection, and the spread of cancer cells [16]. It should be borne in mind that cells will have a beneficial or harmful effect on the malignant process depending on their needs and metabolic activity. Multiple lines of evidence show that inflammation, which is the key factor in the development of prostate cancer, plays a decisive role in TME processes. The generation and release of increased amounts of cytokines by TME-associated cells support the development of the primary tumor and allow the progression of the disease to an advanced state by activating EMT and angiogenesis [10; 23; 24]. Recently, it has been suggested that the periprostatic adipose tissue is part of the PCa tumor microenvironment and is regarded as an active secretory organ. Periprostatic adipose tissue in a paracrine, endocrine, or exocrine manner has the ability to release lipids and adipocytes but also hormones that will later participate in the growth of the tumor, which will be followed by invasion of surrounding tissues and metastasis [1].