Melanoma is one of the most aggressive and progressive skin cancers. It develops from normal pigment-producing cells known as melanocytes, so it is important to know the mechanism behind such transformations. The study of metastasis mechanisms is crucial for a better understanding the biology of neoplastic cells. Metastasis of melanoma, or any type of cancer, is a multi-stage process in which the neoplastic cells leave the primary tumour, travel through the blood and/or lymphatic vessels, settle in distant organs and create secondary tumours. MicroRNA (miRNA) can participate in several steps of the metastatic process. This review presents the role of miRNA molecules in the development and progression as well as the immune response to melanoma.

Melanoma is the most serious type of skin cancer, causing a large majority of deaths but accounting for only ~1% of all skin cancer cases. The worldwide incidence of malignant melanoma is increasing, causing a serious socio-economic problem. Melanoma is diagnosed mainly in young and middle-aged people, which distinguishes it from other solid tumors detected mainly in mature people. The early detection of cutaneous malignant melanoma (CMM) remains a priority and it is a key factor limiting mortality. Doctors and scientists around the world want to improve the quality of diagnosis and treatment, and are constantly looking for new, promising opportunities, including the use of microRNAs (miRNAs), to fight melanoma cancer. This article reviews miRNA as a potential biomarker and diagnostics tool as a therapeutic drugs in CMM treatment. We also present a review of the current clinical trials being carried out worldwide, in which miRNAs are a target for melanoma treatment.

In sports research, genetic studies linked to the traits of the temperament, in addition to medical examinations and other physiological and biochemical tests, would enrich the scope of possibilities and successes that a competitor can accomplish. This could be beneficial for the protection of both mental and physical health. The study group comprised 391 male volunteers. Out of these, 222 sports subjects and 186 were non-addicted. The temperament and character questionnaire (TCI-R) was used to determine personality traits such as novelty seeking, harm avoidance, reward addiction and perseverance, as well as self-direction, cooperation and self-transcendence. Genotyping OPRM1 rs1799971 was carried out with the real-time PCR method. In the present study polymorphic variants of selected genotypes were associated with self-direction - A/A genotypes in the study group. Higher values were observed compared to the control group (p = 0.045). Similarly, the A/G genotype occurred statistically significantly more frequently in the study group compared to the control group. The G/G genetic variant was less common in the study group compared to the controls. Conclusions: The study reveals the validity of analysing connections between personality traits and selected gene polymorphisms in athletes, a relatively new field. The presence of the OPRM1 rs1799971 AA genotype is associated with higher self-management scores, indicating genetic predispositions in the study group for better results in sports.

Introduction: Addictive substances act on a number of neurotransmitter systems, and the end result of this action is the activation of the reward system in the brain. The cellular and neuronal mechanisms that underlie addiction have long been searched for. One of such neurotransmitters is dopamine, a catecholamine synthesized in neurons located mainly in the midbrain. Material and method: The available literature was reviewed on the Pubmed platform and from other sources. The analysis included original studies, reviews. The aim of the study was to review the literature on the relationship between the DRD2 gene and the occurrence of substance addiction. Discussion: This work presents several currently discussed biological mechanisms, especially at the molecular and genetic level, involved in the process of addiction to various psychoactive substances. They discovered the brain structures that are most at risk, as well as other neurotransmitter systems and receptor proteins through which they can exert their pathological effects. It has also been established that exposure to psychoactive substances causes significant changes in expression in over 100 genes (including genes for dopaminergic, serotonergic and signaling pathways). The DRD2 receptor (present, among others, in the nucleus accumbens) plays an important role in the reward system, in the transmission of information. The weakening of this conductivity is a significant risk factor for the onset of clinical features that are associated with reward system deficiency syndrome. The expression of the D2 receptor gene may take up to 2 isoforms: short D2S and long D2L. Conclusions: Further research at the molecular level may result in the modification of psychotherapy and pharmacotherapy in terms of their personalization.

The complement system is traditionally recognized as a major effector of innate immunity, essential for pathogen clearance, inflammation and the maintenance of tissue homeostasis. In recent years, however, its role in cancer has been substantially redefined. Beyond its canonical extracellular activity, complement has emerged as a multifaceted regulator of tumor biology, acting not only within the tumor microenvironment but also intracellularly through the recently described intracellular complement system (complosome). While extracellular complement primarily shapes immune responses and the tumor microenvironment, the complosome directly regulates fundamental cellular processes, including metabolism, proliferation, autophagy, stress responses and cell survival. In this review, we discuss current evidence on the canonical and non-canonical roles of complement in cancer. Importantly, complement signaling exhibits a strong context-dependent duality, exerting either tumor-promoting or tumor-restraining effects depending on the tumor type, disease stage, cellular source, and localization. Taken together, the available evidence indicates that the complosome is not merely an extension of classical complement biology, but a distinct and biologically significant signaling network that rewrites our understanding of complement in cancer. Its growing relevance in tumor development and therapy resistance positions it as a promising target for future mechanistic studies and innovative therapeutic interventions.