Gastric cancer is one of the most common worldwide types of cancer. It is a multifactorial disease and both environmental and genetic factors play an important role in its etiology. Evaluation of the relative expression level of NFKB2 gene in two groups of patients: peptic ulcer and gastric cancer and its role in the pathomechanism of these diseases was the aim of this study. RNA was isolated from: 79 samples of peptic ulcer, 22 gastric cancer and 11 control tissue. The real-time PCR technique was used to study the expression of NFKB2 gene. The relative expression level of NFKB2 gene was a variable in all three studied groups. The relative NFKB2 gene expression depends on the type of a disease. Peptic ulcer cases showed the increased relative NFKB2 gene expression to control group (p = 0.0000). Cancer cases presented decreased relative NFKB2 gene expression to normal stomach tissue (p = 0.0183). There are statistically important differences in the investigated gene expression between peptic ulcer, where the expression level is higher comparing to gastric cancer and control tissue which confirmed that such an activation is connected with an inflammatory process. The relative expression level of NFKB2 is decreased in cancer cases as opposed to control tissue and peptic ulcer cases which could suggest that during carcinogenesis of gastric cancer inhibition of NF-kB pathway takes place which could be a promising factor for patients.

The PI3K/AKT pathway plays a pivotal role in cellular processes, and its dysregulation is implicated in various cancers, including colorectal cancer. The present study correlates the expression levels of critical genes (PIK3CA, PTEN, AKT1, FOXO1, and FRAP) in 60 tumor tissues with clinicopathological and demographic characteristics. The results indicate age-related variation in FOXO1 gene expression, with higher levels observed in patients aged 68 and above. In addition, tumors originating from the rectum exhibit higher FOXO1 expression compared to colon tumors, suggesting region-specific differences in expression. The results also identify the potential correlation between PTEN, PIK3CA gene expression, and parameters such as tumor grade and neuroinvasion. The bioinformatic comparative analysis found that PTEN and FOXO1 expressions were downregulated in colorectal cancer tissue compared to normal colon tissue. Relapse-free survival analysis based on gene expression identified significant correlations, highlighting PTEN and FRAP as potential indicators of favorable outcomes. Our findings provide a deeper understanding of the role of the PI3K/AKT pathway in colorectal cancer and the importance of understanding the molecular basis of colorectal cancer development and progression.

In the course of lung cancer, normal cells are transformed into cancerous ones, and changes occur in the microenvironment, including the extracellular matrix (ECM), which is not only a scaffold for cells, but also a reservoir of cytokines, chemokines and growth factors. Metalloproteinases (MMPs) are among the elements that enable ECM remodeling. The publication focuses on the problem of changes in the gene expression of MMP2, MMP9 and tissue inhibitor of metalloproteinases (TIMP1) in the blood of NSCLC patients during therapy (one year after surgical resection of the tumor). The paper also analyzes differences in the expression of the studied genes in the tumor tissue, as well as data collected in publicly available databases. The results of blood tests showed no differences in the expression of the tested genes during therapy; however, changes were observed in cancerous tissue, which was characterized by higher expression of MMP2 and MMP9, compared to non-cancerous tissue, and unchanged expression of TIMP1. Nevertheless, higher expression of each of the studied genes was associated with shorter patient survival. Interestingly, it was not only the increased expression of metalloproteinase genes, but also the increased expression of the metalloproteinase inhibitor (TIMP1) that was unfavorable for patients.

The global scope and scale of the SARS-CoV-2 pandemic led to huge amounts of important data from clinical observations and experimental analyses being collected, in particular, regarding the long-term impact of COVID-19 on lung tissue. Visible changes in lung tissue mainly relate to the destruction of the alveolar architecture, dense cellularity, and pulmonary fibrosis with myofibroblast proliferation and collagen deposition. These changes are the result of infection, mainly with virus variants from the first pandemic waves (Alpha to Delta). In addition, proper regulation of immune responses to pathogenic viral stimuli is critical for the control of and recovery from tissue/organ damage, including in the lungs. We can distinguish three main processes in the lungs during SARS-CoV-2 infection: damage or deficiency of the pulmonary surfactant, coagulation processes, and fibrosis. Understanding the molecular basis of these processes is extremely important in the context of elucidating all pathologies occurring after virus entry. In the present review, data on the abovementioned three biochemical processes that lead to pathological changes are gathered together and discussed. Systematization of the knowledge is necessary to explore the three key pathways in lung tissue after SARS-CoV-2 virus infection as a result of a prolonged and intense inflammatory process in the context of pulmonary fibrosis, hemostatic disorders, and disturbances in the structure and/or metabolism of the surfactant. Despite the fact that the new Omicron variant does not affect the lungs as much as the previous variants, we cannot ignore the fact that other new mutations and emerging variants will not cause serious damage to the lung tissue. In the future, this review will be helpful to stratify the risk of serious complications in patients, to improve COVID-19 treatment outcomes, and to select those who may develop complications before clinical manifestation.

The present study examines the relationship between circular RNA (circRNA) derived from three genes of the family a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTSs): ADAMTS6, ADAMTS9 and ADAMTS12 and the host gene expression in non-small-cell lung cancer (NSCLC) with regard to various clinical factors. Notably, an association was identified between ADAMTS12 expression and specific circRNA molecules, as well as certain expression patterns of ADAMTS6 and its derived circRNA that were specific to histopathological subtypes. The survival analysis demonstrated that a lower ADAMTS6 expression in squamous cell carcinoma was associated with extended survival. Furthermore, the higher ADAMTS9 expression was linked to prolonged survival, while the overexpression of ADAMTS12 was correlated with a shorter survival. These findings suggest that circRNA molecules may serve as potential diagnostic or prognostic biomarkers for NSCLC, highlighting the importance of considering molecular patterns in distinct cancer subtypes.

Colorectal cancer has become a serious problem, especially in highly developed countries. As reported by the World Health Organization, the number of colon cancer cases in the world in 2012 amounted to 1.36 million. It is the second most common cancer in females (614,000 cases, 9.2% of the total) and the third in males (746,000 cases, 10.0% of the total) worldwide. It is believed that TGFβ pathway elements are involved in the pathogenesis of colorectal cancer. This study assessed one of these elements, the ACVR2A gene. Qualitative and quantitative analyses of the ACVR2A gene in 84 patients with colorectal cancer was performed. There was no statistically significant association between ACVR2A gene expression and age, gender, histological type, grading of tumor, vascular invasion, and presence of lymphocytes in tumor tissue. No association was observed between the ACVR2A gene expression level and the presence of metastases in regional lymph nodes and distant metastases. In this study, larger tumors (T3 and T4) were characterized by higher ACVR2A expression compared to smaller tumors (T1 and T2). This may indicate an association between ACVR2A expression and the severity of pathological changes in the tumor growth process.