Hodgkin lymphoma (HL) is a biologically diverse group of lymphoid tumors, which accounts for 1% of all de novo neoplasms in the world’s population. It is divided into two main groups: the more common classic Hodgkin lymphoma (cHL) and the less common nodular lymphocyte-predominant Hodgkin lymphoma (NLPHL). cHL is further divided into four subtypes, which differ in morphology and the contents of tumor microenvironment. Macrophages are one of the components of tumor microenvironment known to contribute to creating an immunosuppressive microenvironment, which inhibits the activity of cells expressing granzyme B against tumor cells, even when tumor cells are infected with Epstein–Barr virus (EBV). Our research aimed to explore the association between the specific contents of tumor microenvironment and the genetic anomalies in tumor cells. The presence and the relative percentage of cytotoxic T lymphocytes and macrophages was detected by immunohistochemical staining of the antigens specific for certain cell populations. Fluorescent in situ hybridization was used to detect anomalies in the genome of tumor cells and in situ hybridization was used to detect the presence of EBV. Our results show an association between the number of CD163+ macrophages and the number of TP53 copies or BCL6 gene translocation. Patients who had a higher number of CD163+ macrophages infiltrating tumor tissue and three or higher number of copies of TP53 showed poorer survival. We conclude that the presence of macrophages may contribute to genetic instability in cHL, which drives the progression of cHL and decreases survival of the patients.

Hepatocellular carcinoma (HCC) is the most prevalent primary liver cancer, ranking as the sixth most common cancer worldwide and the fourth leading cause of cancer-related deaths. Most HCC cases originate from cirrhotic livers, typically due to chronic liver diseases, such as hepatitis B (HBV) and hepatitis C (HCV) infections, and alcoholism. HCC cells often harbor numerous somatic mutations that are implicated in HCC development, but epigenetic factors, such as miRNA interference, can also affect HCC initiation and progress. miRNA-221 has been explored as a factor affecting HCC development in HCC of viral etiology, but little is known about its effects on gene expression in alcohol-associated HCC. This study aimed to explore potentially similar gene expression aberrations underlying viral and alcohol-induced HCC. We analyzed available transcriptome data from non-tumor hepatocytes and viral-induced HCC tissues. The most notable differences in gene expression associated with miRNA-221 between non-tumor hepatocytes and viral-induced HCC involved NTF-3 and MYBL1 genes. To assess these data in alcohol-induced HCC, we examined 111 tissue samples: tumor tissue and cirrhotic tissue samples from 37 HCC patients and 37 samples from non-tumor liver tissue using RT-Q PCR. We found no significant difference in NTF-3 expression, but MYBL1 expression was significantly lower in HCC tissue compared to non-tumor hepatocytes and cirrhotic tissue. Our findings highlight the importance of the MYBL1 gene in HCC development and emphasize the need for diverse approaches in evaluating tumor mechanisms.

Background/Objectives: Early-onset colorectal cancer (EOCRC) is more frequently characterized by poorly differentiated, aggressive tumors, often diagnosed at advanced stages, and associated with worse prognoses. Despite these differences, current treatment guidelines do not distinguish between EOCRC and late-onset colorectal cancer (LOCRC). Elevated expression of polo-like kinase 1 (PLK-1) has been linked to advanced disease stages and poorer treatment outcomes, including resistance to both chemotherapy and radiotherapy. However, data on PLK-1 expression in EOCRC compared to LOCRC remain limited. Methods: Patients with sporadic CRC, aged >18 years, were included in this study. We categorized the patients into two groups: patients younger than 50 years, and those aged 50 years or older. Immunohistochemical staining was performed to assess PLK-1 expression. The aim of this study was to assess PLK-1 expression considering the age of the patients and its effects on overall survival (OS) and progression-free survival (PFS). Results: A total of 146 patients with metastatic colorectal cancer (mCRC) were included in this retrospective two-center study. Patients with low PLK-1 expression were older than patients with high PLK-1 expression (64 (49–71) years vs. 49 (42–67) years, p = 0.016). Multiple logistic regression confirmed that age is a significant predictor of PLK-1 expression, independent of the covariates (p = 0.036). The Kaplan–Meier analysis revealed no significant association between PLK-1 expression and PFS (p = 0.397) or OS (p = 0.448). Accordingly, Cox proportional hazards regression analysis showed no significant association between PLK-1 expression and OS (HR 1.20, 95% CI 0.73–1.96, p = 0.598) or PFS (HR 0.85, 95% CI 0.51–1.43, p = 0.611) when covariates were taken into account. Finally, no significant differences in PFS (p = 0.423) or OS (p = 0.104) were found between the age groups of interest. Conclusions: PLK-1 expression was not associated with survival or progression in EOCRC and LOCRC patients. Further research on these combinations is necessary, as well as the discovery of new potential targets for targeted therapy and the mechanisms of synergistic effects in tumors with PLK-1 overexpression.