Agnieszka Jeleń

The goals of ulcerative colitis (UC) treatment are focused on improving quality of life, achieving steroid-free remission, and minimizing the risk of cancer. In UC traditional management, a step-up strategy involves introducing increasingly more immunosuppressive medications, thus avoiding unnecessary overexposure to more potent drugs. However, in cases of severe, acute UC, priority is rapid and effective treatment to minimize the risk of complications such as bleeding, intestinal perforation, toxic megacolon or the need for colectomy. Modern approach to UC management shifts to an “accelerated step-up” or “top-down” approach in high-risk patients to prevent bowel damage. A holistic approach—integrating molecular research, clinical management and patient-centered care—enhances our understanding of disease mechanisms and therapeutic strategies, ultimately supporting improved outcomes and overall quality of life. This review aims to present the treatment options for UC along with an overview of the most modern therapies and experimental agents.

Many countries have introduced HPV screening and vaccination programs to reduce the burden of cervical cancer. In Poland, before 2023, HPV vaccination was available only on an individual, non-universal basis, using all types of vaccines, while in 2023, a nationwide vaccination program for boys and girls aged 12–13 years was introduced alongside updated screening guidelines. This retrospective study analyzed 2296 HPV-positive test results obtained from adult patients in Poland, including demographic data, HPV genotypes distribution, infection intensity, and cytological findings. HPV genotyping was performed using the Anyplex™ II HPV28 assay. HR-HPV genotypes accounted for 64.53% of all detected infections, with the highest prevalence observed in individuals aged 26–35 years of both sexes. HPV-18 was significantly more frequently in women (p = 0.0430), whereas HPV-53 predominated in men (p = 0.0030). Men more often presented low-intensity infections, while women showed higher viral load. Multigenotypic infections occurred in 46.5% of cases, particularly among younger patients (p < 0.001), and were significantly associated with LSIL changes in cytology. The HSIL type correlated most strongly with HPV-16 (p < 0.001). These findings confirm the high burden of HR-HPV infections in the Polish adult population and provide an essential epidemiological baseline for evaluating the impact of universal HPV vaccination and updated screening strategies.

Antibodies, also called immunoglobulins, play a key role in the body’s immune response, binding to specific molecular targets. Of the five classes of antibodies, IgG has found the greatest clinical application. The article presents the mechanisms of antibody action, including interactions with FcR receptors on leukocytes, complement activation, and direct cytotoxic interactions, as well as the main methods of antibody production, which include hybridoma technology, phage display, and production using transgenic animals and their modifications, which allowed for the production of antibodies with reduced immunogenicity and increased their effectiveness and safety of use. It also characterizes various types of antibodies and presents the differences between them resulting from the structure and content of individual protein domains encoded by human genes and genes from other species. Antibodies are currently one of the most important groups of biological drugs used in the treatment of autoimmune, infectious, and neoplastic diseases. The properties of these large biomolecules and the achievements in the field of obtaining and modifying antibodies mean that they are currently the subject of many studies. New forms of antibodies, such as antibody–drug conjugates with highly potent cytotoxic agents, bispecific antibodies, and nanobodies, demonstrate an innovative approach to the treatment of cancer and autoimmune diseases. The dynamic development of the antibody market indicates its growing importance in modern pharmacy and medicine. Further research in this area may lead to the development of more effective and precise therapies, as well as to increase the safety of their use.

Background/Objectives: ATP-binding cassette subfamily G member 2 [ABCG2/breast cancer resistance protein (BCRP)] contributes to mechanisms of multidrug resistance (MDR) and is a marker of side population (SP) cells in human cancers. The primary objective of this study was to investigate the impact of ABCG2 gene expression on the non-small cell lung cancer (NSCLC) development, course of cancer disease, and patient prognosis using publicly available data. Obtained results were supplemented with assessment of ABCG2 expression in blood of NSCLC patients. Methods: The dataset of lung cancer was analyzed utilizing the TIMER 2.0, UALCAN, TNMplot, MEXPRESS, cBioPortal, MethSurv, KM Plotter, STRING, and ShinyGO 0.80 databases. Blood samples from 50 patients were assessed using the real-time PCR method. Results: The ABCG2 gene was expressed at a low level in NSCLC, and did not correlate with clinical aggressiveness of lung cancer. Higher ABCG2 expression improved overall survival, but only in LUAD. In addition, CpG sites located on the CpG island affecting the NSCLC patient’s prognosis were indicated. In the case of our own laboratory results, the study did not reveal any changes in the ABCG2 expression levels in blood collected from patients at different time points during the diagnostic–therapeutic procedure. In the in silico analysis, most ABCG2 protein interactors were associated with the development of drug resistance. Conclusions: ABCG2 appears to have a particularly significant impact on the survival of patients with lung cancer and on the effect of immunotherapy related to immune cell infiltration. Presented findings may support personalized medicine strategies based on bioinformatics findings.

Gastrointestinal cancers account for over a quarter of all cancer cases and are associated with poor prognosis and high mortality rates. The IKK complex (the canonical I kappa B kinase), comprising the CHUK, IKBKB, and IKBKG genes, plays a crucial role in activating the NF-kB signaling pathway. This study aimed to analyze publicly available bioinformatics data to elucidate the oncogenic role of IKK genes in selected gastrointestinal cancers. Our findings reveal that IKBKB and IKBKG are significantly upregulated in all examined cancers, while CHUK is upregulated in esophageal carcinoma and stomach adenocarcinoma. Additionally, the expression of IKK genes varies with histological grade and nodal metastases. For instance, in stomach adenocarcinoma, CHUK and IKBKB are upregulated in higher histological grades and greater lymph node infiltration. Lower expression levels of CHUK, IKBKB, and IKBKG in stomach adenocarcinoma and IKBKB in esophageal squamous cell carcinoma correlate with shorter overall survival. Conversely, in esophageal adenocarcinoma, reduced IKBKG expression is linked to longer overall survival, while higher IKBKB expression in colon adenocarcinoma is associated with longer overall survival. Given the significant role of IKK genes in the development and progression of selected gastrointestinal cancers, they hold potential as prognostic markers and therapeutic targets, offering valuable insights for clinical practice.

ABCG2 (ATP-binding cassette superfamily G member 2) is a cell membrane pump encoded by the ABCG2 gene. ABCG2 can protect cells against compounds initiating and/or intensifying neoplasia and is considered a marker of stem cells responsible for cancer growth, drug resistance and recurrence. Expression of the ABCG2 gene or its protein has been shown to be a negative prognostic factor in various malignancies. However, its prognostic significance in colorectal cancer remains unclear. Using publicly available data, ABCG2 was shown to be underexpressed in colon and rectum adenocarcinomas, with lower expression compared to both the adjacent nonmalignant lung tissues and non-tumour lung tissues of healthy individuals. This downregulation could result from the methylation level of some sites of the ABCG2 gene. This was connected with microsatellite instability, weight and age among patients with colon adenocarcinoma, and with tumour localization, population type and age of patients for rectum adenocarcinoma. No association was found between ABCG2 expression level and survival of colorectal cancer patients. In wet analysis of colorectal cancer samples, neither ABCG2 gene expression, analysed by RT-PCR, nor ABCG2 protein level, assessed by immunohistochemistry, was associated with any clinicopathological factors or overall survival. An ABCG2-centered protein–protein interaction network build by STRING showed proteins were found to be involved in leukotriene, organic anion and xenobiotic transport, endodermal cell fate specification, and histone methylation and ubiquitination. Hence, ABCG2 underexpression could be an indicator of the activity of certain signalling pathways or protein interactors essential for colorectal carcinogenesis.

P-glycoprotein (P-gp) has been implicated in lung cancer development, disease progression, and patient survival. Changes in the ABCB1 expression level may correlate with tumorigenesis and the formation of multidrug resistance (MDR). In addition, epigenetic modifications such as DNA methylation are involved in the regulation of the transcriptional activity of this gene. Therefore, we focused on an analysis of changes in the expression of ABCB1 and its methylation, taking into account their potential associations with the clinicopathological parameters of LUAD and LUSC. The TNMplot, UALCAN, cBioPortal, PrognoScan, and MEXPRESS databases were used to investigate the role of this gene in lung cancer progression. ABCB1 expression in lung tissue was significantly downregulated in cancer cells, but differences also resulted from age, gender, ethnicity, and smoking cessation. Moreover, decreased levels of gene transcript were associated with both a higher stage of cancer and a lower probability of survival. It is worth emphasizing that the presence/direction of ABCB1 expression changes are frequently unique to specific histological tumor subtypes. Finally, it is equally important that the main methylation promoter is one of the causes of decreased gene expression in lung cancer cells. Taken together, these data establish the ABCB1 transporter gene as an important prognostic factor that could alter disease progression and contribute to the survival of cancer patients.

Members of the activator protein 2 (AP-2) transcription factor (TF) family are known to play a role in both physiological processes and cancer development. The family comprises five DNA-binding proteins encoded by the TFAP2A to TFAP2E genes. Numerous scientific reports describe differential expression of these TF and their genes in various types of cancer, identifying among them a potential oncogene or suppressor like TFAP2A or TFAP2C. Other reports suggest their influence on disease development and progression, as well as response to treatment. Not all members of this AP-2 family have been comprehensively studied thus far. The aim of the present article is to gather and discuss knowledge available in bioinformatics databases regarding all five members of this family and to differentiate them in relation to the two most common lung cancer subtypes: adenocarcinoma (LUAD) and squamous cell carcinoma (LUSC). In addition, to assess the difference in levels depending on a number of clinicopathological factors, the impact on patient survival and interactions with tumor-infiltrating immune cells. This article may help to identify the target for further original research that may contribute to the discovery of new diagnostic biomarkers and define the molecular differences between LUAD and LUSC, which may affect the therapy effectiveness improvement and longer survival.

P-glycoprotein, product of the ABCB1 (ATP binding cassette subfamily B member 1) gene, has been reported to play an important role in multiple drug resistance during cancer therapy. However, its influence on non-small cell lung cancer (NSCLC) risk has not been clearly defined. The aim of the present study was to examine the association between clinicopathological factors and SNPs T-129C, C1236T, G2677T/A, and C3435T, as well as its haplotype, and to investigate the role of ABCB1 polymorphisms in NSCLC development. The study included 80 patients who suffered from NSCLC and underwent surgery to remove the tumour and 96 healthy controls. The tissues were genotyped by PCR-RFLP and sequencing methods, and the haplotype frequencies in both groups were estimated. The SNP C3435T was identified as a NSCLC risk factor. The presence of mutated allelic variant T ( ) or homozygote TT ( ) was observed significantly more often in cancer patients than in healthy controls. The two groups also demonstrated a highly significant difference in common haplotype frequency ( ). The T₋₁₂₉-T₁₂₃₆-T₂₆₇₇-T₃₄₃₅ haplotype was found to be most closely associated with NSCLC risk. Although the investigated polymorphisms were not related to demographic features, clinicopathological lung tumour characteristics, or blood morphology indices, marginally significant correlations were found with some variables: C1236T with age of disease onset ( ); C3435T with smoking status ( ). As the findings indicate, lung cancer and control groups demonstrate significantly different patterns of −129/1236/2677/3435 haplotype distribution; T-T-T-T haplotype contributes to NSCLC susceptibility, and this effect is probably mainly dependent on C3435T. So far, similar studies were published in other populations.