Glutathione S-transferase (GST) enzymes are responsible for cellular detoxification of many carcinogens and are important anticancer elements. This study assessed potential relationships between GSTM1, GSTT1, and GSTP1 polymorphisms and colorectal cancer (CRC) risk in Polish nonsmokers. We also analyzed the influence of GST gene polymorphisms on CRC clinical and histopathological features. Our study included 197 CRC patients and 104 healthy controls. GSTM1, GSTT1, and GSTP1 polymorphisms were evaluated using qPCR. Polymorphism frequencies observed in our control group corresponded to those in other European populations. The GSTM1 null and GSTT1 null genotypes were observed with similar frequencies in both CRC patients and controls (GSTM1 null: 46.7% vs. 45.2%; GSTT1 null: 15.7% vs. 20.2%). GSTP1 Ile/Ile, Ile/Val, and Val/Val genotype frequencies were respectively 42.1%, 48.2%, and 9.6% in patients and 48.1%, 42.3%, and 9.6% in controls. GSTT1 polymorphism correlated with higher tumor grade in CRC patients, and the GSTM1 null/null genotype was associated with more frequent metastasis to lymph nodes (pN classification). Our results suggest that GST gene polymorphisms may influence CRC tumor grade and stage.

Background and Goals. In light of current knowledge, it seems that alternations underlying GISTs are well explained, although all that is enhanced by various aspects on a daily basis. More recently, attention has been pointed towards exosomes as important particles able to modify healthy and also diseased tissues including cancer. The goal of the present study was an analysis of CD9, CD63, and GLUT-1 as a marker of hypoxia status within 54 cases of GIST and evaluation of their predictive value. Methods. 54 cases of patients suffering from GIST were enrolled into the study, predominantly in the gastric location. All operated cases had no Imatinib and other chemotherapies up to the day of operation. Expression of targeted proteins was performed by immunohistochemistry and, after that, the results with tabulated clinical data were compared by Kaplan-Meier method and multivariate Cox proportional hazard model of statistical analysis. Results. Our results presented a marked dependence of worsening clinical outcome with high expression CD63 (p = 0.008) as well as with GLUT-1 (p = 0.014). We noted a strict correlation of GLUT-1 expression with CD63 expression (p = 0.03), which could confirm the thesis about the contribution of exosomes in intratumoural hypoxia status. The collected material did not confirm CD9 contribution. Conclusions. As presented here, CD63 and GLUT-1 have a prognostic value in GIST cases. The results confirm the other studies in this scope and can be used in future as an additional prognostic factor.

Introduction: Liquid-based cytology allows to apply modern and specific analyses of hrHPV genotyping in p16/Ki-67 test. All of these together could raise accuracy ratio for high-grade squamous intraepithelial lesion above 90%. The purpose of this study was to evaluate the diagnostic accuracy of LBC, hrHPV testing, and p16/Ki-67 testing in diagnosis of high-grade cervical intraepithelial lesions. Material and methods: The study consisted of 176 women, out of which 50 presented with HSIL (CIN2) SCC (cervical intraepithelial lesion grade 2 squamous cell carcinoma). 126 women with a negative Pap test were pooled into the second group of the study. All patients were resampled for LBC, HPV genotyping, and for the p16/Ki-67 test. The research was carried out between May and December 2017, and second sampling were taken from 1 to 4 months. Results: We reported a strong correlation between positive Pap test and hrHPV (p < 0.05) that met accuracy close to 90%. We noted correlations between a positive p16/Ki-67 with a positive Pap test: p

Scoring systems used in prognosticating the course of the disease vary with regard to sensitivity and specificity. The CT severity index scoring system showed the highest precision in prognosticating moderately severe AP (as per the revised Atlanta criteria, 2012); however, in prognosticating a severe course of disease and mortality, APACHE II proved to have the greatest predictive value.

Background: It is postulated that both individual genotype and environmental factors such as diet may modify the risk of developing colorectal cancer (CRC). The influences of GST gene polymorphism and red meat intake on CRC occurrence in the Polish population were analyzed in this study. Methods: Genotyping was performed with the qPCR method. Results: A high frequency of meat consumption was associated with an over 2-fold increase in the risk of colorectal cancer odds ratio (OR) adjusted for sex and age = 2.4, 95% confidence interval (CI); 1.3–4.4). However, after analyzing the genetic profiles, in the absence of polymorphisms of all three analyzed genes, there was no association between a high frequency of meat consumption and the occurrence of CRC. In the case of GSTM1 gene polymorphism, the high frequency of meat consumption increased the risk of CRC by almost more than 4 times (OR adjusted for sex and age = 3.8, 95% CI: 1.6–9.1). For GSTP1 gene polymorphism, a 3-fold increase in CRC risk was observed with a high frequency of meat consumption (OR adjusted for sex and age = 3.4, 95% CI: 1.4–8.1). In the case of GSTT1 gene polymorphism, the increase in risk of CRC was not statistically significant (OR adjusted for sex and age = 1.9, 95% CI: 0.4–8.5). Conclusions: The frequency of red meat intake in non-smokers increases the risk of colon cancer in the case of GST gene polymorphisms.

The technological progress within the range of methods of pancreas imaging and their more common accessibility selects a group of patients requiring a microscopic diagnosis. Percutaneous fine needle aspiration biopsy under the control of ultrasonography (PCFNA/USG) is the method commonly used in determining the character of a focal pancreatic lesion. Aim of the Work. An assessment of the accessibility of PCFNA biopsy in the assessment of solid and cystic changes in a pancreas and the correlation of the results of imaging examination, cytological smear and concentration of a serous marker CA19-9. Material and Methodology. In our material we analysed 43 cases of tumors of the pancreas among the patients who were at the average age of 59 ± 10.4 (14 women, 28 men) diagnosed by PCFNA biopsy. Results. In a group we are 23 cases of cancer, 12 cases of inflammation and 7 cases of cellular atypia for which 2 cases of IPMN were included. The sensitivity of the method was 92.5% but specificity was 68%. In our opinion PCFNA/USG is a method of the comparable sensitivity and specificity with fine needle aspiration biopsy with EUS control and its efficiency depends to a considerable degree on experience and interdisciplinary collaboration.

Here we present the case of a 73-year-old woman with an ulcerated, advanced, hepatoid, and α-fetoprotein-producing poorly differentiated (G3) primary gastric adenocarcinoma pT3 N3a M1 with multinucleated cells and evident neuroendocrine component. This tumor was consistent with giant cell tumor type gastric carcinoma with osteoclast-like giant cells (OGCs). The cancer was HER2 and E-cadherin negative, chromogranin A dispersedly and moderately positive, and strongly α-fetoprotein-positive with evident CK AE1/AE3 immunoreactivity, while OGCs expressed CD68. To provide an insight into the molecular background of this peculiar neoplasm, next-generation sequencing (NGS) was performed to analyze the 50 most frequently mutated oncogenes and tumor suppressors. We detected mutations in the primary tumor in the following genes: KIT, EGFR, PTEN, ATM, and RB1. In the liver metastasis, we revealed mutations in 3 genes: PIK3CA, KIT, and CDKN2A.

Epidermal growth factor (EGF) stimulates the proliferation of many different types of cells and plays an important role in the formation and growth of tumours. The interaction of EGF with cells is possible by the EGF receptor (EGFR) anchored in the cell membrane. Excess EGFR expression is found in approximately 25-82% of colorectal cancer cases. Attachment of EGF to EGFR results in a conformational change in the receptor, an increase in affinity for neighbouring receptors, receptor dimerisation, and activation of tyrosine kinase in the intraplasmic domain. Activation of EGFR leads to the initiation of the signal transduction pathway to the cell nucleus, via a number of proteins with enzymatic activity-secondary messengers, including KRAS and BRAF proteins. The assessment of the presence of mutations in the KRAS gene has become a standard element in the qualification of patients with advanced colorectal cancer for therapy with the use of monoclonal antibodies. Streszczenie Naskórkowy czynnik wzrostu (EGF) stymuluje proliferację wielu różnych typów komórek i odgrywa ważną rolę w po wstawaniu i rozwoju nowotworów. Oddziaływanie EGF z komórkami jest możliwe dzięki receptorowi EGF (EGFR) zako twiczonemu w błonie komórkowej. Nadmierna ekspresja EGFR występuje w ok. 25-82% przypadków raka jelita grubego. Przyłączenie EGF do EGFR powoduje konformacyjną zmianę receptora, wzrost powinowactwa do sąsiednich receptorów, dimeryzację receptora i aktywację kinazy tyrozynowej w domenie wewnątrzplazmatycznej. Aktywacja EGFR prowadzi do inicjacji szlaku transdukcji sygnału do jądra komórkowego za pośrednictwem wielu białek o aktywności enzymatycz nej-wtórnych przekaźników, w tym białek KRAS i BRAF. Ocena obecności mutacji w genie KRAS stała się standardowym elementem kwalifikacji pacjentów z zaawansowanym rakiem jelita grubego do leczenia z zastosowaniem przeciwciał mono klonalnych.