Introduction: The invasion of blood and lymph vessels with tumor tissue represents a negative prognostic factor of the disease course in patients with non-small cell lung cancer. Aim: The aim of the study was to determine the marker value of a preoperatively determined size of pulmonary squamous cell carcinoma and adenocarcinoma and its impact on lymphovascular invasion (LVI) in resected lung tissue. Materials and Methods: The conducted observational cross-sectional study included 322 patients with a complete resection of confirmed squamous cell lung carcinoma and lung adenocarcinoma. Preoperative size and type of tumor were determined by a preoperative chest computed tomography scan and cytological/histological analysis of obtained samples, while LVI status was determined by pathohistological analysis of resected tumor lung tissue. Receiver operating characteristic (ROC) curve analysis was performed to assess whether tumor size could serve as a reliable marker for LVI. P < 0.05 was considered statically significant. Results: A statistically significant difference in the frequency of tumor size (P = 0.580) along with LVI (P = 0.656) was not established between the patients with squamous cell lung cancer and lung adenocarcinoma. A ratio between the size of lung adenocarcinoma and LVI status (P < 0.001) was determined as statistically significant, while such a difference was not established in squamous cell lung cancer (P = 0.052). The ROC analysis revealed that tumor size >39 mm in patients with lung adenocarcinoma has obtained a sensitivity of 70.8% and a specificity of 60.9% to differentiate patients with a LVI (areas under the curve [AUC] = 0.70; 95% CI 0.60‒0.79; P < 0.001). A tumor size >4.6 cm in patients with squamous cell lung cancer obtained a sensitivity of 56.5% and a specificity of 60.3% to differentiate patients with a LVI (AUC = 0.59; 95% CI 0.50‒0.67; P = 0.043). Conclusion: The preoperative size of lung adenocarcinoma could be an acceptable marker of LVI presence in resected lung tissue, while in the squamous cell lung cancer, a potential biomarker role of the preoperative size of the tumor was inadequate.

OBJECTIVES The aim of this systematic review was to critically analyze available data on gene polymorphisms in odontogenic keratocysts and ameloblastomas, including their possible relationship with clinical and histological features of these lesions. MATERIALS AND METHODS A comprehensive search of Web of Science Scopus, PubMed, Cochrane Central Register of Controlled Trials and EMBASE was conducted using relevant key terms and supplemented by a gray literature search. Quality assessment of included studies was performed using criteria from the Strengthening the Reporting of Genetic Association (STREGA) statement. RESULTS Ten studies were included in the final review. Survivin -31G/C, interleukin IL-1α -889 C/T, p53 codon 72 G/C, tumor necrosis factor TNF-α (-308G>A) and its receptor TNF-R1 (36A>G), glioma-associated oncogene homolog 1 rs2228224 and matrix metalloproteinase 2 rs243865 gene polymorphisms were reported to be associated with odontogenic keratocysts. For ameloblastomas, p53 - codon 72 G/C, X-ray repair cross-complementing protein 1 - codons 194 and 399 and matrix metalloproteinase 9 rs3918242 gene polymorphisms were identified as risk factors. It wasn't possible to establish a relationship between specific polymorphisms and clinical and histological features of investigated lesions. CONCLUSIONS Several gene polymorphisms might be considered as a risk factor for the development of these lesions. Future studies should investigate whether these polymorphisms might be used to identify patients with increased risk of recurrence or aggressive disease.

Histological diagnosis of differentiated vulvar intraepithelial neoplasia (dVIN), the precursor of human papillomavirus (HPV)-independent vulvar squamous cell carcinoma (VSCC), can be challenging, as features of dVIN may mimic those of non-dysplastic dermatoses. To aid the diagnosis, p53-immunohistochemistry (IHC) is commonly used, and mutant expression patterns are used to support a histological diagnosis of dVIN. However, a proportion of dVIN can show wild-type p53-expression, which is characteristic of non-dysplastic dermatoses. Furthermore, recent research has identified a novel precursor of HPV-independent VSCC—the p53-wild-type differentiated exophytic vulvar intraepithelial lesion (de-VIL). Currently, there are no established diagnostic IHC-markers for p53-wild-type dVIN or de-VIL. We evaluated IHC-markers, cytokeratin 17 (CK17), and SRY-box 2 (SOX2), as diagnostic adjuncts for dVIN. For this, IHC-expression of CK17, SOX2, and p53 was studied in dVIN (n = 56), de-VIL (n = 8), and non-dysplastic vulvar tissues (n = 46). For CK17 and SOX2, the percentage of cells showing expression, and the intensity and distribution of expression were recorded. We also performed next generation targeted sequencing (NGTS) on a subset of dVIN (n = 8) and de-VIL (n = 8). With p53-IHC, 74% of dVIN showed mutant patterns and 26% showed wild-type expression. Median percentage of cells expressing CK17 or SOX2 was significantly higher in dVIN (p53-mutant or p53-wild-type) and de-VIL than in non-dysplastic tissues (p < 0.01). Diffuse, moderate-to-strong, full epithelial expression of CK17 or SOX2 was highly specific for dVIN and de-VIL. With NGTS, TP53 mutations were detected in both dVIN and de-VIL. We infer that immunohistochemical markers CK17 and SOX2, when used along with p53, may help support the histological diagnosis of dVIN.

During cancer evolution constituent tumour cells compete under dynamic selection pressures. Phenotypic variation can be observed as intratumour heterogeneity, which is propagated by genome instability leading to mutations, somatic copy number alterations and epigenomic changes. TRACERx was set up in 2014 to observe the relationship between intratumour heterogeneity and patient outcome. By integrating multi-region sequencing of primary tumours with longitudinal sampling of a prospectively recruited patient cohort, cancer evolution can be tracked from early to late stage disease and through therapy. Here we review some of the key features of the studies and look to the future of the field.

Here we describe the major genetic and genomic aberrations found in myeloid malignancies and how those markers are used in patients' diagnosis, prognosis, and targeted treatment. In Bosnia and Herzegovina, cytogenetic and molecular diagnostics for myeloid malignancies have been established and continually improved since 2005. We report the current state of available diagnostic tools for myeloid malignancies in Bosnia and Herzegovina. Myeloid malignancies are a heterogeneous group of clonal blood diseases characterized by defects in hematopoietic stem cells and myeloid progenitors that lead to abnormal proliferation, differentiation, localization, and self-renewal. Most common myeloid malignancies include myeloproliferative neoplasms (MPNs), myelodysplastic syndrome (MDS), and acute myeloid leukemia (AML). Molecular diagnostics of myeloid malignancies have significantly expanded in the last decade with new genetic and genomic markers for diagnosis, prognosis, and treatment. CONCLUSION: In the last decade, several new genomic markers important for patient diagnosis, prognosis, and therapy have been discovered that need to be implemented in routine molecular diagnostics not only in developed nations but also in developing nations such as Bosnia and Herzegovina.