an important role in stage III non-small cell lung cancer outcome.The 2017 revision of WHO Classification of tumors of hematopoietic and lymphoid tissues contains separate chapters on the immunodeficiency-associated lymphoproliferative disorders. In this mini-review, the brief description of pathological, immunophenotypical and clinical features of lymphoid neoplasms associated with primary immune disorders, HIV infection, those arising in post-transplant setting and other lymphoproliferative disorders (excluding those induced by radiation) is given. The heterogeneous spectrum of these lymphoid malignancies is specified by the nature of those factors that are capable to induce immune suppression or chronic antigenic stimulation of immune system. Taking into account the full swing of SARS-CoV-2 pandemic and our ignorance of the ability of this virus to induce the sustained stimulation of immune system, we could not exclude the high risk of autoimmune diseases and lymphoid neoplasms in the long-term post-pandemic period. In this context, the role of angiotensin-converting enzyme 2 as well as some recently reported cell receptors for SARS-CoV-2 cell entry should be considered as far as some of them (CD147, CD26) could be tumor-associated antigens.
To study cellular localization of full-length breakpoint cluster region (BCR), Pleckstrin homology domain of BCR and cortactin and determine whether they can coexist in cell nucleus.

HEK293T cell line was transfected with pECFP-BCR, pEGFP-PH and pmTagRFP-N1-CTTN using polyethyleneimine. Live cells were imaged in cell culture dishes with glass coverslip attached to the bottom with Leica SP8 STED 3D confocal microscope in the environmental chamber. Obtained images were processed and analyzed with Fiji software.

We identified colocalization of full-length BCR and cortactin in nucleus of cell undergoing terminal phase of cell division. https://www.selleckchem.com/products/pik-iii.html We did not observe nuclear localization of cortactin in non-dividing cell. Both Pleckstrin homology domain and full-length BCR exhibited cytoplasmic as well as nuclear localization.

Colocalization of BCR with cortactin in cell nucleus indicates their potential role in regulation of actin network allowing for the maintenance of nuclear architecture and DNA integrity.
Colocalization of BCR with cortactin in cell nucleus indicates their potential role in regulation of actin network allowing for the maintenance of nuclear architecture and DNA integrity.
Toll-like receptor 4 (TLR4) is known to be involved in carcinogenesis and cancer progression. Changes in TLR4expression are associated with changes in the expression of key cellular cytokines (transforming growth factor-β (TGF-β), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ)), which affect cancer progression and metastasis.

To study changes in the expression of TLR4, TGF-β, TNF-α, IFN-γ genes, the level of apoptosis and cell cycle distribution in human invasive urothelial carcinoma T24/83cells under the treatment with polyphenolic adjuvant compound of fungal origin melanin, cytotoxic drug cisplatin, and combination of both.

T24/83cells were incubated with cisplatin (0.05mM), melanin (5µg/ml), or their combination. The expression level of TLR-4, TGF-β, INF-γ, TNF-α was evaluated by the real time polymerase chain reaction. The flow cytometry was used to study cell cycle distribution, proliferative activity and level of apoptosis. Morphological analysis of the Т24/83cells was performed as well.

4, TNF-α, TGF-β, INF-γ expression, cell cycle distribution and morphology in T24/83 cells suggesting their transition to less aggressive phenotype.
To assess the functional state of macrophages based on various manifestations of their activity at the different stages of metastatic tumor growth in C57Bl mice.

On days 7, 14, 21and 28after Lewis lung carcinoma transplantation to C57Bl mice, macrophages from various anatomic sites were isolated and tested on their cytotoxicity, metabolic activity, NO production and arginase activity.

In the populations of peritoneal and splenic macrophages, on days 7and 21of tumor growth antitumor (M1) cells prevailed while on days 14and 28tumor-promoting (M2) macrophages predominated. In the population of lung macrophages, cells with M1phenotype were in the majority in the early stages of tumor growth. On days 21and 28, M1cells were gradually substituted by cells exhibiting M2phenotype. This shift correlated with metastasis to lungs.

Lewis lung carcinoma growth is accompanied by the gradual change in macrophage polarization from antitumor (M1) towards tumor-promoting (M2) type. These changes were more evident in population of lung macrophages and correlated with the parameters of metastasis.
Lewis lung carcinoma growth is accompanied by the gradual change in macrophage polarization from antitumor (M1) towards tumor-promoting (M2) type. These changes were more evident in population of lung macrophages and correlated with the parameters of metastasis.Vulvar carcinoma corresponds to the fourth gynecological malignancy in incidence, with more than forty thousand new cases being estimated worldwide in 2020. It is a disease characterized by locoregional spread presenting high recurrence rates although distant metastases are an uncommon event. The purpose of this work is to describe the diagnosis, treatment, and clinical course of vulvar carcinoma in a patient who presented regional recurrences and late metastasis to the mammary gland. Vulvar cancer is a disease with a well-defined natural history; but with the advancement of therapeutic possibilities in recent years, it has been possible to improve the prognosis, reducing the chance of locoregional recurrence. Thus, the possibility of distance recurrence must be remembered in inpatient follow-up with locally advanced vulvar carcinoma, even if atypically, as in the case reported.
To investigate the features of expression of miRNA-21and miRNA-375in tumor cells of patients with cancer of oral cavity(COC) and to determine the possibility of their use to predict the aggressiveness of COC course.

The work is based on the results of examination and treatment of 50patients with stage II-IV COC. miRNA expression in tumor cells was analyzed by real time reverse transcription polymerase chain reaction.

High levels of miRNA-21expression (> 0.26a.u.) and miRNA-375 (> 0.36a.u.) were determined in 72.0% and 63.0% of cases. We revealed a tendency to decreased miRNA-21expression and increased miRNA-375expression in tumors of patients with recurrence-free survival less than 12months and the presence of metastatic lesions in regional lymph nodes. In patients with COC of low differentiation grade, the level of miRNA-21was 2.0times lower compared with tumors of moderate differentiation grade (p< 0.05), while the expression of miRNA-375, on the contrary, was higher in tumors of low differentiation grade. A decreased expression of miRNA-21 (< 0.26a.u.) against the background of decreased levels of miRNA-375 (< 0.36a.u.) in tumor cells was associated with worse recurrence-free survival.

The obtained results indicate the relation between the main clinical and pathological characteristics of patients with COC and the levels of miRNA-21and -375expression in tumor tissue, which indicates the involvement of these miRNAs in the formation of COC malignancy evidencing on their potential usefulness as additional prognostic markers.
The obtained results indicate the relation between the main clinical and pathological characteristics of patients with COC and the levels of miRNA-21 and -375 expression in tumor tissue, which indicates the involvement of these miRNAs in the formation of COC malignancy evidencing on their potential usefulness as additional prognostic markers.In October 2020, passed away Ada Leonidivna Vorontsova, our esteemed colleague, well known specialist in experimental oncology, doctor of sciences in biology, professor, leading researcher, who devoted all her life to the R.E. Kavetsky Institute of Experimental Pathology, Oncology and Radiobiology, the National Academy of Sciences of Ukraine.
To assess the level of erythropoietin (EPO) in blood sera of patients with different subtypes of myelodysplastic syndromes (MDS) from different risk subgroups and to determine its prognostic role.

EPO was measured by enzyme-linked immunosorbent assay in peripheral blood of 54patients with different MDS subtypes according to the French-American-British (FAB) classification. The comparison group consisted of 15healthy individuals. Complete blood count (hemoglobin, leukocyte and platelet levels) was determined and bone marrow cells were characterized morphologically. The overall and leukemia-free survivals were estimated by Kaplan- Meier method.

The level of ЕРО in MDS was reliably higher in comparison with healthy persons (p< 0.01, Mann- Whitney test). No statistically significant difference was found in serum EPO concentration between the groups of patients with low- and high-risk MDS (603.5pg/ml vs 721.0pg/ml; p> 0.05). In transfusion-dependent patients, the level of EPO was significantly higher tprognostic factors in MDS patients.
This study shows that lower serum EPO level may be considered as one of the additional adverse prognostic factors in MDS patients.
Somatic mutations in coding regions of the genome may result in non-functional proteins that can lead to cancer or other diseases, however cancer mutations in the non-coding regions have rarely been studied and the interpretation of their effects is difficult. Non-coding mutations might act by breaking or creating transcription factor binding motifs in promoters, enhancers or silencers resulting in altered expression of target gene(s). A high number of mutations have been reported in coding and non-coding regions in cells of liver cancer. Hepatocyte nuclear factor 4α is a transcription factor that regulates the expression of several genes in liver cells, while the motifs it binds are frequently mutated in promoters and enhancers in liver cancer.

The aim of the study is to evaluate the genetic effects of a non-coding somatic mutation frequently observed in liver cancer.

We evaluated experimentally the effects of a somatic mutation frequently reported in liver cancer as a motif-breaker for the binding of hepatocyte nuclear factor 4α. The effects of the mutation on protein binding and enhancer activity were studied in HepG2cells via electrophoresis mobility shift assay and dual luciferase reporter assays. We also studied genome-wide promoter-enhancer interactions performing targeted chromosome conformation capture in liver tissue to identify putative target genes whose expression could be altered by the mutation.

We found that the mutation leads to reduced protein binding and a decrease in enhancer activity. The enhancer harboring the mutation interacts with the promoters of ANAPC13, MAP6D1and MUC13, which have been implicated in liver cancer.

The study highlights the importance of non-coding somatic mutations, vastly understudied, but likely to contribute to cancer development and progression.
The study highlights the importance of non-coding somatic mutations, vastly understudied, but likely to contribute to cancer development and progression.