IntroductionThe subject of the experiment was bacterial nanocellulose, a natural polymer produced by bacteria – Gluconacetobacter xylinus. Following a specific modification process a cartilage-like material for restoration of damaged tissues may be produced. The obtained implants with excellent biocompatibility, mouldability, biophysical and chemical properties perfectly fit the needs of reconstructive surgery. The goal of the experiment was to develop and analyze cellulosic guidance channels in vivo for the reconstruction of damaged peripheral nerves.Material and methodsThe experiments were conducted on Wistar rats, femoral nerve. Cellulose was produced according to a self-patented method. In the experimental group tubulization was applied, whereas in the control traditional end-to-end connection was used. Observation time was 30, 60, 90, and 180 days. Results evaluation included histological analysis and postoperative observation of motor recovery.ResultsThe overgrowth of connective tissue and disorganisation of neural structures was evident in 86.67% of control specimens, while for cellulosic group it was only 35% (p = 0.0022). Tubulization prevented the excessive proliferation of connective tissue and isolated from penetration with scar tissue. Autocannibalism, being probably an evidence of neurotrophic factors amassment, was observed in cellulosic group but not in the control one. Motor recovery did not differ significantly (p > 0.05). Biocompatibility of implants was affirmed by very small level of tissue response and susceptibility to vascularisation.ConclusionsCellulosic neurotubes effectively prevent the formation of neuromas. They are of very good biocompatibility and allow the accumulation of neurotrophic factors inside, thus facilitating the process of nerve regeneration.

Glioblastoma multiforme is the most common type of primary brain tumor in adults. WWOX is a tumor suppressor gene involved in carcinogenesis and cancer progression in many different neoplasms. Reduced WWOX expression is associated with more aggressive phenotype and poor patient outcome in several cancers. We investigated alternations of WWOX expression and its correlation with proliferation, apoptosis and signal trafficking in 67 glioblastoma multiforme specimens. Moreover, we examined the level of WWOX LOH and methylation status in WWOX promoter region. Our results suggest that loss of heterozygosity (relatively frequent in glioblastoma multiforme) along with promoter methylation may decrease the expression of this tumor suppressor gene. Our experiment revealed positive correlations between WWOX and Bcl2 and between WWOX and Ki67. We also confirmed that WWOX is positively correlated with ErbB4 signaling pathway in glioblastoma multiforme.

Glioblastoma is a highly aggressive tumour of the central nervous system, characterised by poor prognosis irrespective of the applied treatment. The aim of our study was to analyse whether the molecular markers of glioblastoma (i.e. TP53 and IDH1 mutations, CDKN2A deletion, EGFR amplification, chromosome 7 polysomy and EGFRvIII expression) could be associated with distinct prognosis and/or response to the therapy. Moreover, we describe a method which allows for a reliable, as well as time- and cost-effective, screening for EGFR amplification and chromosome 7 polysomy with quantitative Real-Time PCR at DNA level. In the clinical data, only the patient’s age had prognostic significance (continuous: HR = 1.04; p<0.01). At the molecular level, EGFRvIII expression was associated with a better prognosis (HR = 0.37; p = 0.04). Intriguingly, EGFR amplification was associated with a worse outcome in younger patients (HR = 3.75; p<0.01) and in patients treated with radiotherapy (HR = 2.71; p = 0.03). We did not observe any difference between the patients with the amplification treated with radiotherapy and the patients without such a treatment. Next, EGFR amplification was related to a better prognosis in combination with the homozygous CDKN2A deletion (HR = 0.12; p = 0.01), but to a poorer prognosis in combination with chromosome 7 polysomy (HR = 14.88; p = 0.01). Importantly, the results emphasise the necessity to distinguish both mechanisms of the increased EGFR gene copy number (amplification and polysomy). To conclude, although the data presented here require validation in different groups of patients, they strongly advocate the consideration of the patient’s tumour molecular characteristics in the selection of the therapy.

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A b s t r a c tIntroduction: TP53 and MGMT alterations play a crucial role in glioblastoma (GB) pathogenesis. TP53 and MGMT function is affected by several pathologic mechanisms, such as point mutations or promoter methylation, which are well characterized. Expression of both genes can be regulated by other mechanisms as well, e.g., microRNAs (miRNAs). Moreover, cross-talk among various pathologic processes may occur, further affecting MGMT and TP53 functionality. Material and methods: In 49 GB patients, we analyzed the possible associations between TP53 and its miRNA regulators miR-125b, miR-21, and miR34a, as well as MGMT and its miRNA regulators miR-181d and miR-648. We evaluated the possible influence of mutational and methylation status on the pre-identified associations. Results: In patients with immunohistochemistry-detected TP53 overexpression, expression levels of miR-34a and TP53 were negatively correlated (r = -0.56, p = 0.0195), and in patients with TP53 mutations, expression levels of TP53 and miR-21 were negatively correlated (r = -0.67, p = 0.0330). In patients with MGMT methylation, expression levels of MGMT were negatively correlated with miR-648 and miR-125b expression levels (r = -0.61, p = 0.0269 and r = -0.34, p = 0.0727, respectively).Conclusions: Our findings demonstrate that selected miRNAs are significantly correlated with MGMT and TP53 levels, but the extent of this correlation differs regarding the TP53 and MGMT mutational and promoter methylation status.

Revision of the fourth edition of the World Health Organisation (WHO) Classification of Haematopoietic and Lymphatic Tissues, which was published in 2017, introduced important changes updating the biology, pathology, genetics, and clinical presentation of aggressive B-cell lymphomas. High grade B-cell lymphomas (HG-BLs) replaced B-cell lymphoma, unclassifiable, with features intermediate between diffuse large B-cell lymphoma and Burkitt lymphoma, the new provisional entityBurkitt-like lymphoma with 11q aberration was identified, and some categories were upgraded, e.g. EBV-positive diffuse large B-cell lymphoma, not otherwise specified. Still the histopathological diagnostics is based on morphology and immunoprofile, but to define the HGBLs evaluation of MYC, BCL2, and BCL6 gene statuses is required. According to the presented WHO criteria, in the comprehensive histopathological diagnostics of aggressive B-cell lymphomas a highly specialised diagnostic team including a pathologist, a molecular biologist, a geneticist, a haematologist, and immunophenotyping technicians is needed.

Hairy cell leukemia (HCL) is a rare and indolent form of small mature B-cell leukemias. The annual incidence of HCL is estimated to be 0.3 cases per 100 000, and the disease comprises 2%-3% of all leukemias. 1,2 It was estimated that 1100 new cases of HCL and 4060 deaths occurred in 2016 in the USA. 3,4 It is mostly a disease of middle-aged males (median age 55 years and 4:1 male predominance). Patients present most frequently with splenomegaly, pancytopenia, and bone marrow infiltration. Hairy cells characteristically stain strongly positive for tartrate-resistant acid phosphatase (TRAP) and have a typical pattern of B-cell antigen expression (CD19, CD20) with co-expression of CD11c, CD25, and CD103. Cell surface markers associated with normal B-cell activation, especially CD22, CD72, and CD40, are also strongly expressed. 3,4 The BRAF V600E mutation is present in all patients and is regarded as a disease-defining genetic event. 5 Purine nucleoside analogs (PNA), cladribine (2-CDA), and pentostatin (DCF, deoxycoformycin) are the drugs of choice in first-line treatment of HCL 3,4 ; they induce durable and unmaintained complete response (CR) in more than 70% of patients, with relapse rates of 30%-40%, after 5-to 10-year follow-up. However, despite very high initial response rates, many patients ultimately relapse or develop refractory disease and will require novel therapies after these agents. 3 Unusual clinical manifestations of HCL are occasionally reported. 6-14 These rare symptoms may include bulky abdominal lymphadenopathy, tumor masses in the mediastinum, paravertebral masses,

IntroductionSolitary fibrous tumors of the pleura (SFTP) are primary tumors arising from mesenchymal cells. Immunohistochemical studies have demonstrated that the origin of these tumors is mesenchymal rather than mesothelial. The aim of this study is to present our experience with diagnosing and treating patients with SFTP.Material and methodsWe analyzed 18 patients treated at the Department of Thoracic Surgery of the Medical University of Lodz. The patients’ medical histories and the results of postoperative histopathological investigation of the tumors were analyzed. Postoperative histopathological samples were evaluated with regard to the current criteria of malignancy.ResultsIn 17 patients, the tumors were surgically removed. Benign and small lesions (less than 3 cm in size) were removed by video-assisted thoracoscopic surgery (VATS). In 5 cases, malignant tumors were found in the postoperative material.ConclusionsSolitary fibrous tumors of the pleura is a tumor with frequently asymptomatic clinical course. Treatment consists in resection which includes the adjacent structures, especially if the tumor is malignant.