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Hodgkin's lymphoma is a malignant disease of the lymphatic system. Hodgkin's lymphoma was first described by Dr. Thomas Hodgkin in 1832 and later named “Hodgkin's disease” by Samuel Wilkes. Hodgkin's lymphoma accounts for about 24 % of all lymphomas. Hodgkin's lymphoma is classified as classical and nodular lymphoid-predominant (Nodular type of lymphoidpredominant Hodgkin's lymphoma). Classical Hodgkin's lymphoma includes the following histologic variants: nodular sclerosis variant (types I and II), mixed cell variant, classic lymphocyte-rich variant, and rare lymphoid depletion variant. Epidemiological and serological studies showed the involvement of the Epstein-Barr virus into Hodgkin's lymphoma etiology, since its genome was found in the study of the biopsy material samples from patients with Hodgkin's lymphoma. A relationship with the human immunodeficiency virus (HIV) was revealed as well, and patients infected with HIV have a significantly increased risk of developing Hodgkin's lymphoma compared to healthy people. An in-depth study of the Hodgkin's lymphoma pathophysiology revealed new therapeutic targets in the treatment of this disease. All these discoveries changed the understanding of the Hodgkin's lymphoma pathogenesis, and were important for the development of new methods of treatment. The history of therapy begins on the cusp of the 19th and 20th centuries. Over the past four decades, achievements in radiation therapy and combined chemotherapy have significantly improved overall survival of patients with Hodgkin's lymphoma. Currently, more than 80 % of patients under 60 years old with first diagnosed Hodgkin's lymphoma can be cured from this disease after first-line chemotherapy.

Purpose of the study. An analysis of blood levels of TGF-β, TGFR2, TNF-α, TNF-αR1, TNF-αR2, CD44 and MMP9 in patients with various biological subtypes of breast cancer receiving neoadjuvant chemotherapy.Materials and methods. This article presents an analysis of levels of growth and progression factors (TGF-β, TGFR2, TNF-α, TNF-αR1, TNF-αR2, CD44 and MMP9) in the blood of 162 patients with various biological subtypes of locally advanced breast cancer receiving 8 cycles of neoadjuvant chemotherapy.Results. Levels of TGF-β, TGFR2, TNF, TNF-α, TNFR1, TNFR2, CD44, MMP9 in patients with all BC subtypes were high before the treatment. After chemotherapy cycles, the values decreased statistically significantly in all BC subtypes: CD44 decreased by 25.2 %, 30 % and 54.7 % in luminal A, luminal B and TNBC, respectively; TNFα– by 26.2 %, 48.3 % and 50.8 %, respectively; TNFα-R1 – by 52.1 %, 39.2 % and 50.3 % respectively; TNFα-R2 – by 31.7 %, 32.8 % and 41.9 % respectively; MMP9 – 35.3 %, 32.6 % and 43.3 % respectively.Conclusions. We identified a combination of growth and progression factors which determines the chemotherapy sensitivity and resistance in all subtypes of breast cancer; so, a decline in the levels of TGF-β, TNFα, MMP9 and CD44 after neoadjuvant chemotherapy predicts further remission for at least 3 years. On the contrary, stabilization or an increase of these indicators leads to the early tumor progression.

Introduction: About 5% of endometrial cancer cases can be genetic and inherited. Lynch syndrome, also called hereditary non-polyposis colorectal cancer (HNPCC), is an autosomal dominant syndrome. Caused by a germline mutation in one of the DNA mismatch repair genes, it is responsible for most hereditary cases. Lynch syndrome is associated with the early onset and the development of many types of cancer, especially colon and endometrial cancer. Methods: The review of publications regarding Lynch syndrome-associated endometrial cancer and methods for screening, diagnosis and its prevention. State of knowelage: Endometrial cancers related to Lynch syndrome are mostly sentinel (they reveal the predisposition in 50% of families) and are characterized by young age at onset (commonly before 60 years). The lifetime cumulative risk of endometrial cancer for women with Lynch syndrome is about 40% to 60%, which equals or exceeds their risk of colorectal cancer. Lynch syndrome, the current gynecologic cancer screening guidelines include annual endometrial sampling and transvaginal ultrasonography beginning at age of 30-35 years, which is very important in the early detection of this cancer. Risk-reducing surgery consisting of prophylactic hysterectomy and bilateral salpingooophorectomy should be offered to women aged 35 years or older who do not wish to preserve their fertility. Summary: Diagnosis of endometrial cancer in patients with Lynch syndrome has important clinical implications for the individual and family members.

Objective: To examine the applicability of IHC staining method: with TGF-β1 antibodies (serial examination, statistically processed results) and with mast cell tryptase antibodies for injuries vitality determination., Material and Methods: 261 skin autopsy samples with mechanical injuries from 29 persons were divided to 3 groups (87 in each group): vital injuries, postmortal injuries, control non-injured samples. A routine histological examination using standard H&E stain and IHC both with TGF-β1 and mast cells tryptase antibodies was performed., Results and Conclusion: The positive TGF-β1 staining (score 2-3) was found in keratinocytes in vitally injured skin and the negative or weak one (score 0-1) was found in control postmortally injured and non-injured samples. Additionally, dermal TGF-β1 expression was found in some vitally injured skin samples. The difference between vitally injured skin and control samples was statistically significant ( p <0.05). No significant difference of dermal mast cells density in groups 1, 2, 3 was found.

New and original values (coefficient of phosphorylation and coefficient of intracellular distribution) proposed. They are reflecting a functional state of the heat shock protein 27 kDa (Hsp27) in tumor cells of breast cancer. These coefficients are more clearly reflect the functional state of Hsp27, than classical evaluation of chaperone expression only in the cytoplasm. It has been shown that in tumors with high expression of receptor Her2/neu on the membrane in the absence of gene amplification cerb2/neu (Her2/neu (3+) FISH (-)) there are low coefficients of phosphorylation and intracellular distribution as compared with Her2/neu-positive (Her2/neu (2+/3+) FISH (+)) and Her2/neu-negative tumors (Her2/neu (0/1+) FISH (-)). The possible molecular mechanisms of the phenomenon of dissonance cerb2 / neu gene amplification and receptor Her2/neu expression on the membrane of tumor cells breast cancer are discussing.

A forensic pathological case of rare T-cell leukemia is reported. Autopsy samples (paraffine blocks and slides) from 32 years old female with long-term existing anemia and leukopenia, number of chronic inflammatory diseases, died from fulminant pneumonia, were presented for forensic pathological re-examination. A routine histological examination was done using standard H&E stain. Additionally, we used IHC stain with antibodies to CD3 and CD20 when examining bone marrow and liver samples. The T-cell infiltration in bone marrow (interstitial and intrasinusoidal type) were found. The next step was IHC bone marrow examination with CD4, CD5, CD8, CD56 antibodies. We concluded that the patient had unrecognized T-cell leukemia, based on anamnestical, clinical data and results of our histological and IHC examination. In this case, the T-cell leukemia was not found neither vitally nor at primary forensic pathological examination after autopsy. The necessity of minimal IHC stain sets usage in primary forensic pathology units and IHC's decisive role in bone marrow pathological examination are discussed.

The Aim of the Study: Is to examine the applicability of IHC staining method with TGFβ1 antibodies for injuries vitality determination. 72 skin autopsy samples with mechanical injuries from 12 persons were divided to 3 groups ( n =24 in each group): vital injuries, postmortal injuries, control non-injured samples. A routine histological examination using standard H&E stain and IHC with TGFβ1 antibodies was performed. We concluded the positive TGFβ1 staining was in keratinocytes in vitally injured skin and the negative one in postmortally injured and control non-injured samples. The role of TGFβ1 in the injuries healing process and the further examinations of the TGFβ1 staining method application for determination of injuries vitality are discussed.