Biomedical subjects

Rajko Kusec

Publications and source records attributed to Rajko Kusec.

21 records · Page 2Linked to original sources

PubMed2002

Molecular and genetic mechanisms of lymphomagenesis.

The analysis of the molecular characteristics of immunoglobulin or T-cell receptor genes of lymphomas allows us to determine the cell origin in terms of pre- or postgerminal center cells. Most molecular oncogenic events are associated with the activity of otherwise physiologically active enzymatic and protein machinery for Ig/TCR gene modeling, where normal molecular sequence of events can be disrupted, leading to pathogenic molecular lesion and neoplastic cell transformation. Our current knowledge on the molecular and genetic basis of neoplastic transformation of lymphoid cells resulting in clinical phenotype of malignant lymphoma is further reviewed, and basic specific molecular mechanisms of Ig/TCR gene deregulation are presented, as well as recent achievements in molecular genetic profiling of malignant lymphoma.

Cell Transformation, Neoplastic↗

PubMed2002

Diffuse large B-cell lymphoma and its variants.

According to the World Health Organization classification of neoplastic diseases of the hematopoietic and lymphoid tissues, diffuse large B-cell lymphoma comprises about 40% of adult cases of non-Hodgkin s lymphoma. It consists of the following morphological variants: 1) centroblastic (with or without multilobulated nuclei); 2) immunoblastic (>90% of immunoblasts); 3) T cell/histiocytes rich; and 4) anaplastic. Rare morphological variants plasmablastic type, mediastinal (thymic) diffuse large B-cell lymphoma, intravascular, and primary effusion B-cell lymphoma are considered distinct variants of diffuse large B-cell lymphoma due to their unique topographic presentation and clinical behavior, as well as immunophenotypic and genetic characteristics. T-cell/histiocyte-rich B-cell lymphoma is morphologically characterized by up to 25% of large neoplastic B cells and 75-90% of reactive, non-neoplastic T cells. Mediastinal (thymic) diffuse large B-cell lymphoma is considered a subtype of diffuse large B-cell lymphoma arising in the mediastinum, with distinctive morphological, immunohistochemical, genotypic, and clinical features. Mediastinal diffuse large B-cell lymphoma is an aggressive disease with poor outcome, which probably originates from thymic B cells at the terminal stage of differentiation. During the 1997-2001 period, 720 patients were diagnosed with non-Hodgkin s lymphoma in our institution. Out of 101 (14%) patients with diffuse large B-cell lymphoma, 17 had T-cell-rich B-cell lymphoma and their median survival was less than 20 months, with no difference regarding sex, bone marrow involvement, CD30 positivity, or histiocytic component of the tumor. Twenty out of 101 patients had mediastinal B-cell lymphoma and their median survival was 21 months, with sex or degree of necrosis of the involved lymph node having no impact on survival. We studied the frequency of bcl-2 gene rearrangement in fusion with immunoglobulin receptor gene of t(14;18) and found no such event among 20 of our patients with mediastinal diffuse large B-cell lymphoma. Despite extensive efforts and constant progress in our understanding of non-Hodgkin s lymphoma pathogenesis, the diffuse large B-cell lymphoma group remains heterogeneous entity awaiting further pathological and clinical stratification.

Adult↗

PubMedDate not supplied

[Occurrence of chronic B-cell lymphocytic leukemia in Hodgkin's disease: case report].

We present a case of a female patient (79 years) with pathohistologic diagnosis of Hodgkin's lymphoma (HL) (stage IIIB, histologic type MC) for which she was treated with chemotherapy according to LVPP protocol (6 cycles) with good therapeutic response. Unexpectedly, 18 months after HL diagnosis leukocytosis occurred (19.4 x 10(9)/L) with 65% of lymphocytes with lymphoplasmocytic differentiation. Immunophenotype of these cells is typical for B-chronic lymphocytic leukemia (B-CLL) (CD5/CD19+, CD23-, CD38 +/-; with weak expression of monoclonal light chains lambda). Molecular analysis confirmed clonal immunoglobulin heavy chain gene (IgH) rearrangement of peripheral blood lymphocytes. The diagnosis of B-CLL imposed the question of the connection between two neoplasms of lymphocytic origin. Molecular analysis of lymph node biopsy taken at the time of lymphoma diagnosis revealed clonal population of B lymphocytes. That test undeniably proved coexistence of both diseases from the beginning. The latest PCR analysis of archive peripheral blood smears confirmed B lymphocyte clonality without diagnostic criteria for lymphoproliferative disease of CLL type. This finding etiologically excludes secondary leukemia. The possibility of untypical presentation of CLL in transformation to Richter's syndrome with morphologic characteristics of HL from the beginning stays unconfirmed. The hypothetical question that remains unanswered is: "Was it one disease in different clinical forms?"

Aged↗