NK cell lymphoma, nasal type, with massive lung involvement: a case report

Extranodal NK/T cell lymphoma, nasal type, is an Epstein–Barr virus-associated lymphoma that most commonly involves the nasal cavity and upper respiratory tract. Lung involvement by NK/T cell lymphoma is rare and seldom reported in the literature. We describe the unusual case of a 41-year-old male with NK cell lymphoma, nasal type, who presented with massive secondary lung involvement 2.5 years after the detection of a retroperitoneal mass. The diagnosis was made by open lung biopsy. Despite aggressive treatment, the patient died shortly after the initiation of therapy. Lung involvement by NK/T cell lymphoma occurs most commonly as part of widely disseminated disease and carries a poor prognosis for the patient. Novel agents and innovative therapies need to be developed for this aggressive lymphoma.     

Detection of B cell lymphoma involvement in T cell-rich serous fluid by immunoglobulin gene rearrangement: a report of 2 cases

BACKGROUND: Cytology, flow cytometry and gene rearrangement studies are methods to detect lymphoma involvement of body fluid. The cytology of the effusion is equivocal for lymphoma involvement. CASES: We report 2 cases of diffuse large B cell lymphoma with massive lymphocyte predominant serous fluid, ascites in one case and pleural effusion in the other. Immunophenotypic analysis by flow cytometry showed that lymphoid cells express only T cell markers. Lymphoma involvement of effusion was confirmed by immunoglobulin gene rearrangement detected by polymerase chain reaction. CONCLUSION: Our case demonstrated the value of gene rearrangement study in establishing diagnosis of equivocal cases.     

The centrosome as the main integrator of endothelial cell functional activity

The centrosome is an intracellular structure of the animal cell responsible for organization of cytoplasmic microtubules. According to modern concepts, the centrosome is a very important integral element of the living cell whose functions are not limited to its ability to polymerize microtubules. The centrosome localization in the geometric center of the interphase cell, the high concentration of various regulatory proteins in this area, the centrosome-organized radial system of microtubules for intracellular transport by motor proteins, the centrosome involvement in the perception of external signals and their transmission–all these features make this cellular structure a unique regulation and distribution center managing dynamic morphology of the animal cell. In conjunction with the tissue-specific features of the centrosome structure, this suggests the direct involvement of the centrosome in execution of cell functions. This review discusses the involvement of the centrosome in the vital activity of endothelial cells, as well as its possible participation in the implementation of barrier function, the major function of endothelium.     

Involvement of Rac GTPase activation in phosphatidylcholine hydroperoxide-induced THP-1 cell adhesion to ICAM-1

Increasing evidence indicates that phospholipid oxidation plays important roles in atherosclerosis. Here, we investigated the involvement of Rho-family GTPases inphosphatidylcholine hydroperoxide (PCOOH)-induced THP-1 cell adhesion to ICAM-1. Isoprenoid depletion by fluvastatin and geranylgeranyltransferase inhibition by GGTI-286 suppressed PCOOH-induced cell adhesion to ICAM-1 and F-actin-rich membrane protrusion formation. Pull-down assays demonstrated the activation of Rac1 and Rac2 in PCOOH-treated cells. Pan-Rho-family GTPase inhibitor Clostridium difficile toxin B, Rac-specific inhibitor NSC23776, and RNA interference of the Rac isoforms suppressed the cell adhesion. These findings indicate the involvement of Rac GTPase activation in PCOOH-induced cell adhesion to ICAM-1 via actin reorganization.     

The role of eukaryotic initiation factor 5A in the control of cell proliferation and apoptosis

Summary. In the past years, the attention of scientists has mainly focused on the study of the genetic information and alterations that regulate eukaryotic cell proliferation and that lead to neoplastic transformation. An increasing series of data are emerging about the involvement of the initiation phase of translational processes in the control of cell proliferation. In this paper we review the novel insights on the biochemical and molecular events leading to the initiation and its involvement in cell proliferation and tumourigenesis. We describe the structure, regulation and proposed functions of the eukaryotic initiation factor 5A (eIF-5A) focusing the attention on its involvement in the regulation of apoptosis and cell proliferation. Moreover, we describe the modulation of its activity (through the reduction of hypusine synthesis) in apoptosis induced either by tissue transglutaminase or interferon α. Finally, we propose eIF-5A as an additional target of anti-cancer strategies. Received July 28, 2000 Accepted September 30, 2000     

The detection of endocervical gland involvement by high grade squamous intraepithelial lesions in smears prepared from endocervical brush specimens

The cytologic features of squamous cell carcinoma in situ with endocervical gland involvement have been described in cervical smears. We evaluated the presence of two types of cellular fragments in 43 cervical smears of high grade squamous intraepithelial lesions (HGSIL) to assess their ability to predict glandular involvement by HGSIL in subsequent cone biopsies. an endocervical brush was used to obtain all endocervical specimens. of 16 cases without glandular involvement, fragments were present in 13 smears. of 27 cases with glandular involvement, fragments were absent in 11 smears. No statistical association was identified between the presence of abnormal cellular fragments on cervical smears of HGSIL and endocervical gland involvement on cone biopsies.     

Involvement of proteases in apoptosis

Genetically programmed (apoptotic) cell death plays a key role in cell and tissue homeostasis and in pathogenesis of various diseases. However, the mechanisms involved in apoptotic cell death are poorly understood. At present, the role of proteases in key events of apoptosis is intensively studied and discussed and the involvement of various proteolytic enzymes in the induction and development of the cell death is well-recognized. Proteases of various classes participating in apoptosis have been identified as well as some substrates of these proteases whose cleavage is critical to cell viability; specific protease inhibitors which prevent the cell death have been synthesized. This review summarizes new data on proteolytic enzymes involved in apoptosis and considers the mechanisms of activation of proteases upon induction of apoptosis and the pathways of their involvement in the cell death. The participation of nuclear proteolytic enzymes in the destabilization of chromatin structure and regulation of DNA fragmentation by endonucleases in apoptotic cells is discussed.     

Cell proliferation and drug sensitivity of human glioblastoma cells are altered by the stable modulation of cytosolic 5′-nucleotidase II

Cytosolic 5′-nucleotidase II (cN-II) has been reported to be involved in cell survival, nucleotide metabolism and in the cellular response to anticancer drugs. With the aim to further evaluate the role of this enzyme in cell biology, we stably modulated its expression the human glioblastoma cell ADF in which the transient inhibition of cN-II has been shown to induce cell death. Stable cell lines were obtained both with inhibition, obtained with plasmids coding cN-II-targeting short hairpin RNA, and stimulation, obtained with plasmids coding Green Fluorescence Protein (GFP)-fused wild type cN-II or a GFP-fused hyperactive mutant (GFP-cN-II-R367Q), of cN-II expression. Silenced cells displayed a decreased proliferation rate while the over expressing cell lines displayed an increased proliferation rate as evidenced by impedance measurement using the xCELLigence device. The expression of nucleotide metabolism relevant genes was only slightly different between cell lines, suggesting a compensatory mechanism in transfected cells. Cells with decreased cN-II expression were resistant to the nucleoside analog fludarabine confirming the involvement of cN-II in the metabolism of this drug. Finally, we observed sensitivity to cisplatin in cN-II silenced cells and resistance to this same drug in cN-II over-expressing cells indicating an involvement of cN-II in the mechanism of action of platinum derivatives, and most probably in DNA repair. In summary, our findings confirm some previous data on the role of cN-II in the sensitivity of cancer cells to cancer drugs, and suggest its involvement in other cellular phenomenon such as cell proliferation.     

Hypersensitive response-related death

The hypersensitive response (HR) of plants resistant to microbial pathogens involves a complex form of programmed cell death (PCD) that differs from developmental PCD in its consistent association with the induction of local and systemic defence responses. Hypersensitive cell death is commonly controlled by direct or indirect interactions between pathogen avirulence gene products and those of plant resistance genes and it can be the result of multiple signalling pathways. Ion fluxes and the generation of reactive oxygen species commonly precede cell death, but a direct involvement of the latter seems to vary with the plant-pathogen combination. Protein synthesis, an intact actin cytoskeleton and salicylic acid also seem necessary for cell death induction. Cytological studies suggest that the actual mode and sequence of dismantling the cell contents varies among plant-parasite systems although there may be a universal involvement of cysteine proteases. It seems likely that cell death within the HR acts more as a signal to the rest of the plant rather than as a direct defence mechanism.     

Hapten-specific T cell responses to 4-hydroxy-3-nitrophenyl acetyl. XIII. Characterization of a third T cell population involved in suppression of in vitro PFC responses

The involvement of a third-order suppressor T cell population (Ts3) in the suppression of in vitro PFC responses was analyzed. It was shown that Ts2 effector-phase suppressor cells, induced by the i.v. injection of NP-coupled syngeneic spleen cells, require a third suppressor T cell population to effect NPb idiotype-specific suppression of an in vitro B cell response. This Ts3 population was shown to be present in NP-primed but not unprimed donors. The Ts3 population specifically binds NP and is Lyt-1-, Lyt-2+, I-J+ and bears NPb idiotypic determinants. The involvement of the Ts3 population in a suppressor pathway that requires recognition of idiotypic determinants is discussed.     

Dna topoisomerase activities in plants: Involvement in cell proliferation

Abstract

The role of DNA topoisomerases in cell processes related to DNA metabolism, their involvement in the regulation of cell proliferation and their distribution in plant tissues are discussed.     

Role of vimentin in cell migration

Cell migration plays a crucial role in embryonic development, wound healing, regeneration, inflammation, and immune response, as well as in dissemination of malignant tumors. Vimentin is the marker of migrating cells, but its role in cell migration is still unclear. However, recent studies have revealed novel functions for vimentin related to the migration, such as determination of cellular polarity, regulation of cell contact formation, and arrangement and transport of signal proteins involved in cell motility. The review sums up the latest data on vimentin functions and its involvement in molecular mechanisms underlying cell migration. Early studies demonstrated that vimentin expression during embryonic development is associated with cell migration. However, having obtained vimentin knockout mice without apparent impairments in development and ability to reproduce, doubts have appeared if vimentin is required for cell migration during embryonic development. In the present review, we also discuss involvement of vimentin in migration processes at different stages of development and try to resolve current contradictions concerning the role of vimentin in various events of cell migration.     

Reticulum Cell Sarcoma of the Central Nervous System

One variety of sarcoma of the central nervous system (CNS) has been referred to under such synonyms as perithelial sarcoma, microglioma, and reticulum cell sarcoma. A case of diffuse involvement of the CNS is reported and the author believes that the tumour is a reticulum cell sarcoma because: (1) in addition to involvement of the CNS, lesions characteristic of a diffuse lymphomatous process were present in extraneural sites; (2) silver carbonate impregnation of the tumour cells was demonstrated. This tinctorial property has been reported as characteristic of microgliomas but has been shown to be an unreliable criterion for the differentiation of the cells of microglial from those of reticulum cell sarcomas. It is concluded that in such cases the CNS is the initial and major focus of a multicentric malignant lymphoma which has the histologic characteristics of a reticulum cell sarcoma.     

The role of cell wall in plant embryogenesis

This review presents recent data about cell wall involvement in plant embryogenesis. During plant development, the cell wall is subjected to precise regulation. During this process a bidirectional information exchange between the cell wall and the protoplast is observed. The cell wall also mediates in the cell-cell (apoplastic) and cell to cell (symplastic) information flow. Especially some products derived from the hydrolysis of specific cell wall compounds can act as short distance signal transduction molecules during the development. Oligosaccharins are a group of such products. Their activity and sources focused the researchers' attention on the biochemical composition of the cell wall and the activity of some cell wall enzymes. The dramatic influence on the embryo body shape has also the cell wall synthesis machinery, including vesicular secretion pathways. Moreover, the interplay between the turgor pressure and counteracting cell walls and neighbouring cells (in higher organisms) creates the specific mechanical forces influencing the development of the whole plant. We conclude that discovering factors which can influence cell wall physiology and architecture is crucial for a better understanding of plant embryogenesis. In this review we summarize some recent experimental data reporting plant cell wall involvement in embryogenesis, putting special emphasis on somatic embryogenesis.     

Differential PARP Cleavage: An Indication of Heterogeneous Forms of Cell Death and Involvement of Multiple Proteases in the Infarct of Focal Cerebral Ischemia in Rat

Aim Poly (ADP-ribose) polymerase (PARP) is a nuclear repair enzyme whose role is widely depicted in various physiological and pathological processes. In the present study, we wanted to check the status of PARP and the role of various cell death proteases involved in apoptotic and non-apoptotic forms of cell death during transient focal cerebral ischemia in rat model. The activation of these proteases can result in the production of PARP fragments which can be treated as specific signature fragments to the particular protease involved in the pathology and hence the type of cell death. Results In the ischemic samples, we observed activation of calpain, cathepsin-b, caspase-3, and granzyme-b which were known to act on and cleave PARP to produce specific signature fragments by Western blot and immunohistochemical analysis. Cresyl violet staining showed the presence of apoptotic and necrotic cell deaths. Further we observed interaction of AIF and gra-b with PARP in double immunofluorescence and co-immunoprecipitation experiments. Conclusion Activation of calpains, cathepsin-b, caspase-3, and granzyme-b correlated with either apoptotic or necrotic cell deaths in cresyl violet staining. The appearance of PARP signature fragments gives a clear idea on the involvement of particular protease in the pathology. Appearance of signature fragments like 89- and 50-kDa indicates the involvement of apoptotic and necrotic cell death in the pathology. Further interaction of AIF and gra-b with PARP also indicates the involvement of non-apoptotic modes of cell death during the pathology of focal cerebral ischemia.     

Normal hematopoiesis and hematologic malignancies: Role of canonical Wnt signaling pathway and stromal microenvironment

Wnts are a family of evolutionary-conserved secreted signaling molecules critically involved in a variety of developmental processes and in cell fate determination. A growing body of evidence suggests that Wnt signaling plays a crucial role in the influence of bone marrow stromal microenvironment on the balance between hematopoietic stem cell self-renewal and differentiation. Emerging clinical and experimental evidence also indicates Wnt signaling involvement in the disruption of the latter balance in hematologic malignancies, where the stromal microenvironment favors the homing of cancer cells to the bone marrow, as well as leukemia stem cell development and chemoresistance. In the present review, we summarize and discuss the role of the canonical Wnt signaling pathway in normal hematopoiesis and hematologic malignancies, with regard to recent findings on the stromal microenvironment involvement in these process and diseases.     

Ganglioside GM3 and its biological functions

Metabolism, topology, and possible mechanisms for regulation of the ganglioside GM3 content in the cell are reviewed. Under consideration are biological functions of GM3, such as involvement in cell differentiation, proliferation, oncogenesis, and apoptosis.     

Modulation of the tumor cell death pathway by androgen receptor in response to cytotoxic stimuli

Despite an initial response from androgen deprivation therapy, most prostate cancer patients relapse to a hormone-refractory state where tumors still remain dependent on androgen receptor (AR) function. We have previously shown that AR breakdown correlates with the induction of cancer cell apoptosis by proteasome inhibition. However, the involvement of AR in modulating the cell death pathway has remained elusive. To investigate this, we used an experimental model consisting of parental PC-3 prostate cancer cells that lack AR expression and PC-3 cells stably overexpressing wild type AR gene. Here, we report that both chemotherapeutic drugs (cisplatin) and proteasome inhibitors induced caspase-3-associated cell death in parental PC-3 cells whereas non-caspase-3 associated cell death in PC3-AR cells. The involvement of AR in modulating tumor cell death was further confirmed in PC-3 cells transiently expressing AR. Consistently, treatment with the clinically used proteasome inhibitor Bortezomib (Velcade/PS-341) of (AR+) LNCaP prostate cancer cells caused AR cleavage and cell death with low levels of caspase activation. However, co-treatment with Bortezomib and the AR antagonist Bicalutamide (Casodex) caused significant decrease in AR expression associated with an increase in caspase-3 activity in both LNCaP and PC3-AR cells. Thus our results provide compelling evidence for involvement of AR in deciding types of tumor cell death upon cytotoxic stimuli, and specifically, blockade of AR activities could change necrosis to apoptosis in tumor cells. Our findings may help guide clinicians based on AR status in the design of favorable treatment strategies for prostate cancer patients.