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At least 577 records · Page 32Linked to original sources
PubMed1981

Ultrastructural aspects of colchicine ultrasensitivity in CLL lymphocytes.

Circulating lymphocytes from patients with chronic lymphatic leukaemia show extreme sensitivity to colchicine, with 80%-90% cell death after exposure to 10(-7) M colchicine for 20 h in vitro. This is 100,000-times greater than the dose required (10(-2) M) for a similarly toxic effect on normal lymphocytes. A time course series of fixations during the 20-h exposure of chronic lymphoid leukaemia (CLL) lymphocytes to 10(-7) colchicine revealed an entire spectrum of ultrastructural alterations well in advance of any sign of cell death, previously only ascertained by nuclear pycnosis in the light microscope. The changes included the appearance of large numbers of intermediate filaments, loss of surface microvilli, mitochondrial alterations and the formation of annulate lamellae. Mitochondrial changes included disruption of the cristae, swelling and tight clumping of the entire mitochondrial population into a single region of the cytoplasm.

Adolescent↗
PubMed1993

Interleukin-4 priming enhances a target for human complement-mediated cytotoxicity of CLL.

JD118 is a murine immunoglobulin M monoclonal antibody (mAb) under study as a therapeutic agent that is capable of potent human complement-mediated cytotoxicity (CMC) against B-cell lymphoma and leukemia targets. The JD118 antigen target was upregulated on fresh human B cells and B-cell neoplasms after brief in vitro incubation in media containing calf serum. To determine if cytokines could also lead to upregulation of JD118 antigen, alpha-interferon (alpha-IFN), gamma-interferon (gamma-IFN), interleukin 2 (IL-2), or IL-4 were added to fresh neoplastic B cells in serum-free media and changes in JD118 antigen expression were evaluated by flow cytometry (FCM). IL-4 was found to be the predominant cytokine responsible for inducing upregulation of the JD118 antigen. Marked JD118 upregulation by IL-4 was seen in 14 out of 14 chronic lymphocytic leukemia (CLL) samples tested, with 50 to 750-fold increases in four samples, 11 to 49-fold increases in four samples, and up to 10-fold increase in six samples. One B-cell lymphoma specimen was upregulated 18-fold, but no up-regulation was demonstrated in one hairy cell leukemia and two acute myelogenous leukemia specimens tested. The specificity of the IL-4 up-regulation was demonstrated by the elimination of its activity by blocking with a neutralizing anti-IL-4 mAb. IL-4 upregulation allows JD118 mAb CMC against otherwise antigen-negative targets and argues for phase I trials using a combination of IL-4 cytokine and mAb for B-cell neoplasms.

Antibodies, Monoclonal↗
PubMed1996

Current approach to the biology and treatment of chronic lymphoid malignancies other than CLL.

A number of discrete disease entities are now well recognised within the lymphoproliferative disorders of B and T lymphocytes. By means of detailed morphologic and immunophenotypic analysis it is possible to distinguish these disorders from chronic lymphocytic leukemia (CLL) and thereby learn about their biology, natural history and response to treatment. We review here the main diagnostic and therapeutic issues of two B-cell disorders: B-prolymphocytic leukemia (B-PLL) and splenic lymphoma with circulating villous lymphocytes (SLVL) and discuss aspects of management and the role of splenectomy and of the nucleoside analog fludarabine in the treatment of B-PLL and SLVL.

Chronic Disease↗
PubMed1997

[A case of polyneuropathy with B-CLL and HTLV-I associated myelopathy (HAM)].

We report a case of polyneuropathy associated with chronic B lymphoid leukemia (B-CLL) and HAM. A 65-year-old man had an initial onset with polyneuropathy, then myelopathy appeared. High HTLV-I antibody and anti-ganglioside antibodies were observed. The biopsy examination of the sural nerve showed mainly demyelinated changes. Muscle weakness gradually improved after cyclophosphamide therapy. Anti-ganglioside antibodies were also decreased in titer. This case suggested that the production of antiganglioside antibodies and the occurrence of polyneuropathy might be caused by both factors of HTLV-I infected T cells and B cell tumors.

Aged↗
PubMed1998

[Advances in the treatment of chronic lymphocytic leukemia (CLL)].

CLL is a chronic lymphoproliferative disorder which is characterized by the proliferation of a CD5 positive B cell clone. At diagnosis most patients are in early stage of the disease (stage A). It is well established that an early treatment in stage A is not associated with a survival advantage. Therefore, the disease should be treated only when signs of progression are present. The standard initial therapy is chlorambucil +/- prednisone. By this treatment remissions (mostly partial remissions) are achieved in about half of the patients. Fludarabine, a purine analogue, is more effective than chlorambucil as initial treatment (75% remissions, 27% complete remissions, 33 months progression free survival). However, the overall survival is not prolonged when compared to chlorambucil treatment. Fludarabine has a high efficacy in patients with recurrent disease, in particular in those who are resistant to alkylating agents. The allogeneic and autologous stem cell transplantation is an experimental treatment which may be indicated in younger patients who show a response to conventional treatment. With both procedures hematological remissions are frequently achieved and in some of the patients long lasting molecular remissions were obtained. Currently, it is unknown whether patients can be cured by stem cell transplantation and longer follow-up will be necessary to clarify this question. Monoclonal B-cell antibodies are effective in vivo and partial remissions can be obtained in chemotherapy refractory patients. Antibodies have a high efficacy in clearing lymphoma cells from peripheral blood and bone marrow but are less effective on the organomegaly.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2004

Modern diagnostics in chronic myeloproliferative diseases (CMPDs).

According to the new WHO classification a group of chronic myeloproliferative diseases (CMPDs) were defined: chronic myeloid leukemia (CML), chronic neutrophilic leukemia (CNL), chronic eosinophilic leukemia and hypereosinophilic syndrome (CEL/HES), polycythemia vera (PV), chronic idiopathic myelofibrosis (with extramedullary hematopoiesis, CIMF), essential thrombocythemia (ET), and so called CMPD/unclassifiable. As clinical features and laboratory findings differ widely between these diseases several diagnostic approaches are mandatory at diagnosis for classification and are needed also for follow up studies, especially for the measurement of minimal residual disease (MRD). We here outline the laboratory set up at diagnosis and during follow up in CMPDs with specific focus on the respective therapeutical consequences. Only by using a comprehensive diagnostic panel including cytomorphology, cytogenetics, and molecular genetic methods establishing the correct diagnosis, optimizing treatment as well as evaluating treatment response is possible in CMPDs today.

Blood Cell Count↗
PubMed2001

Successful treatment of paraneoplastic pemphigus in follicular NHL with rituximab: report of a case and review of treatment for paraneoplastic pemphigus in NHL and CLL.

Paraneoplastic pemphigus is a severe mucocutaneous disease associated in most cases with B-cell lymphoproliferative disorders. Independent of the course of the underlying malignancy, this autoimmune skin disease is resistant to any treatment in most cases and may lead to death by infectious complications. We observed a patient with recovery of paraneoplastic pemphigus associated with follicular non-Hodgkin's-lymphoma after therapy with rituximab. In addition, we reviewed the literature and analyzed the few cases with comparable outcome with other treatment modalities.

Aged↗
PubMed1983

A case of T-cell chronic lymphocytic leukemia (T-CLL) expressing a peculiar phenotype (E+, OKM1+, Leu 1+, OKT3- and IgG EA-).

A case of chronic leukemia is reported. Malignant cells had the morphology of lymphocytes and an affinity for skin. Cytochemically, they were peroxidase negative, and NaF-resistant alpha-naphthyl esterase positive. The peripheral mononuclear cells formed E-rosettes and reacted with Leu 1 and OKM1. They were unreactive with OKT3, OKT4, OKT6, OKT8, and OKIa1. The cells did not possess surface IG, C3b receptors, or IgG Fc receptors (EAIgG). They responded weakly to phytohemagglutinin, and did not respond to concanavalin A. The cells did not adhere to Petri dishes or phagocytose latex beads. It is concluded that it was a case of OKT3-, OKM1+, EAIgG- T-cell chronic lymphocytic leukemia. This suggests that OKT3 does not recognize all peripheral T-cells, and that OKM1 is not specific for the monocyte-myeloid lineage. These cells may be useful in the characterization of E+, OKM1+ subset of peripheral mononuclear cells.

Adult↗
PubMed1979

Intensive leukapheresis in the management of cytopenias in patients with chronic lymphocytic leukaemia (CLL) and lymphocytic lymphoma.

The role of leukapheresis was explored in the management of anaemia and thrombocytopenia complicating the accumulation of lymphoid cells in patients with chronic lymphocytic leukaemia and lymphoma. The aim of this study was to determine the efficiency of this procedure in correcting these complicating features and to assess the length of response and the clinical well being of the patients. Twenty such patients with either chronic lymphocytic leukaemia or lymphocytic lymphoma were studied using a Continuous Flow Cell Separator (Aminco Celltrifuge). All had persistent significant anaemia and/or thrombocytopenia prior to the institution of leukapheresis. The procedure was carried out on alternate days until significant reduction in total circulating lymphoid cells had been achieved, an average of 2.9 x 10(11) cells being removed on each occasion. Thirteen of the twenty patients showed a significant elevation of both haemoglobin and platelet level concomitant with reduction in lymphoid cells. A reduction in organomegaly was also observed. These patients were classified as "responders," but the other patients failed to show correction of the haematologic parameters. This procedure permitted a number of responder patients to receive more specific treatment but in some it obviated the necessity for any further management for up to 12 months. Surface marker studies were also carried out on the lymphocytes of these patients. The patients who showed the best response to leukapheresis had cells characteristic of those seen in chronic lymphocytic leukaemia. The reduction of cells (82%) was greater in those who responded to this treatment than in the non-responder group (72%). The procedure was well tolerated by all patients and overall provided a long-term control of disease which outweighed the initial cost incurred.

Aged↗
PubMed1990

Sequence homologies, N sequence insertion and JH gene utilization in VHDJH joining: implications for the joining mechanism and the ontogenetic timing of Ly1 B cell and B-CLL progenitor generation.

Sequence analysis of rearranged VHDJH genes of B lineage cells from various stages of ontogeny indicates that short sequence homologies at the breakpoints of recombination contribute to V region gene assembly. Such homologies are regularly seen at DJH junctions of neonatal pre-B cells, most of which do not contain N sequences. In the same cells, but not at later developmental stages, preferential usage of the JH1 element is observed. After birth, N sequence insertion increases with time and is always more prominent at the VHD border than the DJH border. In pre-B cells from adult animals and in mature B cells, in cases where N sequences were not detectable, sequence homologies at the DJH border were found in only half of the instances. This lower incidence could be due to N sequence addition to one of the recombining DNA ends and/or cellular selection. Inspection of VHDJH junctions for N sequence insertion, sequence homologies at the DJH border and JH1 usage allows the estimation of the timepoint in ontogeny at which particular B cell subsets are seeded into the immune system. Specifically, the present data show that the cells of the Ly1 B cell subset are generated not only neonatally but also beyond the first weeks of life. However, the DJH junctions of the progenitors of chronic B cell leukemias which originate from the same B cell subset resemble those of neonatal pre-B cells, suggesting that these cells have already undergone a transforming event at this early developmental stage.

Animals↗