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Biomedical subjects

J Góra-Tybor

Publications and source records attributed to J Góra-Tybor.

18 recordsLinked to original sources
PubMed2005

Richter syndrome first manifesting as cutaneous B-cell lymphoma clonally distinct from primary B-cell chronic lymphocytic leukaemia.

Richter syndrome (RS) is a transformation to high-grade non-Hodgkin lymphoma in patients with chronic lymphocytic leukaemia (CLL). RS may develop in lymph nodes or rarely extranodally. Skin localization of RS has been described in only a few cases. We present a 77-year-old woman who developed isolated diffuse large B-cell lymphoma (LBCL) in the skin of the nose without any other symptoms of RS. The LBCL in the skin was clonally distinct from the original bone marrow CLL cells. Moreover, LBCL cells were positive for LMP-1 segment of Epstein-Barr virus and overexpressed p53 protein. The patient was successfully treated with CHOP (cyclophosphamide, doxorubicin, vincristine and prednisone) and adjuvant local radiotherapy.

Aged↗
PubMed2001

Cladribine in combination with mitoxantrone and cyclophosphamide(CMC) in the treatment of heavily pre-treated patients with advanced indolent lymphoid malignancies.

The aim of our study was to determine the effectiveness and toxicity of combined chemotherapy consisting of cladribine (2-chloro-deoxyadenosine, 2-CdA), mitoxantrone and cyclophosphamide (CMC regimen) in the treatment of refractory or relapsed indolent lymphoproliferative disorders. The treatment course consisted of 2-CdA given at a dose of 0.12 mg/kg/24 h in a 2-h intravenous infusion for 5 (CMC5) or 3 (CMC3) consecutive days, mitoxantrone 10 mg/m2 on day 1 and cyclophosphamide 650 mg/m2/iv on day 1. Thirty-three patients (19 with B-CLL and 14 with LG-NHL) entered the study and all of them were eligible. Twenty patients (60.6%) were recurrent after prior therapy and 13 (39.4%) had refractory disease. All patients received 5 or more cycles of chemotherapy before CMC treatment. Twenty-one patients were treated with CMC5 regimen and 12 with CMC3 regimen. The overall response rate, including CR and PR, was 48.6% (95% CI 32-66). There were no differences in the frequency of responses between the CMC3 and CMC5 treated groups (p>0.05). One patient with B-CLL and three patients with lymphocytic lymphoma achieved CR (12.1%). Among 12 patients (36.4%) who achieved PR there were 6 CLL patients, and 6 lymphoma patients. The major toxicity was myelosuppression. Severe neutropenia was seen in 11/33 (33.3%) patients, more frequently in patients who received CMC5 than in the patients who received CMC3, both in the CLL (50.0% and 28.5%, respectively) and in the LG-NHL group (22.2% and 0%, respectively). The rate of thrombocytopenia was similar in both groups. Infections and fever of unknown origin complicated the treatment with CMC5 more often than with CMC3: five episodes were seen in 3 patients treated with CMC3 when compared to 15 episodes in 12 patients treated with CMC5. In conclusion, the CMC programme is an active combined regimen in heavily pre-treated CLL and LG-NHL patients. However, its toxicity is significant and we suggest a shortening of 2-CdA infusion from 5 to 3 d in further studies. Whether a combination of 2-CdA with cyclophosphamide and mitoxantrone would result in improved outcome as compared to 2-CdA alone, is being investigated in a prospective, randomised trial.

Aged↗
PubMed2001

Toxic epidermal necrolysis in a patient with severe aplastic anemia treated with cyclosporin A and G-CSF.

Toxic epidermal necrolysis (TEN) and severe aplastic anemia (SAA) are rare nonpredictable side effects of several drugs. To our knowledge there are no reports on the coexistence of these two disorders. This study presents a 23 year-old man with TEN diagnosed 6 days after treatment with aminophenazone, paracetamol and phenoxymethylpenicillin. The resolution of the skin disorder was observed after few days of treatment with G-CSF and cyclosporin A. In contrast, SAA only partially responded to treatment with these agents.

Acetaminophen↗
PubMed2001

Cladribine combined with mitoxantrone in the treatment of blastic phase of chronic myeloid leukemia.

A phase II clinical study was performed to evaluate the effectiveness and toxicity of cladribine (2-CdA) combined with mitoxantrone (CM regimen) in the treatment of chronic myeloid leukemia in blastic phase (CML BP). A total of 12 adult patients with CML BP were included in this study. 2-CdA was given at a dose 0.12 mg/kg in 2-hour iv infusion on days 1-5 and mitoxantrone 10 mg/m2 i.v. day 1. The cycles were repeated at 4 week intervals in most cases. Complete remission (CR) was defined as the presence of < 5% of blasts in a normo- or hypercellular bone marrow in addition to normal peripheral blood counts and with normal physical examination. A partial response (PR) required normal peripheral blood counts but 5 to 25% marrow blasts. Toxicity was assessed according to WHO criteria. The patients received 21 courses of CM (median 2, range 1-3). Of 12 patients only 2 (17%), achieved PR. Responses were observed in patients with myeloid BP, after 3 and 2 courses, respectively. Myelosuppression was the main toxicity. Four patients (33.3%) had grade 3 or 4 neutropenia and 3 (25%) had grade 3 or 4 thrombocytopenia. Infections occurred in 4 patients (33.3%) and 2 of them died of sepsis shortly after CM treatment. This preliminary results in a small group of patients suggest that CM programme has limited value in pre-treated patients with CML BP. However, this regimen may be used as palliation in the end stage of disease.

Adult↗
PubMed1996

Fulminant 2-chlorodeoxyadenosine-related peripheral neuropathy in a patient with paraneoplastic neurological syndrome associated with lymphoma.

2-chlorodeoxyadenosine (2-CdA) has been demonstrated to be a neurotoxic agent when used at significantly greater doses than currently recommended for clinical use. In this report we describe a case of a 37-years-old man lymphoplasmacytoid malignant lymphoma and pre-existing paraneoplastic neurological syndrome who died of an apparent rapidly progressive sensorimotor peripheral neuropathy after completing treatment with two courses of low-doses of 2-CdA.

Adult↗
PubMed1996

[Clinical pharmacology of 2-chlorodeoxyadenosine (Cladribine)].

2-chlorodeoxyadenosine (2-CdA) is a simple nucleoside derived from deoxyadenosine by substituting chloride for hydrogen in 2' position of the purine ring, which renders it resistant to degradation by adenosine deaminase. Many studies have revealed high efficiency of 2-CdA in the treatment of lymphoid malignancies. Hairy cell leukemia is notably responsive to 2-CdA, with 85% of patients entering complete remissions after treatment of this drug.

Animals↗
PubMed1996

Treatment of drug-induced agranulocytosis with colony stimulating factors (G-CSF or GM-CSF).

The application of granulocyte-macrophage and granulocyte colony stimulation factors (GM-CSF and G-CSF) has been progressively increased in the treatment of patients with agranulocytosis. The aim of our study was to compare the time of neutrophil recovery in patients with severe agranulocytosis treated with G-CSF or GM-CSF and the historical control group. We have studied 6 patients with agranulocytosis treated with stimulating factors and 7 patients in historical control group. Most of the patients have been exposed to thiamazole or non-steroid antiinflammatory drugs. Our results demonstrate that patients receiving colony stimulating factor have a significantly shorter period of recovery (the mean time 8.7 +/- 1.98 days) than the historical control group (the mean time 11.0 +/- 2.24 days). We observed also a shorter time of antibiotico-therapy and hospitalization in the group of patients treated with colony stimulating factor.

Adult↗
PubMed1995

[Clinical pharmacology of hydroxyurea].

Hydroxyurea, an antineoplastic drug evaluated clinically more than 30 years ago, is still the principal drug in patients with myeloproliferative syndromes. It is suggested now that it should be used as initial therapy for chronic myelogenous leukemia. Recently hydroxyurea is used in the treatment of patients with sickle cell disease. It has been shown to augment production of fetal hemoglobin and decrease the propensity of abnormal hemoglobin to polymerize and from the sickle cells in this way.

Anemia, Sickle Cell↗
PubMed1994

The interaction of 2-chlorodeoxyadenosine (2-CDA) and interferon alpha (IFN-alpha) on normal and myeloid leukemia hematopoiesis in vitro.

The influence of 2-CDA and interferon alpha (IFN-alpha) on the CFU-GM cells from ten normal individuals as well as on the CFU-GM from ten patients with chronic myeloid leukemia (CML) and on clonogenic leukemic blasts (CFU-L) from ten patients with acute myeloid leukemia (AML) in semi-solid cultures in vitro was investigated. The agents were added to the cultures alone and in combinations at concentrations of 20, 40 and 80 nM/l of 2-CDA and 10(2), 10(3) and 10(4) U/ml of IFN-alpha. A dose-dependent growth inhibition of CFU-GM as well as of CFU-L was observed. The inhibitory effect of both drugs used alone was significantly greater on the CFU-GM cells from patients with CML than on cells from normal donors. However, 2-CDA and IFN-alpha used together showed greater additive effect on the CFU-L than on the CFU-GM from normal donors and from CML patients.

Adult↗
PubMed1994

Influence of 2-chloro-2'-deoxyadenosine alone and in combination with cyclophosphamide or methotrexate on murine leukemia L1210.

The influence of 2-CdA administrated alone and in combination with CY or MTX on the survival time of mice bearing L1210 leukemia was investigated. 2-CdA treated mice lived longer than control animals. Survival times of mice receiving combined therapy of 2-CdA and CY were significantly prolonged as compared with mice treated with these agents separately. Survival times of mice treated with 2-CdA and MTX were not significantly prolonged, compared with animals receiving 2-CdA alone.

Animals↗
PubMed1994

[Apoptosis--programmed cell death].

Apoptosis is a structurally distinct programmed cell death pathway. It takes place during embryogenesis, after withdrawal of the trophic hormones and in the course of normal tissue turnover. Defective regulation of apoptosis may play a very important role in the aetiology of cancer and other diseases. In this paper these and other problems concerning with apoptosis are reviewed.

Animals↗
PubMed1993

The influence of 2-chlorodeoxyadenosine alone and in combination with cyclophosphamide or methotrexate on normal hematopoiesis in mice.

The influence of 2-chlorodeoxyadenosine (2-CDA) administered alone or in combination with cyclophosphamide (CY) or methotrexate (MTX) on normal hematopoiesis in mice was investigated. The peripheral blood counts such as the number of leukocytes, platelets, and erythrocytes, hematocrit values and hemoglobin concentration were measured. The number of mononuclear cells and multipotential stem cells (CFU-S) in bone marrow was also checked. 2-CDA caused both the decrease in white cell count (granulocytes, monocytes, lymphocytes) and the suppression of mononuclear cells and multipotential stem cells in the bone marrow. The addition of CY significantly enhanced the suppression of these parameters. In contrast to CY, MTX did not augment myelotoxic effect of 2-CDA. 2-Chlorodeoxyadenosine administered singly and in combination with CY or MTX had no influence on the number of erythrocytes, hemoglobin concentration, hematocrit values and number of platelets.

Animals↗
PubMed1993

Synergistic action of 2-chlorodeoxyadenosine and cyclophosphamide on murine leukemias L1210 and P388.

The influence of 2-chlorodeoxyadenosine (2-CDA) administered alone and in combination with cyclophosphamide (CY) or methotrexate (MTX) on the survival time of mice bearing L1210 or P388 leukemia was investigated. 2-CDA given alone significantly prolonged survival time of mice bearing L1210 leukemia and caused only a slight prolongation of survival time in mice bearing P388 leukemia. Survival times of mice bearing both kinds of leukemia, receiving combined therapy of 2-CDA and MTX were not significantly prolonged as compared with mice treated with these agents separately. The groups of mice with both leukemia L1210 and P388 treated with 2-CDA and CY lived significantly longer as compared with the control group and with mice receiving only single cytostatic.

Animals↗
PubMed1992

The influence of recombinant human tumor necrosis factor (rh-TNF alpha) on granulocyte-macrophage progenitor cells (CFU-GM) and clonogenic leukaemic blasts (CFU-L) in cultures in vitro.

We investigated the influence of recombinant human tumor necrosis factor alfa (rh-TNF alpha) on the clonal growth of CFU-GM from 14 normal individuals and clonogenic blasts (CFU-L) from 16 patients with acute myeloid leukaemia (AML) in semi-solid cultures in vitro. Recombinant human TNF was produced by the Center of Molecular and Macromolecular Studies of the Polish Academy of Sciences (Lódź, Poland) as a lyophylized powder. This factor was added to the culture medium at the concentrations of 10, 100, 1000 U/ml. A dose-dependent growth inhibition of CFU-GM and AML CFU-L was observed. The inhibitory effect of rh-TNF alpha was significantly greater on CFU-L than CFU-GM.

Colony-Forming Units Assay↗