Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q06643 (non-Hodgkin's lymphoma)
 11,307 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe four cases of Fournier's gangrene complicating the postchemotherapy aplastic phase (polymorphonuclear cells [PMN] less than 500/microliter) in three patients with acute leukemia and one patient with non-Hodgkin's lymphoma. Blood and local cultures from two patients contained Pseudomonas aeruginosa, and local cultures from another patient grew both P. aeruginosa and Proteus rettgeri. Early recognition and aggressive antibiotic and surgical treatment with granulocyte recovery were fundamental factors in resolution of the gangrene in three of the four patients. Hyperbaric oxygen therapy, never reported in hematologic patients, was also very useful in one patient in whom the clinical course was particularly acute.
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PMID:Acute gangrene of the scrotum and penis in four hematologic patients. The usefulness of hyperbaric oxygen therapy in one case. 311 13

Diffuse pulmonary infiltrates and acute respiratory compromise frequently occur in patients with cancer who are undergoing chemotherapy, and treatment remains controversial. We initiated a prospective randomized trial in 22 nonneutropenic patients to compare the efficacy of immediate open lung biopsy with that of empirical trimethoprim-sulfamethoxazole and erythromycin therapy with delayed open lung biopsy if no clinical improvement occurred after 4 days of therapy. Diagnoses included non-Hodgkin's lymphoma (15 patients), T-cell lymphoma (2), acute lymphoblastic leukemia (3), Hodgkin's disease (1), and breast cancer (1). The median age was 40 years, and fever (18) and tachypnea (13) were the most frequent signs. Median room air arterial oxygen tension in 18 hypoxic patients was 53 mm Hg; 19 patients had diffuse pulmonary infiltrates. Eight of the 10 patients randomized to empirical antibiotic therapy showed improvement after 4 days. The 2 patients whose condition did not improve and who underwent delayed open lung biopsy had Pneumocystis carinii pneumonia. One of them did show improvement, and the other died of respiratory failure. Time to clinical resolution in the 9 surviving patients was 14 days; 4 required prolonged ventilation (longer than 24 hours). Findings for the 12 patients randomized to immediate open lung biopsy were P. carinii pneumonia in 7 and nonspecific pneumonitis in 5; there were 3 deaths related to open lung biopsy. Time to resolution in the surviving patients was 13 days for those with P. carinii pneumonia and 5 days for those with nonspecific pneumonitis; 7 required prolonged ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Prospective randomized study of open lung biopsy versus empirical antibiotic therapy for acute pneumonitis in nonneutropenic cancer patients. 406 96

Four of 12 Chinese patients receiving BACOP, in combination with recombinant human granulocyte colony-stimulating factor, for aggressive non-Hodgkin's lymphoma developed a rapidly progressive pneumonic illness characterised by diffuse pulmonary infiltrates and hypoxaemia. The condition proved fatal in three, and in none could an infective cause be identified. A retrospective analysis revealed only one episode of pneumonia in the previous 24 patients in whom the same BACOP regimen was administered without granulocyte colony-stimulating factor support. Granulocyte colony-stimulating factor, by augmenting white cell production, pulmonary sequestration and margination and production of toxic oxygen species, may exacerbate underlying subclinical bleomycin pulmonary toxicity. Caution should be exercised before using granulocyte-stimulating factors in bleomycin-containing regimens.
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PMID:Serious pulmonary complications in patients receiving recombinant granulocyte colony-stimulating factor during BACOP chemotherapy for aggressive non-Hodgkin's lymphoma. 752 99

Microangiopathic disease and diffuse alveolar haemorrhage (DAH) are uncommon serious complications of bone marrow transplantation (BMT), but an association between these two conditions has not been previously recognised. We report 4 patients in whom these two complications occurred after allogeneic BMT for haematological malignancy. The patients were 16-39 years of age, and received transplants for acute myeloid leukemia, chronic myeloid leukemia and non-Hodgkin's lymphoma (n = 2). Donors were HLA-identical siblings (n = 3), and a matched unrelated volunteer. The patient with AML was receiving a second transplant for relapse 3 years after her first BMT, and was prepared with busulphan and melphalan; other patients received total body irradiation and cyclophosphamide. Microangiopathy occurred 20-48 days after BMT, and was associated with renal impairment in all cases, and mental confusion in 3. Cyclosporin levels were in the toxic range in 2 cases. DAH occurred 18-55 days after BMT, in 3 cases 2-7 days after the onset of microangiopathy, but preceding it by 14 days in the other case. Patients were treated with fresh frozen plasma, plasma exchange, supplemental oxygen and ventilation in 2 cases. Two patients died of progressive respiratory failure, while 2 patients recovered with evidence of continuing microangiopathic disease, and died of myocardial infarction or fungal infection. We report an association between microangiopathic disease and DAH in these BMT patients, and suggest that damage to the pulmonary vascular endothelium may be the common pathophysiological event, although no specific causative factor could be identified.
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PMID:Diffuse alveolar haemorrhage associated with microangiopathy after allogeneic bone marrow transplantation. 758 Oct 82

The management of patients with treated malignant lymphomas requires functional methods to differentiate a residual soft tissue mass. Patients with treated Hodgkin's lymphoma (HL, n = 20, 68 malignant lesions, three benign lesions) or non-Hodgkin's lymphoma (NHL, n = 26, 46 malignant lesions, one benign lesion) were studied with positron emission tomography (PET) and fluorine-18 deoxyglucose (FDG). Oxygen-15 labelled water was used (n = 14, 25 lesions) in addition to FDG in order to obtain information on the tissue perfusion. Long-term follow-up studies with PET and FDG were performed in nine patients up to 511 days after the initiation of second-line therapy. Fourteen patients underwent single-photon emission tomography (SPET) with technetium-99m sestamibi immediately prior to the first PET examination. PET with FDG displays a high sensitivity for the detection of viable tumour tissue, all the malignant lesions being correctly classified in this study. The possible limitations are inflammatory processes, which may obscure tumour detection due to increased FDG uptake, and malignant lesions with low FDG uptake due to reduced perfusion. Difficulties exist in the prognosis of long-term response, since the change in FDG uptake may be variable. Long-term therapy outcome was correlated with the slope values obtained from the standardized integral uptake (SIU) data, which provides a new approach for the evaluation of PET follow-up studies. 99mTc-sestamibi, which should reflect the multidrug resistance, was evaluated with respect to therapy outcome. A high uptake of 99mTc-sestamibi was observed in patients with stable disease or better. The data support the hypothesis that sestamibi may reflect multidrug resistance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Evaluation of tumour metabolism and multidrug resistance in patients with treated malignant lymphomas. 764 52

In radiotherapy, use of an enormous radical dose may be necessary. However, it is sometimes limited by the poor tolerance of the surrounding normal tissues. Transient systemic hypoxia induced by breathing 10.5% oxygen gas during radiotherapy may protect the normal tissues. In treating non-Hodgkin's lymphoma (NHL) involving the Waldeyer's ring, radioprotective effects of hypoxia on radiation responses of the pharyngeal mucosa and saliva secretion were observed, giving a radioprotective factor (RPF) of 1.43 in saliva quantity and 1.31 in ptyalin secretion. Other responses were milder and occurred later.
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PMID:[Radioprotective effects of hypoxyradiotherapy on saliva secretion]. 768 31

We analyzed active oxygen (hydroperoxide; H2O2) production by peripheral neutrophils in various hematological diseases by flow cytometry. One hundred microliters of heparinized fresh blood was sequentially incubated at 37 degrees C with 2',7'-dichlorofluorescein diacetate and with or without phorbol myristate acetate (PMA). After hemolysis, the pelleted white blood cells were subjected to flow cytometry, and the neutrophil fraction was gated on the cytogram. Production of H2O2 by the fraction was estimated by determining the increase in the relative intensity of fluorescence emitted from the fraction in response to stimulation by PMA. In controlled chronic myelogenous leukemia (CML) (WBC < 1 x 10(10)/1), H2O2 production was normal, while in uncontrolled CML (WBC > or = 1 x 10(10)/1), it was reduced. In myelodysplastic syndrome (MDS), H2O2 production was also reduced, but no significant difference was observed among FAB classification disease types in MDS patients. In untreated acute non-lymphocytic leukemia (ANLL), H2O2 production was reduced, while in the complete remission stage of ANLL, its level was normal, suggesting recovery from normal clones. In aplastic anemia, the H2O2 production level was normal. Steroid therapy might be responsible for the reduction of H2O2 production in non-Hodgkin's lymphoma and multiple myeloma. The production of H2O2 is closely related to the oxygen-dependent bactericidal activity of neutrophils, and, hence, can be utilized as an index to indicate susceptibility to infection. This neutrophil function can be determined easily in ordinary clinical facilities by using flow cytometry, and care should be taken to prevent infection when H2O2 production is reduced.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Flow cytometric determination of active oxygen (hydroperoxide) produced by peripheral blood neutrophils in patients with hematological disorders. 836 85

The ready access to blood (plasma and formed cellular elements) makes it unusually susceptible to the deleterious effects of pollutants whose origins may be in the air. The red blood cells' hemoglobin may be rendered useless for oxygen transport by combination with carbon monoxide or conversion to methemoglobin or sulfhemoglobin. Lead and arsine can damage the erythrocytes' membranes, resulting in anemia. Metabolites of benzene and other volatile polycyclic hydrocarbons are implicated in the causation of leukemias. The extensive use of pesticides and herbicides may be associated with the development of Hodgkin's disease, non-Hodgkin's lymphoma, and aplastic anemia. The carcinogenic risks from ionizing radiation, especially for leukemia, are well known. More information is needed concerning the epidemiology of environmental factors responsible for damage to blood. Enhanced knowledge about the molecular biology of toxins' effects on the hematopoietic system and improved detection and prevention technologies are needed to answer environmentally related health questions.
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PMID:Blood and air pollution: state of knowledge and research needs. 863 33

Redox mechanisms have been shown to be important in malignant cell survival and are a system that may be modified for the treatment of hematologic malignancies. Motexafin gadolinium (MGd) is a synthetic expanded porphyrin that selectively accumulates in tumor cells and oxidizes various intracellular metabolites, including ascorbate, nicotinamide adenine dinucleotide phosphate, glutathione, and protein thiols, to generate reactive oxygen species in a process known as futile redox cycling. The rationale for its use in hematologic malignancies is that, like naturally occurring porphyrins, it tends to concentrate selectively in cancer cells, and it has a novel mechanism of action of inducing redox stress and triggering apoptosis in a broad range of malignancies. MGd induces apoptosis in B-cell non-Hodgkin's lymphoma, chronic lymphocytic leukemia, and highly resistant myeloma cell lines. Furthermore, MGd is additive or synergistic with ionizing radiation, several chemotherapy agents, and rituximab in vitro and in vivo tumor models. Through gene expression profiling, various stress-related genes are upregulated in response to MGd, including genes encoding metallothioneins, heat shock proteins, and heme oxygenase. Preliminary results from clinical trials with MGd in hematopoietic malignancies have shown that it is well tolerated, with minimal hematologic side effects in both; it has single agent activity in very heavily pretreated chronic lymphocytic leukemia /small lymphocytic lymphoma patients, and it has induced prompt complete remissions in combination with 90Yttrium-ibritumomab (Y-90 Zevalin; Biogen Idec Inc., Cambridge, MA) for relapsed non-Hodgkin's lymphoma in the first two cohorts of patients enrolled. Various clinical trials studying MGd as a single agent and in combination with radiation and/or chemotherapy for the treatment of hematologic malignancies are ongoing.
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PMID:Motexafin gadolinium induces oxidative stress and apoptosis in hematologic malignancies. 1596 82

TNFSF14/LIGHT is a member of the tumor necrosis factor superfamily that binds to lymphotoxin-beta receptor (LTbetaR) to induce cell death via caspase-dependent and caspase-independent pathways. It has been shown that cellular inhibitor of apoptosis protein-1 inhibits cell death by binding to LTbetaR-TRAF2/TRAF3 complexes and caspases. In this study, we found that both Kaposi's sarcoma-associated herpesvirus K7 (KSHV-K7), a viral inhibitor of apoptosis protein, and the structurally related protein survivin-DeltaEx3 could inhibit LTbetaR-mediated caspase-3 activation. However, only survivin-DeltaEx3 could protect cells from LTbetaR-mediated cell death. The differential protective effects of survivin-DeltaEx3 and KSHV-K7 can be attributed to the fact that survivin-DeltaEx3, but not KSHV-K7, is able to maintain mitochondrial membrane potential and inhibit second mitochondria-derived activator of caspase/DIABLO release. Moreover, survivin-DeltaEx3 is able to inhibit production of reactive oxygen species and can translocate from nucleus to cytosol to associate with apoptosis signal-regulating kinase 1 after activation of LTbetaR. Furthermore, survivin-DeltaEx3 protects LTbetaR-mediated cell death in caspase-3-deficient MCF-7 cells. Thus, survivin-DeltaEx3 is able to regulate both caspase-dependent and caspase-independent pathways, whereas inhibition of caspase-independent pathway is both sufficient and necessary for its protective effect on LTbetaR-mediated cell death.
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PMID:Inhibition of lymphotoxin-beta receptor-mediated cell death by survivin-DeltaEx3. 1654 Jun 54


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