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)

A new radioreceptor assay for insulin-like growth factor-II (IGF-II), using receptors on ovine placental membranes, is described. Half-maximal displacement of specifically bound radioiodinated human IGF-II tracer was seen at 1.0 ng/tube of unlabelled IGF-II. The cross-reactivity of IGF-I was 1%, and insulin was entirely without effect. Measured on serum samples from 100 healthy adults, the mean IGF-II concentration (+/- SD) was 576 +/- 160 ng/ml. Identical mean values were seen for all adult age groups up to 65 years. The mean value for 10 acromegalic adults was 583 +/- 155 ng/ml, and for 9 GH-deficient subjects, 161 +/- 26 ng/ml (P less than 0.001 compared to normals). Of eight patients with chronic renal failure, none had an IGF-II level less than 2SD above the normal mean. No significant effect of renal dialysis was seen. In groups of patients with gastric, breast, lung, testicular, oat cell, ovarian, colonic and prostatic carcinoma, Hodgkin's lymphoma, non-Hodgkin's lymphoma, sarcoma and teratoma (5-12 patients per group), mean IGF-II levels were in the lower part of the normal range. Thus this study does not provide evidence supporting a role for excessive IGF-II production in the growth of any of these tumour types.
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PMID:Measurement of insulin-like growth factor-II by radioreceptor assay using ovine placental membranes. 301 20

In 28 of 45 patients suffering from non-Hodgkin's lymphoma, the blood levels of substances detectable by the insulin-specific radioimmunoassay were supranormal, while the C-peptide levels were almost normal or even low. Such a ratio of these substances was also found in a diabetic non-Hodgkin's lymphoma patient. Two sera with the highest concentrations of these substances were investigated by gel filtration. In one case, the insulin cross-reactive material was eluted at the position of the insulin marker; in the other serum, its molecular mass was approximately 120,000.
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PMID:C-peptide does not parallel increases of serum levels of substances immunologically cross-reactive with insulin in non-Hodgkin's lymphoma patients. 633 76

We report 34 patients (aged 5-18 years) with acute (n = 26) or chronic (n = 1) leukemia, non-Hodgkin's lymphoma (n = 3) or severe aplastic anemia (n = 4) evaluated for pancreatic beta-cell function 9 months to 10.2 years after autologous (n = 19) or allogeneic (n = 15) BMT. Before BMT, all patients received cytotoxic drugs, combined with total body irradiation (TBI) in 24 cases or thoracoabdominal irradiation (TAI) in 4 children. Patients were investigated for fasting blood glucose (FBG), HbA1C, anti-insulin (IAA) and islet cell antibodies (ICA), first-phase insulin response (FPIR) and insulinemia/glycemia (I/G) ratio on i.v. glucose tolerance test (GTT) and C-peptide response after glucagon 1 mg i.v. Results were compared with those obtained in 21 age- and sex-matched controls. None of the patients or controls had IAA and/or ICA. FBG and HbA1C were normal in all children. In the patients, glycemia on i.v. GTT was similar to controls whereas insulin levels I/G ratio and FPIR were significantly higher in patients than in controls, as well as C-peptide levels. We divided the patients on the basis of the radiotherapy into group I with TBI (n = 18), group II with TAI (n = 4) and group III who were not irradiated (n = 4). The I/G ratio, FPIR on i.v. GTT and C-peptide response were significantly higher in group I compared with the other two groups and controls. The increased insulin and C-peptide levels in our patients with normal glycemia might be interpreted as a state of insulin resistance, more evident in patients who received TBL.
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PMID:Hyperinsulinemia in children and adolescents after bone marrow transplantation. 758 Oct 84

The interleukin-2 receptor (IL-2R) is expressed on proliferating T-lymphocytes following antigen stimulation. Activated IL-2R bearing lymphocytes accumulate as cellular infiltrates in autoimmune thyroiditis, insulin-dependent diabetes mellitus, rheumatoid arthritis and graft rejection. Affected cells in Hodgkin's disease, hairy cell leukaemia, non-Hodgkin's lymphoma, cutaneous T-cell lymphoma and lymphoid blast crises of chronic myeloid leukaemia also express IL-2R. Anti-IL-2R monoclonal antibodies or chimeric IL-2R toxins provide a way of selective elimination of such cells. These have been used in experimental models of autoimmunity and transplantation with beneficial results, providing a novel way of selective immunosuppression. In open uncontrolled trials, chimeric IL-2R toxin was found to be safe and effective in patients with refractory rheumatoid arthritis, insulin-dependent diabetes mellitus and IL-2R bearing leukaemias and lymphomas.
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PMID:Immunomodulation by interleukin-2 receptor targeted therapy. 801 99

Tumor lysis syndrome is a catastrophic complication of the treatment of certain neoplasms. It most commonly occurs in association with hematologic malignancies and manifests a few hours to a few days after initiation of specific chemotherapy. It has rarely been encountered as a complication of steroid therapy only. Tumor lysis syndrome is a potentially fatal condition if it is not recognized promptly and managed aggressively. We report on a patient with high-grade non-Hodgkin's lymphoma who developed severe metabolic acidosis, hyperkalemia, hyperphosphatemia, and hypocalcemia within 2 days of starting corticosteroid therapy. He was managed with intravenous fluids, bicarbonate infusion, calcium gluconate, and 25% dextrose with insulin. He did not respond to these measures and died within a few hours of the diagnosis of tumor lysis syndrome. Increasing awareness of this complication and proper prophylactic measures are necessary to improve the outcome.
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PMID:Dexamethasone-induced tumor lysis syndrome in high-grade non-Hodgkin's lymphoma. 813 69

A 71-year-old patient with high-grade non-Hodgkin's lymphoma stage IVB, severe lactic acidosis and tumor-associated hypoglycemia is described. Endocrine causes of hypoglycemic episodes were excluded because of low serum concentrations of insulin and "insulin-like growth factor 1", and normal concentrations of growth hormone and thyroid hormone. Clinical conditions associated with lactic acidosis such as diabetes mellitus, biguanide intoxication, septicemia, acute hypoxemia, or circulatory insufficiency were ruled out. Enhanced glucose metabolism within the tumor was visualized by positron emission tomography employing 2-fluro-2-deoxy-D-glucose (FDG) as a tracer. A markedly elevated tumor necrosis factor-alpha (TNF-alpha) level was found which decreased after cytoreductive therapy paralleling the normalization of serum lactate. In contrast to the majority of cases of lymphoma-associated lactic acidoses reviewed to date, in our case lactate elimination was not reduced.
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PMID:Lactic acidosis and hypoglycemia in a patient with high-grade non-Hodgkin's lymphoma and elevated circulating TNF-alpha. 859 16

In a boy with non-Hodgkin's lymphoma (NHL), two different complications developed concurrently associated with L-asparaginase (L-ASP) therapy. A non-ketotic hyperglycemic state was observed simultaneously with bilateral acute parotitis after the patient was subjected to L-ASP. The hyperglycemia with normal insulin levels and the absence of plasma and urine ketones was controlled with insulin therapy and no residual impairment of glucose tolerance was demonstrated later. Bilateral acute parotitis, which is a rare complication associated with L-ASP, resolved spontaneously within a week after cessation of L-ASP. The rarely observed toxic effects of L-ASP, such as parotitis, should be recognized as promptly as the better-known complications, e.g., hyperglycemia, to avoid the continuation of this antineoplastic agent.
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PMID:Hyperglycemia and acute parotitis related to L-asparaginase therapy. 900 80

Multiple endocrine neoplasia type 1 (MEN1) is tightly linked to the muscle-type glycogen phosphorylase (PYGM) gene in 11q13. This region of the human genome contains additional disease-related loci implicated in the development of insulin-dependent diabetes mellitus, familial paraganglioma type 2, spinocerebellar ataxia type 5, Bardet-Biedl syndrome and translocation t(11;17) described in B-cell non-Hodgkin's lymphoma. We approached cloning of candidate disease genes from 11q13 by large-scale genomic sequencing. We obtained > 106 kb of sequence around the PYGM gene and established a transcriptional map that includes: (i) two genes previously localized to 11q13, PYGM and a zinc-finger protein (ZFM1) gene; (ii) the germinal center kinase (GCK, human B-lymphocyte serine/threonine protein kinase) gene; (iii) a novel human CDC25-like (HCDC25L) gene; (iv) a dystrophia myotonica protein kinase-like (DMPKL) gene; and (v) a novel ubiquitously expressed gene of unknown function (germinal center kinase- neighboring gene, GCKNG).
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PMID:The germinal center kinase gene and a novel CDC25-like gene are located in the vicinity of the PYGM gene on 11q13. 934 81

A 43-year-old Japanese man who was positive for hepatitis B surface (HBs) antigen and HB e antibody, underwent chemotherapy for non-Hodgkin's lymphoma. After the chemotherapy he suffered from acute exacerbation of hepatitis because of reactivation of HBV. Recovery was achieved with interferon-alpha, glucagon-insulin therapy, and plasma exchange. Mutations were detected in codons 97, 100, 129, and 131 of the core region of HBV. The peptide encoded from the core region including such mutations possibly had greater antigenicity to induce cytotoxic T cell activity in the host. Core region mutations may be a crucial cause of the acute exacerbation of hepatitis B seen after chemotherapy.
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PMID:Acute exacerbation of hepatitis due to reactivation of hepatitis B virus with mutations in the core region after chemotherapy for malignant lymphoma. 934 95

Lymphotoxin (LT, LT alpha, TNF beta) is a member of the immediate TNF family that also includes TNF-alpha and lymphotoxin-beta (LT beta). LT is produced by activated lymphocytes and functions as either a secreted homotrimer or a membrane-associated heterotrimer that includes the transmembrane protein LT beta. Secreted LT alpha3 can bind to two cell surface receptors, TNFR1 and TNFR2, while the membrane-bound heterotrimer LT alpha1beta2 has been shown to interact with a distinct receptor, LT betaR. LT alpha induces inflammation at the sites of expression of a rat insulin promoter-driven lymphotoxin (RIPLT) transgene in the pancreas and kidney. To determine the role of the various ligands and their receptors in LT-induced inflammation, mice deficient in either TNFR1, TNFR2, or LT beta were crossed to RIPLT-transgenic mice. Our results indicate that LT alpha-induced inflammation is dependent on the interaction of LT alpha3 with TNFR1, and there is no obvious role for TNFR2, since in its absence, LT alpha-induced inflammation is quantitatively and qualitatively similar to that seen in the wild type. However, the absence of LT beta results in accentuated infiltration of the kidney with an increase in the proportion of memory cells in the infiltrate. These data show a crucial role for the secreted LT alpha3 signaling via TNFR1 in LT alpha-induced inflammation, and a separate and distinct role for the membrane LT alpha1beta2 form in this inflammatory process.
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PMID:Differential activities of secreted lymphotoxin-alpha3 and membrane lymphotoxin-alpha1beta2 in lymphotoxin-induced inflammation: critical role of TNF receptor 1 signaling. 955 7


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