Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect on carbohydrate metabolism of a high dose growth hormone (GH) regimen (1.2 U/kg per week) was assessed on 24 children who had previously been treated for leukaemia. Sixteen patients received high dose GH and eight patients received a conventional dose of GH (0.6 U/kg per week). Oral glucose tolerance tests (OGTT) were performed at baseline and after 3 months of treatment with GH. For the entire group between 0 and 3 months, there was a significant increase in mean (and standard deviation) fasting plasma glucose (0.3 +/- 0.6 mmol/L), fasting insulin level (11 +/- 26 mU/L), and 2 h insulin level (20 +/- 40 mU/L). One patient, who received a conventional dose of GH, developed substantial carbohydrate intolerance. For the entire group, there was no change in response to a carbohydrate load at 3 months as measured by the area under the plasma glucose or insulin curve. There was no significant difference between conventional and high dose groups at 3 months as assessed by these parameters. This study demonstrates that a higher dose of GH may be used in these children in an attempt to improve their final height, without increased risk of carbohydrate intolerance in the short term.
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PMID:Carbohydrate metabolism on high dose growth hormone therapy in children treated for leukaemia. 259 Jan 20

The rat mast cell protease gene, RMCP II, is specifically expressed in the mucosal subclass of rat mast cells. We show here that the 5'-flanking region of this gene contains a mast cell-specific enhancer that directs preferential expression of a linked reporter gene (human growth hormone) transfected into rat basophilic leukemia cells. A DNA fragment containing the enhancer sequence is capable of binding specifically to mast cell nuclear trans-acting factors. The sequence of this enhancer element contains a region of homology to a consensus core sequence present in the enhancer region of the pancreatic protease genes.
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PMID:The mast cell-specific expression of a protease gene, RMCP II, is regulated by an enhancer element that binds specifically to mast cell trans-acting factors. 264 95

Following an initial report from Japan in 1987, 15 growth hormone (GH)-deficient patients developed leukaemia during or following GH treatment. Nearly all available pituitary and biosynthetic growth hormones have been used. In 14 of these 15 patients GH treatment was initiated in 1975 or later with doses between 4.5 and 18IU/m2 per week. The therapy period was between 0.17 and 8.0 years. Leukaemia occurred 0.2-11 years after the start of GH treatment. GH affects normally and abnormally growing blood cells in vitro and in animal experiments, but the clinical data in humans do not indicate GH induction of tumour growth. Seven out of the 14 patients under discussion had an additional increased leukaemia risk. Two other patients had been treated only for a very short time. Though no clear evidence of a strikingly augmented leukaemia incidence in GH-treated patients is found worldwide, the available data call for increased attention.
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PMID:Growth hormone therapy and leukaemia. 266 11

An 18-year-old male patient who had suffered from polyuria, nocturia and easy fatigability since childhood is described. A germ cell tumor in the suprahypophyseal region was diagnosed at the age of 13 years, and was treated by cranial irradiation. Growth retardation and other signs of hypophyseal deficiency successively occurred, and human growth hormone was administered for two years and five months from the age of 16 years until acute lymphoblastic leukemia developed. Adriamycin, vincristine and prednisolone therapy induced complete remission, but the patient died of disseminated intravascular coagulation two months later. The relationship between the occurrence of leukemia and administration of growth hormone is discussed.
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PMID:Occurrence of acute lymphoblastic leukemia in a boy treated with growth hormone for growth retardation after irradiation to the brain tumor. 283 38

Three transcriptional regulatory regions including a human cytomegalovirus immediate-early region (CMVIE) promoter, the simian virus-40 early region (SV40E) promoter, and Moloney murine leukemia virus (MoMLV) long terminal repeat (LTR) were ligated to the bovine growth hormone (bGH)-coding gene. Using a bGH transient expression system, the CMVIE and SV40E gene transcriptional regulatory regions were found to be approximately two-fold more efficient than the MoMLV LTR in directing expression of bGH in mouse L cells.
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PMID:A comparison of bovine growth-hormone gene expression in mouse L cells directed by the Moloney murine-leukemia virus long terminal repeat, simian virus-40 early promoter or cytomegalovirus immediate-early promoter. 285 91

Tumour relapse rates in 14 patients with medulloblastoma, 8 with glioma, 2 with ependymoma, 6 with leukaemia, and 1 with T-cell lymphoma who received growth hormone (GH) treatment for growth failure secondary to cranial irradiation were compared with rates among patients treated with radical radiotherapy for the same types of tumour. Five relapses (in 5 patients) occurred (1 optic nerve glioma, 2 medulloblastomas, and 2 ependymomas), three during and two after completion of GH treatment. Patients with medulloblastoma and ependymoma who relapsed were older at tumour diagnosis, underweight at the start of GH therapy, and entered puberty later than similar relapse-free patients. The late relapse rate of medulloblastoma and glioma was unaltered by GH therapy. Ependymoma carries a poor prognosis, and of the 4 late survivors, the 2 who received GH relapsed. No leukaemic relapse has been associated with GH treatment. The findings indicate that GH therapy does not increase the relapse rate of medulloblastoma, glioma, and leukaemia.
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PMID:Does growth hormone cause relapse of brain tumours? 288 31

The MT-2, derived from an adult T-cell leukaemia (ATL) cell, the Molt-4F, a human T-cell line, and the Isk, an EB virus-transformed B-cell line, were found to have high-affinity receptors for somatostatin, a cyclic tetradecapeptide that inhibits the release of substances such as growth hormone, TSH, glucagon, insulin, secretin, gastrin and cholecystokinin. The quantity of radioactivity bound varied linearly with the number of cells, and was displaced by non-radioactive somatostatin in a concentration-dependent manner. Specific binding of 125I-somatostatin was time- and temperature-dependent and at 22 degrees reached equilibrium within 120 min. Scatchard analysis demonstrated one class of specific-binding sites on MT-2 cells, Isk cells and Molt-4F cells that had respective densities and dissociation constants of 109 pM and 0.64 nM, 102 pM and 1.1 nM, and 5.8 pM and 0.22 nM.
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PMID:Identification of lymphoid cell lines bearing receptors for somatostatin. 289 85

Growth was assessed in 82 children with acute lymphoblastic leukaemia (ALL) who achieved complete continuous first remission following treatment. 34 received prophylactic cranial irradiation at a total dose over 2000 cGy (group I) and 48 at a dose of 1800 cGy (group II). Chemotherapy was given over two or three years and was more intense in group II. Both groups showed a similar significant decrease in height standard deviation score (SDS) over four years (group I -0.31, group II -0.39). 15 children in group I were followed to ten years and continued to show restricted growth with a mean height SDS decrease of -0.84 (range 0 to -1.7). The greatest reduction in yearly decrements in height SDS occurred in the first year after diagnosis. In both groups height SDS increased significantly on completion of chemotherapy. Thus chemotherapy protocols contribute to growth retardation in ALL. In most of these children the mean loss of height over ten years was not sufficiently great to justify long-term growth hormone (GH) therapy.
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PMID:Growth in children treated for acute lymphoblastic leukaemia. 289 77

By virtue of its immediate contact with the circulating blood, the endothelium provides an attractive target for retroviral vector transduction for the purpose of gene therapy. To see whether efficient gene transfer and expression was feasible, rabbit aortic endothelial cells were infected with three Moloney murine leukemia virus-derived retroviral vectors. Two of these vectors carry genes encoding products that are not secreted: N2, containing only the selectable marker gene neoR, and SAX, containing both neoR gene and an SV40-promoted adenosine deaminase (ADA) gene. The third vector, G2N, contains a secretory rat growth hormone (rGH) gene and an SV40-promoted neoR gene. Infection with all three vectors resulted in expression of the respective genes. A high level of human ADA expression was observed in infected endothelial cell populations both before and after selection in G418. G2N-infected rabbit aortic endothelial cells that were grown on a synthetic vascular graft continued to secrete rGH into the culture medium. These studies suggest that endothelial cells may serve as vehicles for the introduction in vivo of functioning recombinant genes.
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PMID:High-level recombinant gene expression in rabbit endothelial cells transduced by retroviral vectors. 291 35

The patient had a low birth weight and was born with appearance anomalies including microcephalus, microphthalmia, hypoplastic mandible, double chin due to cutaneous fold, micropenis. Ability to move and intelligence appeared to develop normally, but growth was markedly retarded. In June 1982, at the age of 2 yr 4 mo, the patient underwent tolerance tests whereby a deficiency of human growth hormone (GH) was proved by poor GH secretion response. GH was administered until April 1985 when acute lymphoblastic leukemia developed. The patient's younger brother, born in 1986, had similar birth anomalies and was diagnosed as having Fanconi's anemia. It therefore seems possible that our patient developed his acute leukemia through the stimulatory effect which GH had on a predisposition to leukemia.
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PMID:Acute lymphoblastic leukemia following treatment with human growth hormone in a boy with possible preanemic Fanconi's anemia. 292 16


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