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Query: UMLS:C0023418 (leukemia)
 93,477 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report a girl with acute lymphoblastic leukaemia presenting hypothalamic syndrome characterized by meningeal leukaemia, hyperphagia and obesity. Insulin and growth hormone secretion, studied with arginine and insulin stimulation tests, showed a high peak of serum insulin and no response of growth hormone. Insulin and growth hormone responses to these tests reverted to normal after intrathecal methotrexate.
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PMID:Insulin and growth hormone secretion in a leukaemic girl with hypothalamic syndrome. 26 33

Administration of ovine growth hormone to young C3Hf mice inhibited Gross passage A virus-induced leukemogenesis as manifested by a delayed onset and a lower incidence of thymus leukemia. These results can be interpreted that growth hormone inhibited thymus-dependent leukemogenesis perhaps through thymotrophic influences which prevented or delayed the thymus involution believed to be essential for leukemia change. In female but not in male Gross passage A virus-infected mice, development of a thymus-independent leukemia appeared to be promoted by growth hormone.
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PMID:Inhibitory effect of growth hormone on Gross passage A virus-induced thymus leukemia in C3Hf mice. 76 Dec 14

Because the delivery of growth hormone (GH) was centralized from 1977 in France, it has been possible to conduct, during the second half of 1990, a nationwide survey of the health status of patients treated with GH from the year 1959. A questionnaire regarding the 5,546 patients recorded for the period 1959-1990 was sent to the prescribers or the patients. 5,418 more or less completely documented reports were obtained. The mean age of the patients at the onset of GH treatment was 11.0 +/- 4.1 years. 1,937 of them had at this time some important disease associated with GH deficiency. The mean duration of treatment was 3.99 +/- 3.05 years. 3,446 patients were still under follow-up. Very recent information (1990-1991) was given for 82.7% of patients, less recent data (1985-1989) for 13.4%. For 3.9%, no data beyond 1985 were obtained. 77 patients had died, 38 from neoplastic disease (mainly recurrence of a primary malignancy), 10 from accident, 3 by suicide, 7 with neurological disease [only 1 case of Creutzfeldt-Jakob disease (CJD) was reported at the time of the survey], the others from various causes. No abnormal frequency of posttreatment leukemia, lymphoma, malignancies, hip diseases, glucose intolerance or other disease focusing attention, was found in the survey. From the time when this survey was completed (December 1990) to that of this report (May 1992), other cases of CJD have been reported in France: 3 ascertained, 7 clinically resembling but not yet certain. These 10 patients were treated for complete GH deficiency, 6 of congenital or neonatal cause and 4 after neurosurgery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Epidemiologic survey of patients treated with growth hormone in France in the period 1959-1990: preliminary results. 129 11

Since 1960 more than 30,000 children have been treated with growth hormone (GH) in the USA. Ten cases of Creutzfeldt-Jakob disease have been associated with the use of GH purified from pituitaries in the USA, and more cases may appear in the future. Ten cases of leukemia or preleukemia have been reported in patients undergoing GH treatment in the US. Eight of these patients had previously diagnosed tumors of the central nervous system. As the indications for GH treatment broaden, and the dosages of GH increase, more unfavorable clinical events linked directly to the biological actions of GH can be expected to occur. Continued surveillance for clinically important GH-associated events is important.
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PMID:Untoward events in patients treated with growth hormone in the USA. 129 12

There is growing concern about the oncogenic potential of growth hormone (GH) used therapeutically. In rat experiments, a variety of malignant tumours have been induced following administration of supraphysiological doses of GH, whilst in other studies in hypophysectomized animals a lower than normal incidence of carcinogen-induced neoplasms was reported. In acromegaly, in which there is a pathologically sustained high GH level, there is a significantly increased incidence of cancer in general and specifically of colonic neoplasia. To determine whether the use of GH in the treatment of radiation-induced GH deficiency causes tumour recurrence, a comparison was made of tumour recurrence rates between 47 children treated with GH for radiation-induced GH deficiency after treatment for a brain tumour and a control population from the North West Children's Cancer Registry who did not receive GH (n = 160). All cases of acute lymphoblastic leukaemia (ALL), including those that were (n = 15) and were not (n = 146) treated with GH were reviewed. The computerized tomography (CT) scans in the children with brain tumours were reviewed at the time of GH commencement and subsequently. There were 5 brain tumour recurrences after GH therapy: 1 astrocytoma, 2 ependymomas and 2 medulloblastomas. Adjusting for variables other than GH which might affect tumour recurrence, the estimated relative risk of tumour recurrence was 0.82 (95% confidence interval: 0.28-2.37). In each tumour category there was no association between the use of GH and subsequent tumour recurrence.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Tumour occurrence and recurrence. 129 13

Since 1988 the number of growth hormone (GH)-treated patients has markedly increased worldwide. To date, leukemia has been observed in 31 patients during or following GH therapy and related malignancies in 2 further patients. Leukemia occurred in 10 patients in Japan, 10 in the USA, and 10 in Europe, and in 1 patient in Canada. In 29 patients GH therapy had been started in 1975 or later. The onset of leukemia was 1984 or later in 28 patients with a mean time between the start of GH therapy and leukemia onset of 5.0 (0.2-18.8) years. Patients had received both pituitary and recombinant GH in moderate doses. In 15 patients definite additional leukemia risk was evident: Fanconi anemia in 2, myelodysplastic syndrome in 1, Bloom's syndrome in 1, radiation for brain tumor (+chemotherapy) in 9, chemotherapy in 2. The leukemic patients without a strong additional risk do not represent a definitely higher leukemia incidence worldwide, except for Japan where the occurrence is higher than expected.
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PMID:Leukemia in growth-hormone-treated patients: an update, 1992. 129 14

Infant cats were inoculated intracranially with rabies or feline leukemia viruses in an experimental study of wasting syndrome. The daily pre- and postinoculation body weights were recorded until kittens were moribund. Affected animals in both groups manifested growth failure or wasting syndrome. Immunodepression, manifested by a conspicuous depletion of thymic cortex, the thymus dependent areas of the spleen, and growth hormone producing-alpha adenopituicytes was significantly (p less than 0.01) related to the wasting status of the animals. The ability of pituitary glands from these animals to produce growth hormone was studied by in situ immunoperoxidase staining and showed a significant (p less than 0.01) difference between healthy and wasted animals. Rabies and feline leukemia viruses were each found responsible for the low immunoreactivity of growth hormone producing alpha adenopituicytes. Because the hypothalamus and the hypophysis were both found infected, it was concluded that regardless of the triggering agent in primary wasting, the hypothalamic-hypophyseal-thymic axis was always involved through a decrease in growth hormone production.
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PMID:The microepidemiology of wasting syndrome, a common link to diarrheal disease, cancer, rabies, animal models of AIDS, and HIV-AIDS YHAIDS). The feline leukemia virus and rabies virus models. 132 Aug 42

We studied the growth of 89 patients who were long-term survivors of childhood leukemia and lymphoma. Eight patients with CNS relapse had a greater decrease in height standard deviation score (SDS) after the relapse than 81 patients without CNS relapse (p less than 0.0001). Two patients who received cranial irradiation when they were younger than 2 years of age demonstrated a marked decrease in height SDS more than 3.0 SD. Five patients appeared to have a decline in height SDS before their CNS relapse. There were no apparent changes in the weight of patients with or without CNS relapse. In endocrine studies, all eight patients with CNS relapse failed to show the normal growth hormone (GH) response to arginine, GH-releasing factor, and glucagon-propranolol tests, while spontaneous GH secretion during sleep was normal. Magnetic resonance imaging (MRI) revealed small pituitary glands in seven patients with CNS relapse. These findings suggest that in leukemia and lymphoma patients with CNS relapse, GH secretion is impaired at the hypothalamic level, resulting in a secondary atrophy of the pituitary gland. The MRI together with selected endocrinologic tests may help to clarify the mechanism of growth impairment in such patients. A decline in height SDS in each patient may be a useful marker for predicting a CNS relapse in a child with leukemia or lymphoma.
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PMID:Growth retardation in childhood leukemia and lymphoma. Special reference to patients with CNS relapse. 151 Jan 94

Treatment with human growth hormone in growth hormone deficient patients will improve growth rate significantly, initially demonstrating catch-up growth and later bringing forth a normal growth rate. During childhood, a dose of 0.3-0.6 units/kg body weight per week (or 14 units/m2 body surface area per week) is recommended, but during puberty the dose should be increased by 50-100%. The goal of therapy is the attainment of a normal final height, which in the past has often not been fulfilled. This was partly due to the inadequate supply of growth hormone. Since recombinant human growth hormone is now available in unlimited amounts, all patients can be treated continuously. The shorter the child is at time of presenting for therapy, the lower final height will be. It is mandatory to start therapy as early as possible. Concomitant hormonal deficiencies must be corrected by adequate therapy. Despite the fact that growth hormone is diabetogenic, supplementary therapy will not induce diabetes mellitus. Subtle changes in the immune system can be detected but no clinical correlates, such as increased susceptibility to infection, exist. Induction of leukaemia has been suspected as a possible side-effect of human growth hormone treatment but so far there is insufficient evidence to prove that growth hormone is oncogenic.
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PMID:Therapy of growth hormone deficiency. 152 51

The binding of haemopoietic growth factors and cytokines to specific receptors triggers a cascade of intracellular events which results in cell proliferation and differentiation. The knowledge of ligand-receptor-signal pathways is not only important in understanding the pathophysiology of malignant disease but also essential for devising future therapeutic strategies. The advent of recombinant technology has made it possible to test the efficacy of selective differentiation therapy, and haemopoietic growth factors are undergoing clinical trials for a number of indications. In addition, increasingly the receptors for haemopoietic growth factors and cytokines have come under scientific scrutiny. Recently receptors for IL-2 alpha, IL-2 beta, IL-3, IL-4, IL-5, IL-6, IL-7, erythropoietin, G-CSF and GM-CSF have been isolated and cloned. It has become apparent that they have structural homology that is shared by receptors for growth hormone and prolactin, and this receptor group makes up the new cytokine receptor superfamily. The finding of sequence homology within these receptors suggests their evolutionary relationship. These receptors are transmembrane proteins 257-856 amino acids and their extracellular ligand-binding domain contains four conserved cysteine residues and a Trp-Ser-X-Trp-Ser motif. The secondary structure of the extracellular domain is made up of alpha-helices. High and low affinity binding forms exist for all these receptors. Binding affinity may depend on the formation of receptor heterodimers or multimers, association with other membrane proteins or differential glycosylation. Soluble receptor forms have been described for IL-2 alpha, IL-4, IL-5, IL-6 and IL-7. It is not known whether they are actively secreted or represent the degradation products of cell turnover. Their function may be to mop up excess cytokines and thereby confine the cytokine response. There is no sequence homology of the intracytoplasmic domains although several are rich in proline and serine residues, which may be important in mechanisms of signal transduction. No receptor in this superfamily functions as a receptor tyrosine kinase or has intrinsic protein tyrosine kinase activity. Detailed study of individual receptors holds clues to the regulation of receptor expression, ligand-receptor interactions and mechanisms involved in signal transduction. Such knowledge might explain the pleotropic effects cytokines may have on different cell types and their overlap in biological functions. Elevated levels of soluble IL-2 alpha receptor (Tac) are detected in hairy cell leukaemia, lymphomas and adult T-cell leukaemia (TL), and levels reflect tumour burden.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The cytokine receptor superfamily. 166 10


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