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)

Growth hormone was given to 13 children (nine boys, four girls) with acute leukaemia who had undergone treatment with cyclophosphamide and total body irradiation before bone marrow transplantation. Mean age at total body irradiation and bone marrow transplantation was 9.0 years (range 3.7-15.8). Endocrinological investigation was carried out at a mean of 2.0 years (range 0.4-4.0) after bone marrow transplantation. Peak serum growth hormone responses to hypoglycaemia were less than 10.0 micrograms/l (less than 20.0 mU/l) in 10, 10.5 micrograms/l (21.0 mU/l) in one, greater than 16.0 micrograms/l (greater than 32.0 mU/l) in two patients. Mean age of the patients at the start of growth hormone treatment was 12.2 years (range 5.8-18.2). The mean time between total body irradiation and bone marrow transplantation and the start of growth hormone treatment was 3.2 years (range, 1.1-5.0). Height velocity SD score (SD) increased from a mean pretreatment value of -1.27 (0.65) to + 0.22 (0.81) in the first year, +0.16 (1.11) in the second year, and +0.42 (0.71) in the third year of treatment. Height SD score (SD) changed only slightly from -1.52 (0.42) to -1.50 (0.47) in the first year, to -1.50 (0.46) in the second year, and -1.74 (0.92) in the third year. Measurement of segmental proportions showed no significant increase in subischial leg length from -0.87 (0.67) to -0.63 (0.65) in the first year, to -0.58 (0.70) in the second year, and -0.80 (1.14) in the third year of treatment. Our data indicate that children who have undergone total body irradiation and bone marrow transplantation respond to treatment with growth hormone in either of two dose regimens, with an increase in height velocity that is adequate to restore a normal growth rate but not to 'catch up', and that total body irradiation impairs not only spinal but also leg growth, possibly by a direct effect of irradiation on the epiphyses and soft tissues.
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PMID:Growth hormone treatment of growth failure secondary to total body irradiation and bone marrow transplantation. 205 88

An 11-year-old girl being treated with DNA-recombinant growth hormone therapy presented with proximal limb weakness. Laboratory studies were negative. A few months later she presented with acute lymphoblastic leukemia (ALL). A diagnosis of carcinomatous neuromyopathy was made. After successful treatment of the leukemia the symptoms subsided and did not recur.
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PMID:A girl treated with growth hormone presenting with neuromyopathy as first sign of acute lymphoblastic leukemia. 209 12

Three reported cases of Creutzfeldt-Jakob disease (CJD) in young adults who had received human growth hormone (hGH) raised concerns that pituitary-derived GH had been contaminated. Subsequently reported cases have confirmed this suspicion. The US Public Health Service is conducting an investigation to determine the extent of the problem of CJD in recipients of National Hormone Pituitary Program (NHPP) GH. In addition, other possible adverse effects of GH use including leukemia are being investigated. The design, conduct and current status of the study are the subject of this report. Interview data are now available on 5,240 of the 6,284 subjects treated by the NHPP for growth problems. Analysis is underway.
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PMID:Status report on the US human growth hormone recipient follow-up study. 221 Jun 15

Over the past 5 years, reports detailing the production of transgenic pigs have focussed on enhanced growth performance. Phenotypic side-effects observed in pigs harbouring chimaeric constructs containing metallothionein or Moloney murine leukaemia virus transcriptional activators fused to growth hormone (GH) structural genes have been attributed to chronic overexpression of GH. In an effort to regulate a transgene product more effectively, a liver specific 460 bp 5' flanking sequence of the rat phosphoenolpyruvate carboxykinase (PEPCK) gene was ligated to a BamHI site of the first exon of the genomic bovine GH (bGH) structural gene. Following micro-injection of the PEPCK/bGH construct into 1- and 2-cell pig zygotes. 124 offspring were produced of which 7 pigs were determined to be transgenic by dot-blot and Southern analysis. The PEPCK gene expression, in terms of tissue and developmental specificity, appears similar to that observed in PEPCK/bGH transgenic mice. Germ-line transmission was identified in 1 of 3 mated founders. Dramatic influences on backfat thickness were observed including a 41% reduction in backfat depth when compared to non-transgenic sex-matched littermate control pigs. Both the regulation and characterization of gene expression in PEPCK/bGH transgenic pigs are under investigation.
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PMID:Production of transgenic pigs harbouring a rat phosphoenolpyruvate carboxykinase-bovine growth hormone fusion gene. 221 19

In an attempt to elucidate the role of viruses in certain neuroendocrine disorders, we have demonstrated that infection of endocrine cells (GH-3 and Y-1) in vitro by moloney murine leukemia virus (M-MuLV) resulted in diminution of cell-specific secretory function, hormone secretion into culture. In GH-3 (rat anterior pituitary gland) active (initial) and persistent infection by M-MuLV resulted in approximately 80% reduction in prolactin and growth hormone secretion. The adrenal cortex tumor cell line (Y-1), when actively infected with the same virus, showed a transient increase in fluorogenic steroid secretion; however, on subsequent passages of infected cell cultures, steroid secretion was markedly reduced to about 10% of the uninfected Y-1 cells. The virus yield from M-MuLV-infected cultures of Y-1 and GH-3 cells produced a significantly lower amount of virus than the control NIH-3T3-infected cell cultures.
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PMID:Modulation of hormone secretion in vitro by murine retrovirus. 227 77

In eight children, after the termination of therapy for acute lymphoblastic leukaemia (ALL) the secretion of growth hormone (GH) was determined by the stimulation test with clonidine. The children were treated in the period from 1983 till 1988 and they were administered chemotherapy, intrathecal methotrexate therapy and cranial irradiation 60CO in a dose of 1800 rads. In one case a complete GH deficiency was found, in three cases there was a partial deficiency and in the remaining cases the secretion was regular. No correlation was found between the biochemical values of GH and the clinical stature. There was also no interrelation between the duration of therapy (chemotherapy) and the degree of pituitary gland failure. We have compared the results of GH output in children treated for ALL with those of 44 children in whom short stature was diagnosed. The age in both groups was similar.
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PMID:Growth hormone secretion in children after therapy for acute lymphoblastic leukaemia. 235 56

Here we report that the slow-transforming helper component of Friend murine leukaemia virus (Fr-MLV), which produces lymphoid leukaemias in normal mice, induces erythroleukaemia in mice given syngeneic pituitary grafts (SPG). Newborn mice were infected with Fr-MLV and, at one month of age, were transplanted with two pituitary glands under the kidney capsule. Sham-operated infected mice and uninfected transplanted mice served as controls. SPG selectively reduced the mean survival times of infected mice. Histopathology showed that, while most infected non-transplanted mice developed lymphoid leukaemias, virtually all Fr-MLF-infected mice given SPG developed erythroleukaemias. Experiments in vitro showed that Fr-MLV infection markedly depressed concanavalin A induced DNA synthesis in cells from spleen, thymus and lymph nodes. Addition of prolactin or growth hormone further suppressed lectin-induced mitogenesis of lymphoid cells from infected mice, but failed to influence the response of uninfected controls. These experiments indicate that, in mice, pituitary hormones modulate the development and the histological features of Fr-MLV induced leukaemias, and suggest that endocrine-immunological interactions play a role in retrovirus induced tumorigenesis.
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PMID:Fr-MLV infection induces erythroleukaemia instead of lymphoid leukaemia in mice given pituitary grafts. 237 85

The spontaneous secretion of growth hormone during a 24 hour period and the response of growth hormone to growth hormone releasing hormone was studied in 13 girls who had received treatment for acute lymphoblastic leukemia that included cranial irradiation with 20-24 Gy in 12-14 fractions. At the time of investigation the girls were at varying stages of puberty and had normal concentrations of thyroid hormones. The mean interval between the end of treatment and investigation was 4.6 years. The mean age at onset of the disease was 3.2 years and at investigation 10.7 years. The average attained height equalled -0.3 SD at onset, and -1.0 SD at the time of investigation. Secretion of growth hormone was substantially reduced compared with controls and did not increase during puberty. A prompt rise in growth hormone secretion was seen after injection of growth hormone releasing hormone, but the mean maximum growth hormone concentration was, however, only 25 mU/l. There was no correlation between the 24 hour secretion and growth hormone response to growth hormone releasing hormone, or the time since irradiation. These results confirm earlier work that suggested that girls who had received treatment for acute lymphoblastic leukaemia, that included cranial irradiation, have a comparative growth hormone insufficiency characterised by normal prepubertal growth and slow growth during puberty because of an inability to respond to the increased demands for growth hormone at that time.
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PMID:Suppressed spontaneous secretion of growth hormone in girls after treatment for acute lymphoblastic leukaemia. 249 52

A matched case-control study on leukemia occurrence among growth hormone (GH) users was performed to elucidate any risk factor for leukemia. The total doses of GH and administration of other hormones, such as thyroxine, gonadotropin, gonadal hormones, glucocorticoid and anabolic steroid, did not lead to any apparent difference between cases studied and controls. Neither doses of diagnostic X-rays nor therapeutic cranial irradiation was related to leukemia risk. Scintigraphy for thyroid function using radioactive iodide was the only significant risk factor (P = 0.03). Hematological changes and liver function before and one month after GH administration were compared and the cases studied showed more proliferative reaction of white blood cells with rapid increase of neutrophils, but lymphocyte response was variable. Lactic acid dehydrogenase, alkaline phosphatase, glutamic oxalacetic transaminase, glutamic pyruvic transaminase tended to decrease after GH treatment when the patients had shown abnormally increased levels. Other environmental and familial factors did not show any abnormal clusters.
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PMID:Risk factors for leukemia occurrence among growth hormone users. 251 98

Twenty-three patients (13 females, 10 males) with panmyelopathy (N = 9), chronic leukemia (N = 5), and acute leukemias (N = 9) were studied 1 to 6 years following allogenic bone marrow transplantation. All patients had received conditioning treatment with cyclophosphamide prior to aBMT, and 2 of the patients with bone marrow aplasia and all of the leukemia patients had been given radiotherapy. An endocrine assessment was performed by means of TRH, GnRH, oCRF and GHRH tests and estimation of thyroid and gonadal hormones. Whereas pituitary-adrenal function appeared to remain stable, there was a 17.4% incidence of subclinical hypothyroidism (25% of the irradiated patients). Growth hormone reserve was diminished, and ovarian failure occurred in all female patients after radiotherapy, whereas in the men, only a moderate elevation of gonadotropins was observed. Our results warrant observation of thyroid and gonadal function, and in children of growth hormone secretion, after allogenic bone marrow transplantation. They also show that replacement therapy may be needed in some patients.
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PMID:Allogenic bone marrow transplantation in adults: endocrine sequelae after 1-6 years. 253 5


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