Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019829 (Hodgkin's disease)
 30,247 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various tumors of neuroendocrine origin that have amine precursor uptake and decarboxylation (APUD) characteristics can be visualized in vivo after intravenous (IV) injection of the somatostatin analogue, [123I-Tyr3]-octreotide. However, the relatively short effective half-life of this compound and the high background of radioactivity in the abdomen are drawbacks to its application. Therefore, an 111In-coupled somatostatin analogue ([111In-DTPA-D-Phe1]- octreotide) was developed. This analogue is excreted mainly via the kidneys, with 90% of the dose being present in the urine 24 hours after injection. Using 111In-octreotide scintigraphy, seven of seven gastrinomas, four of seven insulinomas, one of one glucagonomas, three of three unclassified APUDomas, and none of 18 exocrine pancreatic carcinomas were visualized. Also, 19 of 19 carcinoids, 15 of 15 glomus tumors, eight of 12 medullary thyroid carcinomas, six of six small-cell lung carcinomas, four of four growth hormone-producing and six of nine clinically nonfunctioning pituitary adenomas were visualized. Apart from APUD cell-derived tumors, 111In-octreotide scintigraphy was also successfully applied in visualizing breast cancer, lymphomas, and granulomas. In 39 of 50 patients with breast carcinoma, 10 of 11 patients with non-Hodgkin's lymphomas, three of three patients with Hodgkin's disease, and eight of eight patients with sarcoidosis, tumor sites accumulated radioactivity during octreotide scintigraphy. In a considerable number of patients with carcinoids and glomus tumors, and also in patients with granulomas and lymphomas, 111In-octreotide scintigraphy showed more tumor sites than did conventional imaging techniques. The results of imaging in vivo correlated with the somatostatin-receptor status on the tumors in vitro.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:111In-octreotide scintigraphy in oncology. 135 91

The interaction between the immune and endocrine systems has recently been investigated. Hodgkin's disease represents a model of immune disturbance frequently associated with endocrine impairment. The present study evaluated the effect of the acute administration of beta-interferon or thymopentin on plasma growth hormone, prolactin and cortisol levels in children with Hodgkin's disease (N = 8) and age- and sex-matched healthy controls (N = 8). beta-interferon (1,000,000 IU), thymopentin (50 mg) or placebo (saline) were injected after two basal blood samples (-15 and 0) and further samples were drawn at 15, 30, 45, 60, 90 and 120 min. Plasma growth hormone, prolactin and cortisol levels were measured by specific RIAs. Plasma prolactin levels did not show significant change following beta-interferon or thymopentin injection in either the controls or the patients. In the patients with Hodgkin's disease, beta-interferon injection induced a significant increase in both plasma growth hormone and cortisol levels, while thymopentin was not effective. In controls both thymopentin and beta-interferon administration increased plasma growth hormone and cortisol levels. These results indicate that beta-interferon and thymopentin are immune substances active on the release of growth hormone and cortisol in healthy children. The lack of effect of thymopentin in children with Hodgkin's disease suggests an impairment of the immune-endocrine interaction in these patients.
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PMID:Acute beta-interferon or thymopentin administration increases plasma growth hormone and cortisol levels in children. 141 49

The effect of radio- and chemotherapy on auxological parameters was investigated in 30 children treated for acute lymphatic leukemia (ALL) or non-Hodgkins lymphoma (NHL). Growth velocity was decreased during the first year of treatment. Catch-up growth was insufficient during the following years. Thus, the whole group experienced a loss of height of 0.49 +/- 1.1 SD at 6.8 +/- 2.6 years after diagnosis. Height and growth velocity were not different between children who received 18 or 24 Gy cranial irradiation; however, growth velocity was significantly lower in children who were treated for more than 2 years or who had the more intensive chemotherapeutic protocol. Evaluation of the growth hormone (GH) response to pharmacological stimulation revealed reduced GH peaks in 47% of the patients, but there was no correlation of GH peak with growth or treatment parameters. In conclusion, the impairment of growth in children after treatment for ALL or NHL might be related to the intensity and duration of chemotherapy.
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PMID:Growth after radiotherapy and chemotherapy in children with leukemia or lymphoma. 147 29

Two weeks after partial resection of the small intestine for an intra-abdominal stenosing centroblastic non-Hodgkin lymphoma, a 65-year-old man began to experience recurrent attacks of hypoglycaemia (down to 30 mg/dl) together with lactic acidosis (lactate 5.13 mmol/l), tachycardia and sensations of heat. Very high parenteral glucose input (up to 750 g/day) was necessary to maintain normal blood sugar levels. There was close correlation between the level of glucose consumption and the degree of lactic acidosis. After chemotherapy the abnormalities improved, but recurred as the neoplasm proliferated once more. An endocrine mechanism for the hypoglycaemic attacks was excluded by the low serum concentrations of insulin and of "insulin-like growth factors" I and II and by the fact that the levels of glucagon, glucocorticoids, growth hormone and thyroid hormone were within the normal ranges. There were pleural and peritoneal effusions containing large numbers of tumour cells. Investigated in vitro, the fluids showed a decline in glucose and a rise in lactate concentration. Studies with an artificial pancreas also showed that glucose utilization rate in vivo was increased to four times the normal and that it could be raised still further by insulin stimulation. These findings provide evidence of direct consumption of glucose by the tumour cells in the form of abnormally increased anaerobic glycolysis.
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PMID:[Recurrent hypoglycemia and lactate acidosis in non-Hodgkin's lymphoma]. 189 54

To assess the neuroendocrine function of long-term survivors of childhood hematologic malignancies, 10 patients who had acute lymphocytic leukemia and two who had non-Hodgkins lymphoma (NHL) (mean age 13.5 +/- 1 year) were studied, who were treated with similar chemotherapeutic regimens with or without 2,400 rads of prophylactic cranial irradiation. Pharmacologic growth hormone (GH) stimulation tests and three graded doses of the GH-releasing hormone (1-40-OH-GRH, 0.1, 0.3, and 1 microgram/kg) were administered. Venous sampling for GH and gonadotropin determinations was done at 20-min intervals for 24 h, and a new computerized pulse detection algorithm was used to analyze pulses. All the patients who had neuroendocrine abnormalities were in the cranially irradiated group. Two of the 12 patients were GH deficient, and had abnormal 24-h secretory profiles, blunted GH responses to pharmacologic stimuli, and minimal responses to the three doses of GRH. The pulsatile properties of luteinizing hormone (LH) were normal in 10 of the 12 nongonadally irradiated patients, irrespective of previous cranial irradiation and pubertal stage, when compared with available normative data.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Neuroendocrine function in survivors of childhood acute lymphocytic leukemia and non-Hodgkins lymphoma: a study of pulsatile growth hormone and gonadotropin secretions. 314 88

Based on clinical findings of patients with some proliferative tumors and experimental data, a hypothesis of positive feedback mechanism by which tumor stimulates its own growth has been formulated. In some patients with Hodgkin's disease and non-Hodgkin's lymphomas, i.e. leukemias, the high levels of substances immunologically cross reactive with insulin (SICRI), low glycemic values and increased values of growth hormone were found in the blood. These findings were in correlation with the status and stages of the disease. In a more advanced stage of the disease, the concentration of insulin-like substances was higher and glucose levels were lower in patients in remission. The high correlation was found between the increased SICRI levels of insulin-like substances showed faster growth. It is certain that some tumor cells excrete these substances. In mice with melanomas, high concentrations of these substances, growth hormone and low glucose levels were found in the blood. On the basis of these findings a hypothesis was formulated about positive feedback mechanism by which tumors stimulates their own growth. Tumor excretes SICRI which decreases glucose concentration in the blood. Hypoglycemia is a stimulation for the pituitary to release growth hormone into the blood. This hormone probably stimulates protein synthesis and replication of tumor cells contributing to increased SICRI excretion, etc. The final results of this positive feedback mechanism is faster growth of tumor and death of host.
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PMID:[Positive feedback mechanisms by which immunoproliferative tumors stimulate their own growth]. 639 65

The levels of substance(s) detectable by insulin specific radioimmunoassay (RIA), glucose and growth hormone (GH) were determined in the blood of patients suffering from Hodgkin lymphoma. In the relapse phase of the disease, the levels of substances immunologically cross-reactive with insulin (SICRI) were elevated and glucose concentrations were below normal. In these patients the basal and hypoglycemia-induced levels of GH in blood were strongly elevated. Contrary to this, both SICRI and glucose levels were normal in the blood of patients in remission, and GH levels were significantly reduced compared to those measured in patients in relapse.
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PMID:Correlation of substance(s) immunologically cross-reactive with insulin, glucose and growth hormone in Hodgkin lymphoma patients. 675 29

Various tumors of neuroendocrine origin that have amine precursor and decarboxylation (APUD) characteristics can be visualized in vivo after intravenous injection of the somatostatin analogue [123I-Tyr3]-octreotide. However, the relatively short effective half-life of this compound and the high background of radioactivity in the abdomen are drawbacks in its application. Therefore, an 111In-coupled somatostatin analogue ([111In-DTPA-D-Phe1]-octreotide) was developed. This analogue is excreted mainly via the kidneys, 90% of the dose being present in the urine 24 h after injection. Using 111In-octreotide scintigraphy, 7 out of 7 gastrinomas, 4 out of 7 insulinomas, 1 out of 1 glucagonoma, 3 out of 3 unclassified apudomas, but none out of 18 exocrine pancreatic carcinomas were visualized. Also, 19 out of 19 carcinoids, 15 out of 15 glomus tumors, 8 out of 12 medullary thyroid carcinomas, 6 out of 6 small cell lung carcinomas, 4 out of 4 growth hormone-producing and 6 out of 9 clinically nonfunctioning pituitary adenomas were visualized. Apart from APUD-cell-derived tumors, 111In-octreotide scintigraphy was also successfully applied to visualize breast cancer, lymphomas and granulomas. In 39 out of 50 patients with breast carcinoma, 10 out of 11 patients with non-Hodgkin lymphomas, 3 out of 3 patients with Hodgkin's disease, and 8 out of 8 patients with sarcoidosis, tumor sites accumulated radioactivity during octreotide scintigraphy. In a considerable number of patients with carcinoids and glomus tumors, but also in patients with granulomas and lymphomas, 111In-octreotide scintigraphy revealed more tumor sites than did conventional imaging techniques.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:111In-octreotide scintigraphy in oncology. 835 73

The CD30 surface molecule is a recently identified member of the tumor necrosis factor/nerve growth factor receptor superfamily. Within the cytoplasmic signal transducing domain, CD30 shares no significant homology to other members of this family. Signaling events engaged via CD30 are still unknown. We here identify the NF-kappabeta transcription factor as a target of the CD30-induced signal pathway in Hodgkin's disease (HD) cells. Exposure of HD cells to CD30 ligand induces release of interleukin-6 (IL-6) that can be duplicated by cross-linking HD-cells to an agonistic anti-CD30 specific monoclonal antibody (alphaCD30), but not by cross-linking to an isotype-identical irrelevant monoclonal antibody. Cross-linking of HD cells to alphaCD30 leads to enhanced accumulation of IL-6 mRNA in a time-dependent fashion resulting from transcriptional activation of the IL-6 promoter. Transient transfection assays using a series of deleted IL-6 promoter constructs linked to the human growth hormone gene as a reporter gene furthermore indicate that transcriptional activation of the IL-6 promoter requires the presence of an intact NF-kappabeta binding site. In addition, introduction of an NF-kappabeta binding site appeared to be sufficient to confer inducibility of an heterologous promoter on activation of CD30 in HD cells. Cross-linking of CD30 promotes rapid and transient binding activity of nuclear proteins to the NF-kappabeta recognition site of the IL-6 promoter. Supershift experiments using a series of monoclonal antibodies recognizing distinct members of the NF-kappaBeta transcription factor family furthermore indicate that in CD30 cross-linked HD cells p50, p65/Rel-A, and Rel-B are present, whereas the c-rel protein is not.
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PMID:Activation of Hodgkin cells via the CD30 receptor induces autocrine secretion of interleukin-6 engaging the NF-kappabeta transcription factor. 1101 49

The major challenge for this generation of children's cancer specialists is to sustain the significant improvement in survival rates, while at the same time minimising treatment-induced late adverse effects. The available evidence suggests that, following first line treatment of acute lymphoblastic leukaemia (ALL), current treatment regimens used in the UK are unlikely to cause sterilisation in either gender. For men who are treated for Hodgkin's disease with 6 or more courses of antineoplastic therapy, azoospermia is the rule. Childhood studies have clearly indicated that the prepubertal testis is not protected from antineoplastic therapy that is potentially sterilising. The interpretation of tests of ovarian function in women treated for cancer in childhood is difficult, but there is increasing evidence of ovarian dysfunction in children treated for Hodgkin's disease. Reassuringly there is no evidence of an increased risk of miscarriage following antineoplastic therapy or an increased number of abnormalities in the offspring. The growth patterns and requirement for growth hormone replacement therapy in children treated for ALL are still unclear. There is good evidence that the intensity and duration of combination cytotoxic antineoplastic therapy received by children with ALL influences the pattern of growth, and that adjuvant antineoplastic therapy for children treated for a brain tumour is an important factor in final height achieved. A child who has been treated for cancer should not be discharged from follow-up. Late effects may have significant implications in later life, and an understanding of these effects is essential to enable balanced decisions to be made regarding the benefits and risks of currently available agents.
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PMID:Late effects of antineoplastic therapy in childhood on growth and endocrine function. 894 94


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