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)

An analysis of red cell membrane proteins in acute and chronic lymphatic leukaemia, Hodgkin's disease, lymphosarcoma, and myeloma was carried out. The electrophoretic pattern after solubilisation in urea or SDS was examined, along with migration on cellulose acetate or acrylamide in different buffers. Protein acid, basic and neutral amino acid percentages were also determined. An increase in low molecular weight and faster anodic migration proteins was noted in the lymphoblastoses, whereas the amino acid spectrum of these proteins showed percent changes in the case of some amino acids, particularly glutamic acid, phosphoserine, lysine and histidine. The alterations observed were compared with those noted previously in other haemoblastoses, congenital haemolytic and anhaemolytic blood diseases, and endoglobular or acquired metabolic defects in a closer assessment of their significance.
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PMID:[Changes in membrane proteins in the erythrocytes of patients with hemolymphoblastosis not directly involving the erythroblastic line]. 106 86

We performed analyses of electrolytes, amino acids, albumin, alpha 2-macroglobulin, gamma-globulin and LDH in the lumbar cerebrospinal fluid of children undergoing treatment for acute lymphoblastic leukemia, non-Hodgkin-lymphoma or acute myeloid leukemia. At the time of diagnosis signs of a disturbance of the blood-brain barrier were found in some patients. During induction treatment with L-asparaginase a rise of glutamic acid and a decrease of glutamine occurred. This finding correlated with slowing of the EEG. Treatment with vincristine was associated with a slight drop of sodium and chloride concentration in serum, but not in the cerebrospinal fluid. Central nervous system prophylaxis with cranial irradiation, and to a lesser degree with intravenous medium-dose methotrexate, gave rise to a further deterioration of the blood-brain barrier function as indicated by an increase in albumin, alpha 2-macroglobulin and LDH levels. During radiotherapy the concentration of several amino acids rose, probably due to a disturbance of active carrier mechanisms. Patients with elevated albumin at the end of radiotherapy more often suffered an early leukemia relapse while still on treatment. No other clinical or electroencephalographic correlations of altered barrier function could be found.
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PMID:Electrolytes, amino acids and proteins in lumbar CSF during the treatment of acute leukemia in childhood. 233 48

We have applied our recently developed approach for quantitative generation and estimation of membrane potential differences (Berteloot, A. (1986) Biochim. Biophys. Acta 857, 180-188) to the reevaluation of glutamic acid transport rheogenicity in rabbit jejunal brush-border membrane vesicles. Membrane diffusion-potentials were created by altering iodide concentrations in the intra- and extravesicular compartments while keeping isosmolarity, isotonicity and ionic strength constant by chloride replacement. The known value of ion permeabilities relative to sodium in this preparation also allows calculation of membrane potential differences using the Goldman-Hodgkin-Katz equation. This strategy appears superior to more classical methods involving ionophore-induced membrane diffusion-potentials of protons or potassium as both cations have been shown to participate in the transport mechanism. In this paper, we demonstrate that this approach is perfectly suitable for the investigation of membrane potential dependency of glutamic acid transport as our results showed that chloride replacement by iodide did not affect uptake in vesicles with membrane potential clamped to zero by gramicidin D (sodium conditions) or by gramicidin D plus valimonycin (sodium + potassium conditions). The method thus allows to dissociate membrane potential effects from possible effects that might be introduced by altering the anion species. In these conditions, our studies clearly demonstrate that glutamic acid uptake, whether analyzed over a 1 min time scale or under initial rate conditions, was sensitive to membrane potential differences. However, our results also show that the electrogenicity of the transport system varied depending upon the intravesicular presence or absence of potassium, its presence stimulating the membrane potential dependency of uptake. This effect is modulated by the internal pH and it is concluded that inside H+ and K+ are not equivalent as countertransported cations. The external pH also seems to modulate the response to potential by acting on the fully loaded form(s) of the transporter. The possibility that outside H+ competes for (an) external Na+ binding site(s) and/or precludes the attachment of (an) extra sodium ion(s) should be considered.
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PMID:Membrane potential dependency of glutamic acid transport in rabbit jejunal brush-border membrane vesicles: K+ and H+ effects. 287 28

Although numerous studies have demonstrated increased expression of p53 protein in the Reed-Sternberg cells of Hodgkin's disease, little data exist as to whether mutations of the p53 gene is a common occurrence in this neoplasm. Using a microdissection technique coupled with PCR, single-strand conformation analysis, and DNA sequencing, we studied 23 cases of Hodgkin's disease for mutations within exons 5 to 8 of the p53 gene. We found seven mutations within six cases; six were missense mutations. An identical missense mutation was found in three cases (codon 243, methionine to isoleucine), and another identical missense mutation was found in an additional two cases (codon 204, glutamic acid to lysine). Verification of the mutations was accomplished either by direct Southern blotting of PCR-amplified p53 exon products from re-extracted DNA or by hybridization of cloned PCR-amplified p53 exon products from re-extracted DNA with a mutant-specific oligonucleotide. There was no good correlation between the presence of p53 mutations and the level of p53 protein expression, which was found to be overexpressed in all cases, the level of MDM2 protein expression, or the proliferation rate as determined by K-67 antibody. None of the cases with p53 mutation had evidence of Epstein-Barr virus within the Reed-Sternberg cells, as compared with 7 of 17 of the other cases (p < 0.06). These results suggest that p53 mutation may represent an important mechanism in the pathogenesis of Hodgkin's disease, and this mechanism may be independent of Epstein-Barr virus.
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PMID:p53 mutations in Hodgkin's disease. 887 83