Serum Myeloperoxidase in Leukaemia and Polycythaemia vera

Malmquist, Jörgen

doi:10.1111/j.1600-0609.1972.tb00946.x

Cited by 17 publications

(2 citation statements)

References 23 publications

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“…IL6 [1383], CSF3 [1384], SOCS3 [1385], CCL3 [1386], CCL5 [1387], VCAM1 [1388], CCL2 [1387], CXCL12 [1389], KLF10 [1390], FRZB (frizzled related protein) [1391], DUSP1 [1392], IL1B [1393], CCL11 [1394], LMNA (lamin A/C) [1395], WIF1 [1396], IL1RN [1397], IFNG (interferon gamma) [1398], CX3CL1 [1399], BMP2 [1400], CDKN1A [1401], BMP4 [1402], ICAM1 [1403], CD34 [1404], IL33 [1405], FASLG (Fas ligand) [1406], KDM6B [1407], TNF (tumor necrosis factor) [1408], GDF15 [1409], IL2 [1410], INPP4B [1411], FABP4 [1412], CYP2C19 [1413], CXCR4 [1414], DKK2 [1415], PLCB4 [1416], ANXA1 [1417], DUSP6 [1418], CORIN (corin, serine peptidase) [1419], F8 [1420], DDIT4 [1421], IL1R2 [1422], S100A4 [1417], CTSL (cathepsin L) [1423], PTX3 [1424], EFNB1 [1425], MCF2L [1426], FZD4 [1427], CCL26 [1428], PHGDH (phosphoglycerate dehydrogenase) [1429] and FDPS (farnesyl diphosphate synthase) [1430] have been identified as predictive biomarkers of osteoporosis. IL6 [1431], SOCS2 [1432], SOCS3 [1432], DUSP1 [1433], MLF1 [1434], EPHA2 [1435], CD34 [1436], IL33 [1437], GDF15 [1438], IL2 [1439], CD177 [1440], G6PD [1441], NFE2 [1442], PTX3 [1443], IDH1 [1444], MPO (myeloperoxidase) [1445] and KLK1 [1446] might be associated with the pathogenesis of polycythemia. The abnormal expression of IL33 [1447] and TNF (tumor necrosis factor) [1448] contributes to the pneumothorax.…”

Section: Discussionmentioning

confidence: 99%

“…A recent study found that the S100A9 [239], FKBP5 [240], SNCA (synuclein alpha) [221] and MPO (myeloperoxidase) [256] are crucial for the progression of depression and anxiety. Regulation of MPO (myeloperoxidase) [1445] and CD177 [1440] levels might be a novel treatment option against polycythemia. The results of this investigation suggest that novel biomarkers include MYC (MYC proto-oncogene, bHLH transcription factor), RPS6KA2, SH2D1A, JUNB (JunB proto-oncogene, AP-1 transcription factor subunit), FOS (Fos proto-oncogene, AP-1 transcription factor subunit), RAB39A and RAB15 might play a key role in the pathogenesis of COPD.…”

Section: Discussionmentioning

confidence: 99%

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Identification of key genes and biological pathways in chronic obstructive pulmonary disease using bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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Identification of accurate biomarkers is still particularly urgent for improving the poor survival of chronic obstructive pulmonary disease (COPD) patients. In this investigation, we aimed to identity the potential biomarkers in COPD via bioinformatics and next generation sequencing (NGS) data analysis. In this investigation, the differentially expressed genes (DEGs) in COPD were identified using NGS dataset (GSE239897) from Gene Expression Omnibus (GEO) database. Subsequently, gene ontology (GO) and pathway enrichment analysis was conducted to evaluate the underlying molecular mechanisms involved in progression of COPD. Protein-protein interaction (PPI), modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network analysis were performed to determine the hub genes, miRNAs and TFs. The receiver operating characteristic (ROC) analysis was performed to determine the diagnostic value of hub genes. A total of 956 overlapping DEGs (478 up regulated and 478 down regulated genes) were identified in the NGS dataset. DEGs were mainly associated with GO functional terms and pathways in cellular response to stimulus. response to stimulus, immune system and neutrophil degranulation. There were 10 hub genes (MYC, LMNA, VCAM1, MAPK6, DDX3X, SHMT2, PHGDH, S100A9, FKBP5 and RPS6KA2) identified by PPI, modules, miRNA-hub gene regulatory network and TF-hub gene regulatory network analysis. In conclusion, the DEGs, relative GO terms, pathways and hub genes identified in the present investigation might aid in understanding of the molecular mechanisms underlying COPD progression and provide potential molecular targets and biomarkers for COPD.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Identification of key genes and biological pathways in chronic obstructive pulmonary disease using bioinformatics and next generation sequencing data analysis

Vastrad,

Vastrad

2024

Preprint

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Tissue peroxidase in the normal and neoplastic salivary gland

Armstrong

Wormer

Dimmitt

1991

Clinical Laboratory Analysis

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Peroxidase activity was measured by two colorimetric methods in six neoplastic tumors of the parotid salivary gland. When p-phenylenediamine was used as the hydrogen donor co-substrate, peroxidase activity was absent or reduced from 6 to 22% of normal in these tumors. Cross reactivity with normal peroxidase antibody could not be demonstrated in tumors exhibiting negative activity. Two neoplastic salivary glands had well-described, encapsulated tumors which showed reduced peroxidase activity when compared with the normal uninvolved portion. However, when guaiacol was substituted for p-phenylenediamine, normal activity was recorded. After dialysis, peroxidase activity was not enhanced. Mixing experiments showed no effect of the tumor extract on the peroxidase activity of normal saliva, nor on salivary gland supernatant. Normal salivary gland peroxidase was inhibited 90% by 10(-2) g/L amino-triazole, but neoplastic tumors were inhibited less (13 and 73%). It is suggested that peroxidase is a simple marker for the detection of neoplasia and can be of value in the differentiation of benign tumors.

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Self-labeling of human polymorphonuclear leucocyte myeloperoxidase with125iodine

Deby‐Dupont

Pincemaïl

Thirion³

et al. 1991

Experientia

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In order to obtain a radioimmunoassay (RIA) technique for the measurement of human plasma myeloperoxidase (MPO), we purified the enzyme from polymorphonuclear granulocytes (neutrophils), and compared three methods of labeling it with 125Iodine:chloramine T, lactoperoxidase, and an original technique of 'self labeling' based on the ability of the enzyme to oxidize and bind 125I in the presence of H2O2. The chloramine T technique produced a degraded protein, as well shown by a high non-specific binding of tracer to antibody. The lactoperoxidase technique did not succeed in labeling MPO with an adequate specific activity. In contrast, the self-labeling method gave a stable tracer with a specific activity of 23 microCi/micrograms MPO (85 MBq), a satisfactory level of immunoreactivity, and a low-specific binding (less than or equal to 3%). After labeling, purification of tracer was achieved by gel filtration chromatography in phosphate buffer (0.05 M; pH7) to which 0.1% poly-L-lysine was added. The labeled molecule remained stable for 40 days and could be used for RIA with a polyclonal antibody raised in rabbits.

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Serum Myeloperoxidase in Leukaemia and Polycythaemia vera

Cited by 17 publications

References 23 publications

Identification of key genes and biological pathways in chronic obstructive pulmonary disease using bioinformatics and next generation sequencing data analysis

Identification of key genes and biological pathways in chronic obstructive pulmonary disease using bioinformatics and next generation sequencing data analysis

Tissue peroxidase in the normal and neoplastic salivary gland

Self-labeling of human polymorphonuclear leucocyte myeloperoxidase with125iodine

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