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Differentiated expression of the lactate dehydrogenase subunit M in pleural fluids of neoplastic aetiology

J Kotyza, D Havel, V Kulda, K Bunatova, M Pesek

. 2009 ; 69 (1) : 73-78.

Jazyk angličtina Země Norsko

Perzistentní odkaz   https://www.medvik.cz/link/bmc11006069
E-zdroje Online

NLK Medline Complete (EBSCOhost) od 1998-05-19 do Před 1 rokem

OBJECTIVE: An anaerobic type of glycolysis exemplified by hyperproduction of the lactate dehydrogenase (LDH) subunit M has been detected in lung tumours, while a similar pattern has been found in concomitant pleural effusions (PE). The aim of this study was to verify the presence of the LDH subunit M in PEs of different aetiology and to compare its expression with markers of inflammation. MATERIAL AND METHODS: LDH isoenzymes were estimated and the LDH5/LDH1 coefficient was calculated in paraneoplastic PEs (n = 99), including subgroups with a different tumour ultrastructure, origin and pleural involvement. The expression pattern was compared with parainflammatory PEs (n = 21), transudates (n = 16) and with the expression of 13 inflammatory markers in PEs. RESULTS: The LDH5/LDH1 coefficient was higher in PEs associated with non-small-cell lung cancer (NSCLC) and with pleura-invading tumours, and lower in PEs of small-cell lung cancer and tumours without a confirmed pleural involvement. The LDH5/LDH1 coefficient positively correlated with uPA, IL-8, IL-10, sICAM, sVCAM, MPO and MMP-9. CONCLUSIONS: In accordance with inflammatory markers, it appears that the expression of LDH and its isoenzymes in PEs reflects the host reaction in pleural space and, in NSCLC, may also feature the anaerobic phenotype of cancer cells.

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$a OBJECTIVE: An anaerobic type of glycolysis exemplified by hyperproduction of the lactate dehydrogenase (LDH) subunit M has been detected in lung tumours, while a similar pattern has been found in concomitant pleural effusions (PE). The aim of this study was to verify the presence of the LDH subunit M in PEs of different aetiology and to compare its expression with markers of inflammation. MATERIAL AND METHODS: LDH isoenzymes were estimated and the LDH5/LDH1 coefficient was calculated in paraneoplastic PEs (n = 99), including subgroups with a different tumour ultrastructure, origin and pleural involvement. The expression pattern was compared with parainflammatory PEs (n = 21), transudates (n = 16) and with the expression of 13 inflammatory markers in PEs. RESULTS: The LDH5/LDH1 coefficient was higher in PEs associated with non-small-cell lung cancer (NSCLC) and with pleura-invading tumours, and lower in PEs of small-cell lung cancer and tumours without a confirmed pleural involvement. The LDH5/LDH1 coefficient positively correlated with uPA, IL-8, IL-10, sICAM, sVCAM, MPO and MMP-9. CONCLUSIONS: In accordance with inflammatory markers, it appears that the expression of LDH and its isoenzymes in PEs reflects the host reaction in pleural space and, in NSCLC, may also feature the anaerobic phenotype of cancer cells.
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