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Titolo:
Serine proteinase activation in esophageal cancer
Autore:
Tang, WH; Friess, H; Kekis, PB; Martignoni, ME; Fukuda, A; Roggo, A; Zimmermann, A; Buchler, MW;
Indirizzi:
Univ Bern, Inselspital, Dept Visceral & Transplantat Surg, CH-3010 Bern, Switzerland Univ Bern Bern Switzerland CH-3010 antat Surg, CH-3010 Bern, Switzerland Univ Bern, Inselspital, Inst Pathol, CH-3010 Bern, Switzerland Univ Bern Bern Switzerland CH-3010 nst Pathol, CH-3010 Bern, Switzerland
Titolo Testata:
ANTICANCER RESEARCH
fascicolo: 4A, volume: 21, anno: 2001,
pagine: 2249 - 2258
SICI:
0250-7005(200107/08)21:4A<2249:SPAIEC>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
UROKINASE-PLASMINOGEN-ACTIVATOR; GROWTH-FACTOR-ALPHA; HUMAN PANCREATIC-CANCER; ENHANCED EXPRESSION; PROSTATE-CANCER; FACTOR RECEPTOR; COLON-CANCER; SERUM LEVELS; METASTASIS; TUMOR;
Keywords:
urokinase plasminogen activator; urokinase plasminogen activator receptor; plasminogen activator inhibitor; Northern blot analysis; immunohistochemistry;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Friess, H Univ Bern, Inselspital, Dept Visceral & Transplantat Surg, CH-3010 Bern, Switzerland Univ Bern Bern Switzerland CH-3010 , CH-3010 Bern, Switzerland
Citazione:
W.H. Tang et al., "Serine proteinase activation in esophageal cancer", ANTICANC R, 21(4A), 2001, pp. 2249-2258

Abstract

Background: Activation of the plasminogen/plasmin system seems to contribute to tumor aggressiveness and shorter post-operative survival. In the present study we examined the relation of uPA (urokinase plasminogen activator), uPAR (uPA receptor) and PAI-1 (plasminogen activator inhibitor type 1) tothe biological growth behavior of esophageal cancer, as well as their influence on survival in esophageal cancer. Materials and Methods: The expression and distribution of uPA, uPAR and PAI-1 were analyzed by Northern blot analysis and immunostaining in 41 resected esophageal cancers and in normal esophagi. Results: Northern blot analysis revealed a 5.0-, 3.6- and 5.4-fold increase in uPA, uPAR, and PAI-1 mRNA levels in esophageal cancer, respectively, in comparison to normal controls (p <0.01). These mRNA moieties were concomitantly increased in 86% of the tumors. uPA activity was 2.3-fold increased in esophageal cancer compared with normal controls (p <0.01). Statistical analysis revealed no differences in uPA, uPAR and PAI-1 immunoreactivity between well-differentiated, moderately-differentiated and poorly-differentiated tumors. Furthermore, survival analysis showed no difference in patients whose tumors exhibited positive uPA and uPAR immunostaining (median 11 months, range 4-36 months) versus patients whose tumors exhibited negative uPA and uPAR immunostaining (median 11 months, range 3-51 months). Conclusion: Our data revealed that overexpression of uPA, uPAR and PAI-1 is often present in human esophageal carcinomas. However, up-regulation of thesefactors is not correlated with tumor differentiation or survival. These findings indicate that, unlike other tumors, uPA, uPAR and PAI-1 seem not to be prognostic markers for esophageal carcinomas.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 13:22:20