High pre‐treatment serum level of vascular endothelial growth factor (VEGF) is associated with poor outcome in small‐cell lung cancer
Vascular endothelial growth factor (VEGF) is an important regulator of angiogenesis and vascular permeability. Increased serum VEGF concentrations (S‐VEGF) have been found in patients with various types of human cancer, including cancer of the lung. However, the clinical and prognostic significance...
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Veröffentlicht in: | International journal of cancer 1998-04, Vol.79 (2), p.144-146 |
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Zusammenfassung: | Vascular endothelial growth factor (VEGF) is an important regulator of angiogenesis and vascular permeability. Increased serum VEGF concentrations (S‐VEGF) have been found in patients with various types of human cancer, including cancer of the lung. However, the clinical and prognostic significance of S‐VEGF in cancer is unknown. We measured S‐VEGF, using enzyme‐linked immunosorbent assay, in sera taken from 68 untreated patients with small‐cell lung cancer (SCLC) at the time of diagnosis. The patients were treated with 6 cycles of cisplatin and etoposide, and were randomly assigned to receive recombinant interferon, leukocyte interferon or neither. S‐VEGF ranged from 70 to 1 738 pg/ml (mean, 527 pg/ml). The patients who achieved partial or complete response to treatment had lower pre‐treatment S‐VEGF than the non‐responding patients (p = 0.0083, Mann‐Whitney test). High (>527 pg/ml) S‐VEGF was associated with poor survival (p = 0.012, Log Rank Test), and all 3‐year survivors had lower than mean pre‐treatment S‐VEGF. In a multivariate analysis, S‐VEGF and stage were the only independent prognostic factors, and the estimated 3‐year survival of the patients with limited stage disease and low pre‐treatment S‐VEGF (n = 17, 25% of all patients) was 41% (p = 0.0055, log rank test). These data show that high pre‐treatment S‐VEGF is associated with poor response to treatment and unfavourable survival in patients with SCLC treated with combination chemotherapy with or without interferon. Int. J. Cancer (Pred. Oncol.) 79:144–146, 1998.© 1998 Wiley‐Liss, Inc. |
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ISSN: | 0020-7136 1097-0215 |
DOI: | 10.1002/(SICI)1097-0215(19980417)79:2<144::AID-IJC8>3.0.CO;2-T |