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Letters to the Editor |
1 Laboratori Anàlisis Clíniques, and,
2
Secció Oncologia, Hospital General de Manresa, Althaia Xarxa Asistencial de Manresa, La Culla, s/n, 08240 Manresa (Barcelona), Spain
aAuthor for correspondence. Fax 34-93-8743859; e-mail hgmlaboratorio{at}aehh.org.
To the Editor:
Vascular endothelial growth factor (VEGF) may play a role in tumor growth. Several biological activities of VEGF favor the growth of solid tumors, including mitogenic activity for vascular endothelial cells and inhibition of immature dendritic cells with a consequent decrease in immunity. VEGF is regulated by hypoxia, growth factors, interleukin-1 and -6, the oncogene ras, and the tumor suppressor gene p53 (1).
The role of VEGF in non-small cell lung cancer (NSCLC) patients treated with chemotherapy in still undetermined. We studied the serum concentrations of this cytokine in NSCLC patients with advanced disease and its correlation with carcinoembryonic antigen (CEA), CYFRA 21-1, CA125, and C-reactive protein (CRP).
We analyzed 33 healthy individuals, 23 patients with benign pulmonary disease (13 with obstructive pulmonary disease and 10 with asthma), and 24 NSCLC patients (5 with stage IIIA, 10 with stage IIIB, and 9 with stage VI) treated with platinum-based chemotherapy [10 treated with cisplatin/etoposide (100/80 mg per m2) and 14 treated with carboplatin/taxol (6 AUC/225 mg per m2)]. Of those, 14 had squamous cell carcinoma, 7 had adenocarcinoma, and 3 had large cell carcinoma.
We measured serum concentrations of VEGF by ELISA [R&D Systems; interassay imprecision (CV), 10%]; CEA (CV, 4.2%), CA125 (CV, 5.3%), and CYFRA 21-1 (CV, 3.7%) by Elecsys 2010 (Roche Diagnostics); and CRP by an immunoturbidimetric method (Roche Tinaquant CRP; CV, 5.7%). Samples were collected at the time of initial diagnosis. Response and staging were determined by physical examination, chest radiography, and thoracic and abdominal computerized tomography scans. Statistical analyses included the 
2 test, Kaplan–Meier analysis, logistic regression, the Pearson correlation coefficient, and the Wilcoxon test.
Serum VEGF concentrations [mean (SD)] were significantly higher in patients with NSCLC [541 (232) ng/L] than in patients with benign disease [231 (144) ng/L] or healthy individuals [208 (122) ng/L; P <0.001]. VEGF showed a sensitivity of 62% and specificity of 95% at a cutoff of 450 ng/L. There were no significant differences in serum VEGF concentrations with histologic type or disease stage.
Shown in Table 1
are the results for the tumor markers, VEGF, and CRP categorized by clinical findings. VEGF was not significantly correlated with response to treatment or with CA125 (r = -0.028; P not significant), CEA (r = 0.084; P not significant), or CYFRA 21-1 (r = 0.035; P not significant), but it was significantly correlated with CRP (r = 0.34; P = 0.040).
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Kaplan–Meier analysis showed no significant survival differences between patients with serum VEGF >450 ng/L (median survival, 9.0 months) and those with VEGF <450 ng/L (median survival, 13.5 months). Patients with a partial or complete response to treatment had a higher survival (median survival, 15 months) than those who showed stabilization or progression of disease (median survival, 6 months; P = 0.001).
NSCLC patients have higher VEGF serum concentration than healthy individuals or patients with benign pulmonary disease. That we found no differences between histologic type or clinical stage in advanced disease may be because all patients had large tumors (stages IIIA–IV). We observed a trend of higher survival in patients who responded to treatment as well as in patients with low VEGF concentrations, although for the latter group the trend lacked statistical significance, as in previous studies (2)(3). The lack of association between tumor markers and VEGF contrasts with the findings in colon cancer (4). In contrast to the expression in tissue (5), we found no relationship between serum VEGF and clinical response. It is possible that plasma VEGF depends on factors other than tumor secretion; hypoxia and inflammation may also alter circulating VEGF concentrations (1)(6).
References
The following articles in journals at HighWire Press have cited this article:
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  B. van de Langerijt, J. M. Gijtenbeek, H.P.M. de Reus, F. C.G.J. Sweep, A. Geurts-Moespot, J. C.M. Hendriks, A. C. Kappelle, and M. M. Verbeek CSF levels of growth factors and plasminogen activators in leptomeningeal metastases. Neurology, July 11, 2006; 67(1): 114 - 119. [Abstract] [Full Text] [PDF]
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 R. Zimmermann, J. Koenig, J. Zingsem, V. Weisbach, E. Strasser, J. Ringwald, and R. Eckstein Effect of Specimen Anticoagulation on the Measurement of Circulating Platelet-Derived Growth Factors Clin. Chem., December 1, 2005; 51(12): 2365 - 2368. [Full Text] [PDF]
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