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The Effects of Standard Anthracycline-Based Chemotherapy on Soluble ICAM-1 and Vascular Endothelial Growth Factor Levels in Breast Cancer

Departments of ¹ Psychiatry, ² Medicine, and ³ Surgery, University of California San Diego, San Diego, California; ⁴ University of California, San Diego Cancer Center, San Diego, California; ⁵ University of California, San Diego General Clinical Research Center, San Diego, California; ⁶ Veterans Affairs San Diego Healthcare System; and ⁷ San Diego State University/University of California, San Diego Joint Doctoral Program in Clinical Psychology, San Diego, California

Purpose: The circulating soluble form of intercellular adhesion molecule-1 (sICAM-1) and vascular endothelial growth factor (VEGF) are elevated in women with breast cancer and associated with tumor progression and poor prognosis. This study examined the effects of anthracycline-based chemotherapy on plasma sICAM-1 and VEGF, as well as soluble P-selectin, von Willebrand factor, and interleukin-6 levels.

Experimental Design: Twenty-six women diagnosed with stage I–IIIA breast cancer (mean age, 48.4 ± 10.4 years; range, 34–79 years) were studied before (week 1) and at weeks 2 and 3 of cycles 1 and 4 of chemotherapy.

Results: The initial effect of chemotherapy was to reduce sICAM-1 levels; compared with pretreatment, sICAM-1 levels were decreased at week 2 of both cycles (P values < 0.01). sICAM-1 levels were elevated, however, at the start of cycle 4 as compared with pretreatment (P < 0.01). Chemotherapy led to an increase in sICAM-1 levels in node-positive but not node-negative patients (P < 0.01). VEGF levels were decreased at week 2 of cycle 4 (P = 0.001) and remained so at week 3. Similar to sICAM-1, VEGF levels were elevated at the start of cycle 4 as compared with pretreatment (P < 0.006). Soluble P-selectin levels decreased during week 2 of cycle 4 (P = 0.026). Neither interleukin-6 or von Willebrand factor were significantly changed in response to chemotherapy.

Conclusions: The findings support prior studies suggesting that sICAM-1 levels derive from sources other than endothelial cells. In addition, whereas the more immediate effect of chemotherapy is to reduce sICAM-1 and VEGF, continued treatment may lead to significant elevations.

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