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Annals of Oncology 14:1660-1666, 2003
© 2003 European Society for Medical Oncology

Original Paper

Paclitaxel for anthracycline-resistant AIDS-related Kaposi’s sarcoma: clinical and angiogenic correlations

J. Stebbing1,2, A. Wildfire1, S. Portsmouth1, T. Powles1, C. Thirlwell1, P. Hewitt3, M. Nelson1, S. Patterson2, S. Mandalia1, F. Gotch2, B. G. Gazzard1 and M. Bower1,+

1 Departments of Oncology and HIV Medicine, Chelsea and Westminster Hospital, London; 2 Department of Immunology, Division of Investigative Science, Faculty of Medicine, Imperial College of Science Technology and Medicine, Chelsea and Westminster Hospital, London; 3 Bristol-Myers Squibb Pharmaceuticals Limited, London, UK

Received 13 March 2003; revised 23 May 2003; accepted 12 August 2003

Background:

Murine data indicate that angiogenesis is central to the aetiopathogenesis of Kaposi’s sarcoma (KS). Therefore, we measured angiogenic cytokines and growth factors in patients with AIDS-related KS during treatment with both antiretrovirals and second-line paclitaxel chemotherapy. Cytokines measured included tumour necrosis factor-{alpha} (TNF-{alpha}), basic fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and the interleukins IL-2, -6 and -12.

Patients and methods:

Enzyme-linked immunosorbent assays (ELISAs) were carried out to measure plasma cytokine levels in 17 patients with AIDS-related KS who had progressed within 6 months of receiving liposomal anthracyclines and were treated with paclitaxel 100 mg/m2 every 2 weeks. Measurements were carried out before progression, at commencement and at the completion of paclitaxel.

Results:

The objective response rate to paclitaxel was 71% (95% confidence interval 60% to 81%). In 17 patients with AIDS-related KS, we observed eight partial responses and four complete responses. Patients with AIDS Clinical Trial Group stage T1 disease had higher plasma VEGF (P = 0.05) and lower plasma TNF-{alpha} levels (P = 0.05) than patients with earlier stage T0 KS. There were no correlations between plasma cytokines (bFGF, VEGF, TNF-{alpha}, and IL-2,-6 and -12) and the CD4 and CD8 cell counts or HIV-1 RNA viral load. Response to paclitaxel was associated with a fall in plasma IL-6 levels (P = 0.04) but no change in other cytokines. There were no significant changes in CD4, CD8, CD16/56, CD19 cell counts and HIV-1 viral loads during chemotherapy.

Conclusions:

Angiogenic cytokines may correlate with KS disease extent but not with cellular immune function or HIV viraemia. Response to paclitaxel therapy correlates with a fall in plasma IL-6 levels and recent data indicate this may be a surrogate marker of KS-associated herpesvirus viral load. Overall, clinical response in KS correlates poorly with known angiogenic cytokines.

Key words: AIDS, angiogenesis, cytokines, human immunodeficiency virus, Kaposi’s sarcoma, paclitaxel


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