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Journal of Clinical Oncology, 2004 ASCO Annual Meeting Proceedings (Post-Meeting Edition).
Vol 22, No 14S (July 15 Supplement), 2004: 578
© 2004 American Society of Clinical Oncology
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Abstract

A pilot study to evaluate response and angiogenesis after treatment with bevacizumab in patients with inflammatory breast cancer

S. B. Wedam, J. A. Low, X. Yang, C. Chow, A. Berman, R. Eulate, D. Danforth, S. M. Hewitt, S. M. Steinberg and S. M. Swain

Cancer Therapeutics Branch, CCR, NCI, Bethesda, MD; DRD, CC, NIH, Bethesda, MD; Medical Oncology Clinical Research Unit, CCR, NCI, Bethesda, MD; Surgery Branch, CCR, NCI, Bethesda, MD; Laboratory of Pathology, CCR, NCI, Bethesda, MD; Biostatistics and Data Mgmt Section, CCR, NCI, Bethesda, MD

578

Background: Inflammatory breast cancer (IBC) is an aggressive form of breast cancer associated with vascular and lymphatic invasion. Previously untreated IBC patients received bevacizumab (BV), a recombinant humanized monoclonal antibody to VEGF, to evaluate endothelial cell proliferation (CD31/Ki67), tumor cell proliferation (Ki67), tumor microvessel density (MVD), VEGF, and vascular permeability (k21) on dynamic contrast enhanced MRI (dMRI). Methods: Treatment consisted of BV alone for cycle (C) 1 (15mg/m2 on day 1) followed by six cycles of BV (15mg/m2) with doxorubicin (50mg/m2) and docetaxel (75mg/m2) q3wk and G-CSF in C2–7. Following mastectomy and radiation, BV was given for eight more cycles with hormonal therapy for ER+ pts. Tumor core biopsies and dMRI were obtained at baseline, after C1, 4, 7. Results: Sixteen pts enrolled received 125 cycles of treatment. Pts: Stage III 87.5% and IV 12.5%, ER+ 38%, Her2 positive 12.5%. Post-chemo, thirteen pts (3 too early to evaluate): 8PRs, 1PR unconfirmed, 1PD. A decrease in CD31/Ki67 was seen after BV treatment alone (-1% median change, p=0.031). There were no decreases in Ki67 or MVD after BV alone (p=0.97 and 0.70) or BV and chemotherapy (p=0.23 and 0.85). There were significant decreases in k21 after treatment (n=12), with a median change of -53% (p=0.019) after C1, -70% (p=0.001) after C4, and -56% (p=0.008) after C7. In patients with PR there were trends towards a decrease in VEGF after C1(-57% median change, p=0.09) and decrease in Ki67 after C4/C7 (-57% median change, p=0.09). There were no correlations between k21and CD31/Ki67 index, Ki67, or VEGF after BV alone (n=11); but a trend towards a correlation between VEGF and k21 after BV and chemotherapy (r=0.62, p=0.10). Most common grade 3/4 toxicities (n=16): neutropenia (63%), diarrhea (25%), HTN (25%), and febrile neutropenia (19%). Conclusions: Preliminary results revealed a decrease in vascular permeability on dMRI and endothelial cell proliferation with BV treatment alone. In responding pts, there were trends toward a decrease in VEGF after BV and tumor cell proliferation after BV and chemotherapy.

No significant financial relationships to disclose.

Abstract presentation from the 2004 ASCO Annual Meeting




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Copyright © 2004 by the American Society of Clinical Oncology, Online ISSN: 1527-7755. Print ISSN: 0732-183X
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