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Your search keyword '"Kerbel, Robert S."' showing total 7 results
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7 results on '"Kerbel, Robert S."'

3. Taxanes Induce a Rapid Mobilization of Different Populations of Circulating Endothelial Progenitors by SDF-1 Modulation in Cancer Patients.

Author

Bono, Anna, primary, Quarna, Jessica, primary, Marighetti, Paola, primary, Calleri, Angelica, primary, Antoniotti, Pierluigi, primary, Mancuso, Patrizia, primary, Voest, Emile E, primary, Langenberg, Marlies, primary, Roodhart, Jeanine, primary, Shaked, Yuval, primary, Kerbel, Robert S, primary, and Bertolini, Francesco, primary

Published
2008
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7. Enhanced natural-killer cell and erythropoietic activities in VEGF-A–overexpressing mice delay F-MuLV–induced erythroleukemia

Author

Cervi, David, Shaked, Yuval, Haeri, Mehran, Usenko, Tatiana, Lee, Christina R., Haigh, Jody J., Nagy, Andras, Kerbel, Robert S., Yefenof, Eitan, and Ben-David, Yaacov

Abstract

We have previously reported that VEGF-A, in combination with MCP-5, contributes to leukemia progression within the splenic microenvironment of mice infected with F-MuLV. To study the influence of constitutively elevated VEGF-A levels on the progression of erythroleukemia, mice heterozygous for a VEGF-A “hypermorphic” allele (Vegfhi/+) were inoculated with F-MuLV. Unexpectedly, a significant delay in erythroleukemia was observed in Vegfhi/+ mice when compared with wild-type controls. These results suggested an altered physiologic response arising from elevated VEGF-A levels that decelerated erythroleukemic progression. Characterization of hematopoiesis in Vegfhi/+ spleens showed a higher natural killer cell activity, elevated B cells, and a decrease in T-cell number. Furthermore, higher erythroid progenitors (ie, CD34+, CD36+, and Ter119+ cells) were evident in the bone marrow, spleen, and peripheral blood of Vegfhi/+ mice. The CFU-E levels were significantly elevated in Vegfhi/+ bone marrow cultures, and this elevation was blocked by a neutralizing antibody to VEGF-A receptor (VEGFR-2). Moreover, erythroleukemic mice were treated with recombinant erythropoietin and, similar to diseased Vegfhi/+ mice, showed a delay in disease progression. We propose that a compensatory erythropoietic response combined with increased natural killer (NK) cell activity account for the extended survival of erythroleukemic, Vegfhi/+ mice.

Published
2007
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