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Rafael Tejada

Researcher at Cornell University

Publications -  6
Citations -  1812

Rafael Tejada is an academic researcher from Cornell University. The author has contributed to research in topics: Haematopoiesis & Progenitor cell. The author has an hindex of 4, co-authored 6 publications receiving 1768 citations.

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Chemokine-mediated interaction of hematopoietic progenitors with the bone marrow vascular niche is required for thrombopoiesis.

TL;DR: It is reported that chemokine-mediated interactions of megakaryocyte progenitors with sinusoidal bone marrow endothelial cells (BMECs) promote thrombopoietin (TPO)-independent platelet production, and progenitor-active chemokines offer a new strategy to restore hematopoiesis in a clinical setting.
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Inhibition of human leukemia in an animal model with human antibodies directed against vascular endothelial growth factor receptor 2. Correlation between antibody affinity and biological activity.

TL;DR: Two fully human anti-KDR antibodies are produced, from Fab fragments originally isolated from a large antibody phage display library, that strongly inhibited VEGF-induced migration of human leukemia cells in vitro, and when administered in vivo, significantly prolonged survival of NOD-SCID mice inoculated withhuman leukemia cells.
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Angiogenic factors reconstitute hematopoiesis by recruiting stem cells from bone marrow microenvironment.

TL;DR: Functional vascular endothelial growth factor receptor‐1 (VEGFR1, Flt‐1) is expressed on a subpopulation of human and mouse Lin−Sca‐1+c‐Kit+ BM‐repopulating stem cells, conveying signals for recruitment of HSCs and reconstitution of hematopoietic recovery.
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Newly Discovered Polymorphism in the CD34+ Stem Cell Specific AC133-P1 Promoter Linked to Leukemias.

TL;DR: Preliminary data suggest that hematopoietic stem cells express only one AC133 isoform and four allelic variants in the AC133-P1 promoter, which differ by the number of short tandem repeats as well as by a single nucleotide polymorphism (SNP), might lay a foundation for testing a risk of susceptibility to AC133+ leukemias.